RESUMEN

Background: The mechanisms through which acculturation influences the onset of cognitive impairment and dementia are not well understood, especially among older Hispanics. Objective: To investigate whether inflammation and psycho-behavioral factors mediate the relationship between acculturation and incident dementia among older Mexican Americans. Methods: We analyzed the Sacramento Area Latino Study on Aging (1998-2007, SALSA), a longitudinal study (N = 1,194) with 10 years of follow-up, and used g-computation for mediation analysis with pooled logistic regression to evaluate whether acculturation (assessed by the Revised Acculturation Rating Scale for Mexican Americans [ARSMA-II]) affected dementia or cognitive impairment but not dementia (CIND) through inflammation (i.e., interleukin 6 [IL-6], tumor necrosis factor-α (TNF-α), high-sensitivity C-reactive protein [hs-CRP]), smoking, alcohol consumption, and depressive symptoms. The potential mediators were assessed at baseline. Results: The 10-year average adjusted risk ratio (aRR) for the effect of high U.S. acculturation and dementia/CIND was 0.66, 95% CI (0.36, 1.30). The indirect effects were: IL-6 (aRR = 0.98, 95% CI (0.88, 1.05)); TNF-α (aRR:0.99, 95% CI (0.93, 1.05)); hs-CRP: (aRR = 1.21, 95% CI (0.84, 1.95)); current smoking: aRR = 0.97, 95% CI (0.84, 1.16); daily/weekly alcohol consumption (aRR = 1.00, 95% CI (0.96, 1.05)); and depressive symptom score (aRR = 1.03, 95% CI (0.95, 1.26)). Hs-CRP yielded a proportion mediated of -26%, suggesting that hs-CRP could suppress the potential effect of high U.S. acculturation. The other factors explored resulted in little to no mediation. Conclusions: The effect of acculturation on time to incident dementia/CIND varied over time. Our study suggests that inflammation could suppress the effect between high U.S. acculturation and dementia risk.

Asunto(s)

Aculturación , Demencia , Inflamación , Americanos Mexicanos , Humanos , Demencia/etnología , Demencia/epidemiología , Demencia/psicología , Americanos Mexicanos/psicología , Americanos Mexicanos/estadística & datos numéricos , Masculino , Femenino , Anciano , Inflamación/sangre , Inflamación/etnología , Inflamación/psicología , Estudios Longitudinales , Anciano de 80 o más Años , Incidencia , Factores de Riesgo , Proteína C-Reactiva/metabolismo , Depresión/etnología , Depresión/psicología , Depresión/epidemiología , Interleucina-6/sangre

RESUMEN

BACKGROUND: Inflammation-related proteins constitute a promising avenue in studying biological correlates of major depressive disorder (MDD). However, MDD is a heterogeneous condition - a crucial aspect to be considered in association studies. We examined whether inflammatory proteins are associated with categorical diagnosis, a dimensional total sum-score, and specific depressive symptoms among youths. METHODS: We analyzed data from the 1993 Pelotas Birth Cohort, a population-based study in Brazil that followed individuals up to age 22 years. Categorical psychiatric diagnoses were derived using adapted modules of the Mini International Neuropsychiatric Interview (MINI). Dimensional symptomatology was assessed using the Brazilian Portuguese version of the Center for Epidemiological Studies-Depression Scale-Revised (CESD-R). We estimated network structures that included individual depressive symptoms as measured by CESD-R items, peripheral inflammatory markers (C-Reactive Protein [CRP] and Interleukin-6 [IL-6]), as well as relevant covariates. RESULTS: We evaluated 2586 participants (mean age = 22.5[SD = 0.33]) There were no associations between concentrations of inflammatory proteins and categorical diagnosis of MDD or with CESD-R total sum-scores. In symptom-specific analysis, CRP and IL-6 were positively connected to somatic and cognitive items. DISCUSSION: We found cross-sectional connections of two commonly studied inflammatory proteins and specific depressive symptoms. Conducting symptom-specific analyses in relation to biological markers might advance our understanding of the heterogeneity of MDD.

Asunto(s)

Proteína C-Reactiva , Trastorno Depresivo Mayor , Interleucina-6 , Adolescente , Biomarcadores , Brasil , Estudios Transversales , Depresión/diagnóstico , Trastorno Depresivo Mayor/diagnóstico , Humanos , Inflamación/psicología , Adulto Joven

RESUMEN

Disgust is hypothesized to be an evolved emotion that functions to regulate the avoidance of pathogen-related stimuli and behaviors. Individuals with higher pathogen disgust sensitivity (PDS) are predicted to be exposed to and thus infected by fewer pathogens, though no studies have tested this directly. Furthermore, PDS is hypothesized to be locally calibrated to the types of pathogens normally encountered and the fitness-related costs and benefits of infection and avoidance. Market integration (the degree of production for and consumption from market-based economies) influences the relative costs/benefits of pathogen exposure and avoidance through sanitation, hygiene, and lifestyle changes, and is thus predicted to affect PDS. Here, we examine the function of PDS in disease avoidance, its environmental calibration, and its socioecological variation by examining associations among PDS, market-related lifestyle factors, and measures of bacterial, viral, and macroparasitic infection at the individual, household, and community levels. Data were collected among 75 participants (ages 5 to 59 y) from 28 households in three Ecuadorian Shuar communities characterized by subsistence-based lifestyles and high pathogen burden, but experiencing rapid market integration. As predicted, we found strong negative associations between PDS and biomarkers of immune response to viral/bacterial infection, and weaker associations between PDS and measures of macroparasite infection, apparently mediated by market integration-related differences. We provide support for the previously untested hypothesis that PDS is negatively associated with infection, and document variation in PDS indicative of calibration to local socioeconomic conditions. More broadly, findings highlight the importance of evolved psychological mechanisms in human health outcomes.

Asunto(s)

Asco , Infecciones/parasitología , Infecciones/psicología , Adolescente , Adulto , Niño , Preescolar , Estudios Transversales , Ecuador/etnología , Humanos , Pueblos Indígenas , Inflamación/etiología , Inflamación/psicología , Estilo de Vida , Persona de Mediana Edad , Factores Socioeconómicos , Adulto Joven

RESUMEN

OBJECTIVE: To investigate the role of IL-33 in gouty arthritis. MATERIAL: 174 Balb/c (wild-type) and 54 ST2-/- mice were used in this study. In vitro experiments were conducted in bone marrow-derived macrophages (BMDMs). Synovial fluid samples from gouty arthritis (n = 7) and osteoarthritis (n = 8) hospital patients were used to measure IL-33 and sST2 levels. METHODS: Gout was induced by injection of monosodium urate (MSU) crystals in the knee joint of mice. Pain was determined using the electronic von Frey and static weight bearing. Neutrophil recruitment was determined by H&E staining, Rosenfeld staining slides, and MPO activity. ELISA was used for cytokine and sST2 measurement. The priming effect of IL-33 was determined in BMDM. RESULTS: Synovial fluid of gout patients showed higher IL-33 levels and neutrophil counts than osteoarthritis patients. In mice, the absence of ST2 prevented mechanical pain, knee joint edema, neutrophil recruitment to the knee joint, and lowered IL-1ß and superoxide anion levels. In macrophages, IL-33 enhanced the release of IL-1ß and TNF-α, and BMDMs from ST2-/- showed reduced levels of these cytokines after stimulus with MSU crystals. CONCLUSION: IL-33 mediates gout pain and inflammation by boosting macrophages production of cytokines upon MSU crystals stimulus.

Asunto(s)

Artritis Gotosa/patología , Inflamación/inducido químicamente , Interleucina-1beta/metabolismo , Interleucina-33/farmacología , Macrófagos/metabolismo , Dolor/inducido químicamente , Animales , Artritis Gotosa/inducido químicamente , Artritis Gotosa/metabolismo , Femenino , Humanos , Inflamación/psicología , Proteína 1 Similar al Receptor de Interleucina-1/genética , Macrófagos/efectos de los fármacos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Noqueados , Persona de Mediana Edad , Infiltración Neutrófila/efectos de los fármacos , Dolor/psicología , Peroxidasa/metabolismo , Superóxidos/metabolismo , Membrana Sinovial/patología , Ácido Úrico

RESUMEN

El tratamiento actual de la depresión mayor, una condición de alta prevalencia a nivel mundial, aún no resulta satisfactorio por las significativas tasas de falta de respuesta o de síntomas residuales. Esto, entre otras razones, ha motivado a la búsqueda de nuevos modelos de comprensión de los procesos biológicos que están a la base de esta enfermedad, con el propósito de encontrar mejores estrategias terapéuticas, al menos desde el punto de vista farmacológico. Se examinan algunas correspondencias entre los fenómenos clínicos y la articulación de los sistemas inmune, nervioso y endocrino, y se revisa algunas relaciones entre depresión y enfermedades inflamatorias sistémicas.

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The current treatment of major depression, a condition of high prevalence worldwide, is still unsatisfactory due to the elevated rates of non-response or residual symptoms. This, among other reasons, has motivated the search for new models of understanding the biological processes that could better explain this disease, with the purpose of finding better therapeutic strategies, at least from the pharmacological point of view. Some correspondences between clinical phenomena and the interplay of the immune, nervous and endocrine systems are examined. Also, some relationships between depression and systemic inflammatory diseases are reviewed.

Asunto(s)

Humanos , Depresión/inmunología , Inflamación/inmunología , Inflamación/psicología , Artritis Reumatoide/inmunología , Artritis Reumatoide/psicología , Lupus Eritematoso Sistémico/inmunología , Lupus Eritematoso Sistémico/psicología

RESUMEN

The use of reliable scores is a constant development in critical illness. According to Sepsis-3 consensus, the use of Sequential Organ Failure Assessment (SOFA) score of 2 or more is associated with a higher mortality of sepsis patients. In experimental research, due murine animal model limitations, the use of a score systems can be an alternative to assess sepsis severity. In this work, we suggest a sickness behavior score (SBS) that uses physiological variables to assess sepsis severity and mortality. Animals were evaluated daily by the presence of six indicators of sickness behavior: temperature alteration, preference of water/sucrose, liquid intake, food intake, body weight, and movimentation. Male adult Wistar rats were evaluated daily after sepsis induction by cecal ligation and puncture (CLP) or laparotomy only (sham) for determination of SBS. Oxidative stress, IL-6, and HPA axis markers (corticosterone and adrenal gland weight) were evaluated 24 h after CLP to determine the correlation with the acute SBS and neuroinflammation. Also, BDNF and four cognitive behavioral tests were correlated with the chronic SBS, i.e., sum of 8 days after surgery. In result, septic rats presented higher SBS than sham animals. Sepsis severity markers were associated with acute and chronic SBS. Also, SBS was negative correlated with the cognitive tests. In conclusion, SBS shows to be reliable score to predict sepsis severity and mortality. The use of score system provides the analysis of global sickness behavior, beyond evaluation of each parameter individually.

Asunto(s)

Coinfección/metabolismo , Modelos Animales de Enfermedad , Conducta de Enfermedad/fisiología , Mediadores de Inflamación/metabolismo , Locomoción/fisiología , Sepsis/metabolismo , Animales , Coinfección/psicología , Ingestión de Alimentos/fisiología , Ingestión de Alimentos/psicología , Inflamación/metabolismo , Inflamación/psicología , Masculino , Estrés Oxidativo/fisiología , Ratas , Ratas Wistar , Sepsis/psicología

RESUMEN

Early adversity, depression, and obesity are associated with increases in low-grade inflammation. However, there are few prospective and longitudinal studies to elucidate how these associations unfold in children. The present study used latent growth curve models to examine pathways between family adversity in infancy, depressive symptoms in childhood, body mass index (BMI) in childhood, and inflammation in adolescence (age = 16-18). The study is an adolescent follow-up of infants from working-class communities around Santiago, Chile, who participated in a preventive trial of iron supplementation at 6 months of age. Anthropometrics, stressful life events, maternal depression, socioeconomic status, and developmental assessments were measured at 12 months, 5 years, 10 years, and adolescence. In adolescence, participants provided blood samples for high-sensitivity C-reactive protein (hsCRP) assessment. Greater exposure to early adversity in the form of interpersonal conflict stress in infancy indirectly associated with increased hsCRP through its association to increased intercept and slope of childhood BMI. Depressive symptoms at any time were not directly or indirectly associated with increased hsCRP. These findings contribute to our understanding of how early family adversity and its associations with obesity and depressive symptoms across childhood are linked to low-grade, chronic inflammation in adolescence. The model identified as best capturing the data supported the pivotal role of childhood BMI in explaining how early-life adversity is associated with inflammation in adolescence.

Asunto(s)

Experiencias Adversas de la Infancia/psicología , Índice de Masa Corporal , Depresión/complicaciones , Depresión/psicología , Inflamación/etiología , Inflamación/psicología , Adolescente , Adulto , Proteína C-Reactiva/análisis , Niño , Preescolar , Chile , Femenino , Humanos , Lactante , Estudios Longitudinales , Masculino , Madres/psicología , Estudios Prospectivos , Saliva/química , Clase Social , Estrés Psicológico

RESUMEN

A higher level of physical activity (PA) is associated with decreased risk of mortality, dementia, and depression, yet the mechanisms involved are not well understood, and little evidence exists for Mexican Americans. With data from the Sacramento Area Latino Study on Aging (1998-2007), we used Cox proportional hazards regression to separately evaluate associations of baseline PA level with mortality, dementia/cognitive impairment without dementia (CIND), and depressive symptoms, and we estimated the mediating effects of inflammatory markers in additive hazard models. A low level of PA (<35 metabolic equivalent of task-hours/week) was associated with increased mortality (hazard ratio (HR) = 1.50, 95% confidence interval (CI): 1.20, 1.88), dementia/CIND (HR = 1.37, 95% CI: 0.96, 1.96), and depressive symptoms (HR = 1.23, 95% CI: 1.00, 1.52). A low PA level added 512 (95% CI: -34, 1,058) cases of dementia/CIND per 100,000 person-years at risk (direct effect), while, through a mediating path, interleukin 6 (IL-6) added another 49 (95% CI: 5, 94) cases, or 9% of the total effect. For mortality, 8%-10% of the PA total effect was mediated through IL-6, tumor necrosis factor α (TNF-α), or TNF-α receptors. None of the inflammatory markers mediated the association between PA and depressive symptoms. Our results suggest that antiinflammation (especially as assessed by IL-6 and TNF-α levels) may partly explain how PA protects against dementia/CIND and mortality.

Asunto(s)

Demencia/epidemiología , Depresión/epidemiología , Ejercicio Físico/psicología , Inflamación/psicología , Americanos Mexicanos/estadística & datos numéricos , Mortalidad , Anciano , Biomarcadores/sangre , Proteína C-Reactiva/metabolismo , California/epidemiología , Cognición , Estudios de Cohortes , Demencia/sangre , Demencia/prevención & control , Depresión/sangre , Depresión/prevención & control , Femenino , Humanos , Inflamación/sangre , Inflamación/epidemiología , Interleucina-6/sangre , Masculino , Americanos Mexicanos/psicología , Persona de Mediana Edad , Factor de Necrosis Tumoral alfa/sangre

RESUMEN

RATIONALE AND OBJECTIVES: Stress-induced alterations in oxidative and inflammatory parameters have been implicated in the pathophysiology of mood disorders. Based on the antioxidant and anti-inflammatory properties of the selenium-containing compound 3-((4-chlorophenyl)selanyl)-1-methyl-1H-indole (CMI), we assessed its ability to reverse depression-like behavioral alterations, neuroinflammation, and oxidative imbalance induced by acute restraint stress. METHODS: Mice submitted to restraint for 240 min received CMI (1 or 10 mg/kg, orally) 10 min after the end of the stress induction. Behavioral and biochemical tests were carried out after further 30 min. RESULTS: Restraint-induced depression-like behavior in the tail suspension test (TST), splash test, and new object exploration test was reversed by CMI. None of the treatments evoked locomotor alteration. In addition, CMI abrogated restraint-induced increases in plasma levels of corticosterone and in markers of oxidative stress and impaired superoxide dismutase and catalase activity in the prefrontal cortex (PFC) and hippocampus (HC). CMI also blocked stress-induced downregulation of mRNA levels of glucocorticoid receptor and brain-derived neurotrophic factor and upregulation of nuclear factor kappa B, inducible nitric oxide synthase, tumor necrosis alpha, indoelamine-2,3-dioxygenase, and glycogen synthase kinase 3 beta in PFC and HC. CONCLUSIONS: These preclinical results indicate that administration of selenium-containing compounds might help to treat depression associated with inflammation and oxidative stress. Graphical abstract ᅟ.

Asunto(s)

Depresión/tratamiento farmacológico , Indoles/uso terapéutico , Estrés Nitrosativo/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Compuestos de Selenio/uso terapéutico , Estrés Psicológico/tratamiento farmacológico , Animales , Antioxidantes/farmacología , Antioxidantes/uso terapéutico , Depresión/metabolismo , Depresión/psicología , Indoles/química , Indoles/farmacología , Inflamación/tratamiento farmacológico , Inflamación/psicología , Masculino , Ratones , Estrés Nitrosativo/fisiología , Estrés Oxidativo/fisiología , Distribución Aleatoria , Restricción Física/métodos , Restricción Física/psicología , Compuestos de Selenio/química , Compuestos de Selenio/farmacología , Transducción de Señal/efectos de los fármacos , Transducción de Señal/fisiología , Estrés Psicológico/metabolismo , Estrés Psicológico/psicología

RESUMEN

Neuropsychiatric disorders (i.e., mood disorders and schizophrenia) and inflammation are closely intertwined, and possibly powering each other in a bidirectional loop. Depression facilitates inflammatory reactions and inflammation promotes depression and other neuropsychiatric disorders. Patients with neuropsychiatric disorders exhibit all cardinal features of inflammation, including increased circulating levels of inflammatory inducers, activated sensors, and inflammatory mediators targeting all tissues. Inflammation may contribute to the pathophysiology and clinical progression of these disorders. Of note, proinflammatory cytokines modulate mood behavior and cognition by reducing brain monoamine levels, activating neuroendocrine responses, promoting excitotoxicity (increased glutamate levels), and impairing brain plasticity. What are the sources of this chronic inflammation? Increasing evidence indicates that changes in neuroendocrine regulation, metabolism, diet/microbiota, and negative health behaviors are important triggers of inflammation. Finally, recent data indicate that early-life stress is associated with overt inflammation prior to the development of neuropsychiatric disorders.

Asunto(s)

Trastornos del Humor/inmunología , Trastornos del Humor/fisiopatología , Esquizofrenia/inmunología , Esquizofrenia/fisiopatología , Estrés Psicológico/inmunología , Encéfalo/fisiopatología , Citocinas/inmunología , Humanos , Inflamación/inmunología , Inflamación/patología , Inflamación/psicología , Plasticidad Neuronal/fisiología , Sistemas Neurosecretores/fisiopatología , Estrés Psicológico/psicología

RESUMEN

BACKGROUND: Systemic inflammation is known as a risk factor of cognitive decline. OBJECTIVE: To investigate the effects of propolis on cognitive decline and systemic inflammation in elderly people living at high altitude. METHODS: Sixty participants (average 72.8 years) living at altitude (2,260 meters) were randomized to receive propolis (0.83 g, n = 30) or placebo (n = 30) for 24 months. Cognitive outcomes were assessed using MMSE and serum cytokine levels were measured for 24 months in a double-blind study. RESULTS: MMSE scores were 26.17 at baseline and 23.87 at 24 months in placebo group. Compared to placebo group, improvements of MMSE scores were significant in propolis-treated subjects (p = 0.007) with a response emerging over time (time points×group interaction, p = 0.016). In addition, the serum IL-1ß and IL-6 levels were significantly different across treatments (p < 0.0001) showing upward and downward trends in placebo- and propolis-treated subjects, respectively (p < 0.0001). Serum levels of TNF-α were not significantly different across treatment (p = 0.0528) but with a response emerging over time (time points×group interaction, p = 0.016). In contrast, serum levels of TGFß1 were significantly different across treatments (p < 0.0001) showing downward and upward trends in placebo- and propolis-treated subjects, respectively. Serum levels of IL-10 were significant for the effect of groups (p = 0.0411). Furthermore, MMSE scores correlated with the decrease in IL-1ß and the increase in TGFß1 in serum. CONCLUSION: Elderly people living at high altitude developed to MCI in 24 months with exacerbation of systemic inflammation. Ingestion of propolis (>12 months) protected against cognitive decline after systemic inflammation was reduced.

Asunto(s)

Altitud , Antiinflamatorios no Esteroideos/uso terapéutico , Apiterapia , Disfunción Cognitiva/prevención & control , Inflamación/tratamiento farmacológico , Própolis/uso terapéutico , Anciano , Biomarcadores/sangre , Disfunción Cognitiva/sangre , Disfunción Cognitiva/inmunología , Citocinas/sangre , Método Doble Ciego , Femenino , Humanos , Inflamación/sangre , Inflamación/inmunología , Inflamación/psicología , Masculino , Pruebas de Estado Mental y Demencia , Resultado del Tratamiento

RESUMEN

OBJECTIVE: To estimate the prevalence of cognitive impairment (CI) among patients recently diagnosed with type 2 diabetes (RDD) and to identify any relationships between CI and RDD comorbidities. METHODS: One thousand seven hundred twelve patients with RDD participated in a cross-sectional study. The patients' sociodemographic and clinical data were registered. RESULTS: The sample population had an average age of 51 ± 11 years, and 63.26% of the patients were female. CI was diagnosed in 38 patients (2.2%) and was more common among both females (2.8% vs. 1.3%, p = 0.063) and the elderly (0% at an age ≤ 30 years vs. 10.4% at an age > 70 years, p = 0.0001). Rheumatoid arthritis (present in 15.8% vs. absent in 2.1%) and asthma (13% vs. 2.1%) correlated significantly with CI based on the results of our logistic regression analysis. CONCLUSION: Age, female gender, rheumatoid arthritis and asthma are risk factors for CI in the setting of RDD.

Asunto(s)

Trastornos del Conocimiento/epidemiología , Diabetes Mellitus Tipo 2/psicología , Inflamación/psicología , Adulto , Anciano , Artritis Reumatoide/epidemiología , Artritis Reumatoide/psicología , Asma/epidemiología , Asma/psicología , Causalidad , Enfermedad Crónica , Trastornos del Conocimiento/etiología , Trastornos del Conocimiento/inmunología , Comorbilidad , Estudios Transversales , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/epidemiología , Progresión de la Enfermedad , Susceptibilidad a Enfermedades , Dislipidemias/epidemiología , Escolaridad , Femenino , Humanos , Hipertensión/epidemiología , Inflamación/epidemiología , Masculino , México/epidemiología , Persona de Mediana Edad , Isquemia Miocárdica/epidemiología , Pruebas Neuropsicológicas , Prevalencia

RESUMEN

Because few studies have examined depression facets or potential moderators of the depression-inflammation relationship, our aims were to determine whether particular depressive symptom clusters are more strongly associated with C-reactive protein (CRP) levels and whether race/ethnicity moderates these relationships. We examined data from 10,149 adults representative of the U.S. population (4858 non-Hispanic White, 1978 non-Hispanic Black, 2260 Mexican American, 1053 Other Hispanic) who participated in the cross-sectional National Health and Nutrition Examination Survey between 2005 and 2010. Depressive symptoms were assessed by the Patient Health Questionnaire-9, and high-sensitivity serum CRP was quantified by latex-enhanced nephelometry. Total (p<.001), somatic (p<.001), and nonsomatic (p=.001) depressive symptoms were each positively related to serum CRP in individual models. However, in the simultaneous model that included both symptom clusters, somatic symptoms (p<.001), but not nonsomatic symptoms (p=.98), remained associated with serum CRP. Evidence of moderation by race/ethnicity was also observed, as six of the nine depressive symptoms×race/ethnicity interactions were significant (ps<.05). Among non-Hispanic Whites, the pattern of results was identical to the full sample; only somatic symptoms (p<.001) remained related to serum CRP in the simultaneous model. No relationships between total, somatic, or nonsomatic symptoms and serum CRP were observed among the non-Hispanic Black, Mexican American, or Other Hispanic groups. Our findings indicate that the link between depressive symptoms and systemic inflammation may be due to the somatic symptoms of sleep disturbance, fatigue, appetite changes, and psychomotor retardation/agitation and may be strongest among non-Hispanic Whites.

Asunto(s)

Población Negra/psicología , Proteína C-Reactiva/análisis , Depresión/etnología , Trastorno Depresivo/etnología , Hispánicos o Latinos/psicología , Inflamación/etnología , Población Blanca/psicología , Adulto , Anciano , Anciano de 80 o más Años , Antihipertensivos/uso terapéutico , Comorbilidad , Estudios Transversales , Depresión/sangre , Depresión/psicología , Trastorno Depresivo/sangre , Trastorno Depresivo/psicología , Femenino , Hormonas/uso terapéutico , Humanos , Hipolipemiantes/uso terapéutico , Inflamación/sangre , Inflamación/psicología , América Latina/etnología , Masculino , México/etnología , Persona de Mediana Edad , Encuestas Nutricionales , Autoinforme , Índice de Severidad de la Enfermedad , Factores Socioeconómicos , Evaluación de Síntomas , Estados Unidos/epidemiología , Adulto Joven

RESUMEN

Temporomandibular disorder (TMD) is prevalent in dental clinics and can involve problems with the masticatory muscles or the temporomandibular joints (TMJ). The pain of TMD is frequently associated with inflammation in the TMJs, but it's etiology is considered to be multifactorial and includes biologic, behavioral, environmental, social, emotional and cognitive factors. The purpose of this investigation was to evaluate the anxiety-like behavior in rats exposed to temporomandibular inflammation via injection of Freund's Adjuvant (CFA) with the elevated plus maze (EPM) and light/dark box (LDB) tests and to evaluate nociceptive behavior with the von Frey test at different periods. Moreover, this study measured TMJ inflammation using plasma extravasation (Evans blue test) and the intraarticular infiltration of polymorphonuclear neutrophils (myeloperoxidase quantification). The results showed that rats that were submitted to TMJ inflammation exhibited a decreased number of entries into the open arms of the EPM and a decrease in the time spent in the light compartment and in the number of transitions in the LDB. Additionally, the number of entries in closed arms in the EPM, used as indicator of locomotor activity, did not alter between treatments. Furthermore, increases in mechanical sensitivity and increases in plasma extravasation in the joint tissue occurred throughout the inflammation process, along with an increase in myeloperoxidase in the synovial fluid of TMJ. Our results suggest that the temporomandibular inflammation induced by CFA produced anxiety-like behaviors in rats and induced nociceptive behavior across different periods of inflammation.

Asunto(s)

Ansiedad/psicología , Inflamación/patología , Inflamación/psicología , Dolor Nociceptivo/patología , Dolor Nociceptivo/psicología , Trastornos de la Articulación Temporomandibular/patología , Trastornos de la Articulación Temporomandibular/psicología , Animales , Ansiedad/complicaciones , Conducta Animal , Extravasación de Materiales Terapéuticos y Diagnósticos/patología , Adyuvante de Freund , Inflamación/inducido químicamente , Inflamación/complicaciones , Masculino , Infiltración Neutrófila , Dolor Nociceptivo/inducido químicamente , Dolor Nociceptivo/complicaciones , Peroxidasa/metabolismo , Ratas , Líquido Sinovial/metabolismo , Trastornos de la Articulación Temporomandibular/inducido químicamente , Trastornos de la Articulación Temporomandibular/complicaciones , Factores de Tiempo

RESUMEN

Sepsis can lead to long-term cognitive changes, including memory and learning deficits, which are known as septic encephalopathy (SE). SE also includes behavioral changes. The underlying mechanism of SE is unknown, and several mechanisms have been proposed. This study investigated late anxiety-like behavior, serum cytokine levels and brain cytokine production in C57BL/6 mice subjected to polymicrobial sepsis induced by sublethal cecum ligature and puncture (CLP). Anxiety-like behavior and locomotor activity were assessed in mice 10 days after sham operation or CLP procedure using the elevated plus maze, contextual fear conditioning, and open field test. Brain and serum concentrations of the cytokines TNF-α, IFN-γ, IL-1ß, IL-6, and IL-10 were determined by ELISA. We found that mice subjected to polymicrobial sepsis presented anxiety-like behavior, which was accompanied by increased serum TNF-α and brain TNF-α, IFN-γ, IL-1ß, and IL-6 levels, 10 days after the surgical procedure. These findings suggest an involvement of central nervous system inflammatory mediators in the anxiety-like symptoms found in SE.

Asunto(s)

Ansiedad/sangre , Coinfección/sangre , Mediadores de Inflamación/sangre , Sepsis/sangre , Animales , Ansiedad/psicología , Coinfección/psicología , Inflamación/sangre , Inflamación/psicología , Masculino , Ratones , Ratones Endogámicos C57BL , Actividad Motora/fisiología , Sepsis/psicología , Factores de Tiempo

RESUMEN

Preclinical studies have demonstrated antinociceptive synergism between dexketoprofen (DEX) and tramadol (TRM) in acute animal models of nociception. The aim of the present study was to investigate the type of interaction between DEX and TRM in a chronic musculoskeletal pain model in mice, which fairly replicates the characteristics of chronic osteoarticular pain in humans. Inflammation was induced by a subplantar injection of complete Freund's adjuvant (CFA) in male CF1 mice. Nociceptive thresholds were evaluated using the hot plate, the nocifensive spontaneous behavior and the acetone tests, while plasma extravasation (PE) was assessed with Evan's blue. We used the following experimental groups: control (no inflammation), acute (1 day after CFA injection), and chronic inflammation (7 days after CFA). Dose-response curves for DEX and TRM, individually and combined in a 1 : 1 proportion based on their potency were obtained, and the doses that produced a 50% inhibition calculated. The isobolographic analysis revealed that in all groups of study (no inflammation, acute, and chronic inflammation), the combination of DEX : TRM was synergistic, for both the inhibition of nociception and the PE. The results suggest that the DEX : TRM (1 : 1) combination could be useful in the management of acute and chronic inflammatory musculoskeletal pains in humans; in addition, the synergistic interaction between the drugs observed both during acute and chronic inflammation suggests that less doses would be required of each drug to obtain effective analgesia.

Asunto(s)

Analgésicos Opioides/administración & dosificación , Antiinflamatorios no Esteroideos/administración & dosificación , Modelos Animales de Enfermedad , Cetoprofeno/análogos & derivados , Dolor/tratamiento farmacológico , Tramadol/administración & dosificación , Trometamina/administración & dosificación , Animales , Combinación de Medicamentos , Sinergismo Farmacológico , Inflamación/sangre , Inflamación/tratamiento farmacológico , Inflamación/psicología , Cetoprofeno/administración & dosificación , Masculino , Ratones , Dolor/sangre , Dolor/psicología , Dimensión del Dolor/efectos de los fármacos , Dimensión del Dolor/métodos

RESUMEN

Injury to the insular cortex in humans produces a lack of appropriate response to pain. Also, there is controversial evidence on the lateralization of pain modulation. The aim of this study was to test the effect of insular cortex lesions in three models of pain in the rat. An ipsilateral, contralateral or bilateral radiofrequency lesion of the rostral agranular insular cortex (RAIC) was performed 48h prior to acute, inflammatory or neuropathic pain models in all the experimental groups. Acute pain was tested with paw withdrawal latency (PWL) after thermal stimulation. Inflammation was induced with carrageenan injected in the paw and PWL was tested 1h and 24h afterwards. Neuropathic pain was tested after ligature of the sciatic nerve by measuring mechanical nociceptive response after stimulation with the von Frey filaments. Another model of neuropathy consisted of thermo stimulation followed by right sciatic neurectomy prior to the recording of autotomy behaviour. Acute pain was not modified by the RAIC lesion. All the RAIC lesion groups showed diminished pain-related behaviours in inflammatory (increased PWL) and neuropathic models (diminished mechanical nociceptive response and autotomy score). The lesion of the RAIC produces a significant decrease in pain-related behaviours, regardless of the side of the lesion. This is a clear evidence that the RAIC plays an important role in the modulation of both inflammatory and neuropathic - but not acute - pain.

Asunto(s)

Conducta Animal/fisiología , Corteza Cerebral/fisiopatología , Hiperalgesia/fisiopatología , Inflamación/fisiopatología , Neuralgia/fisiopatología , Análisis de Varianza , Animales , Hiperalgesia/psicología , Inflamación/psicología , Masculino , Neuralgia/psicología , Dimensión del Dolor , Estimulación Física , Ratas , Ratas Wistar

RESUMEN

The perinatal development of the nervous system is influenced by different external and internal stimuli. Previous data show that maternal care and perinatal inflammation can induce long-term changes in anxiety- and depression-related behavior. Our hypothesis is that both maternal care and perinatal inflammation act through interacting biological pathways to program adult behavior. To evaluate this interaction, we combined a protocol of maternal care variation in mice (C57BL/6J x BALB/c reciprocal F1 offspring) with the administration of bacterial wall lipopolysaccharide (LPS) at a previously reported sensitive development age (postnatal day 3, P3). The analysis of maternal behavior revealed that pups from C57BL/6J dams received more maternal attention than those taken care by BALB/c dams. Pups receiving LPS at P3 showed an acute corticosterone response, and a dose-dependent desensitization of this hormonal response when challenged with LPS at adulthood. We analyzed adult behavior on 6 highly validated tests and found an interaction between maternal care and early postnatal LPS on 7 anxiety-related behaviors in 4 different tests. In particular, early postnatal LPS treatment resulted in higher anxiety-related behavior when administered to females receiving more maternal care (C57 pedigree), but reduced depression-related behavior in males of the same pedigree. These results suggest that specific coping strategies are sensitive to maternal care and/or postnatal inflammation programming of adult anxiety- and depression-related behaviors, suggesting that both divergent and convergent mechanisms participate in this programming.

Asunto(s)

Ansiedad/psicología , Depresión/psicología , Inflamación/psicología , Conducta Materna , Envejecimiento , Animales , Animales Recién Nacidos , Ansiedad/metabolismo , Corticosterona/metabolismo , Depresión/metabolismo , Femenino , Inflamación/inducido químicamente , Inflamación/metabolismo , Lipopolisacáridos/administración & dosificación , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos C57BL , Pruebas Neuropsicológicas , Distribución Aleatoria , Factores Sexuales

RESUMEN

Adult male rats were administered intrapleural (ipl) or intraperitoneal (i.p.) injection of lipopolysaccharide (LPS), 24 h after being submitted to forced swim test (FST). Four hours after LPS challenge, an increase in pleural and peritoneal leukocyte and neutrophil counts in animals not exposed to FST was noted. FST induced a marked increase in pleural, but not in peritoneal, neutrophil leukocytosis. The results suggest that lowered mood may increase inflammatory response to LPS.

Asunto(s)

Leucocitosis/inmunología , Lipopolisacáridos/administración & dosificación , Neutrófilos/inmunología , Neutrófilos/patología , Animales , Líquido Ascítico/patología , Depresión/inmunología , Depresión/psicología , Inflamación/inmunología , Inflamación/psicología , Inyecciones Intraperitoneales , Recuento de Leucocitos/métodos , Leucocitosis/patología , Leucocitosis/psicología , Masculino , Neutrófilos/efectos de los fármacos , Pleura/patología , Ratas , Ratas Wistar , Natación/fisiología , Natación/psicología