RESUMEN

BACKGROUND: Here, we explore the serum levels of anti-oxidized lipid autoantibodies as well as immune complexes in patients with SLE and determine their correlation with disease. METHODS: Serum levels of oxidized-LDL immune complexes, autoantibodies to dsDNA, ox-LDL, MDA-LDL, 9-HODE, 13-HODE and POVPC were detected by ELISA in 64 SLE patients and 9 healthy controls. RESULTS: Active SLE patients exhibited increased serum levels of autoantibodies compared to healthy controls, including anti-MDA-LDL-IgG (p = .003), anti-ox-LDL-IgG (p = .004), anti-9-HODE-IgG (p = .001), anti-13-HODE-IgG (p = .0003), anti-POVPC-IgG (p = .001) and ox-LDL-IC (p = .003). Serum anti-ox-LDL-IgG was positively correlated with SLEDAI (r = 0.34; p = .01), and negatively with C3 (r = -0.40; p = .01). Anti-9-HODE-IgG and anti-POVPC-IgG were positively correlated with SLEDAI and negatively with C4. CONCLUSIONS: Active SLE patients exhibit significantly increased serum levels of IgG anti-oxidized-lipid autoantibodies. Coordinated elevation of oxidized lipids, autoantibodies to these lipids, and immune complexes of these lipid-antibody components could potentially serve as pathogenic drivers and serum markers of SLE disease activity.

Asunto(s)

Autoanticuerpos/inmunología , Lupus Eritematoso Sistémico/inmunología , Estudios de Casos y Controles , Complemento C3/inmunología , Complemento C4/inmunología , ADN/inmunología , Humanos , Inmunoglobulina G/inmunología , Inmunoglobulina M/inmunología , Ácidos Linoleicos/inmunología , Ácidos Linoleicos Conjugados/inmunología , Lipoproteínas LDL/inmunología , Malondialdehído/análogos & derivados , Malondialdehído/inmunología , Éteres Fosfolípidos/inmunología , Índice de Severidad de la Enfermedad

RESUMEN

Conjugated linoleic acid (CLA) is a prime substrate for intra-gastric nitration giving rise to the formation of nitro-conjugated linoleic acid (NO2-CLA). Herein, NO2-CLA generation is demonstrated within the context of acute inflammatory responses both in vitro and in vivo. Macrophage activation resulted in dose- and time-dependent CLA nitration and also in the production of secondary electrophilic and non-electrophilic derivatives. Both exogenous NO2-CLA as well as that generated in situ, attenuated NF-κB-dependent gene expression, decreased pro-inflammatory cytokine production and up-regulated Nrf2-regulated proteins. Importantly, both CLA nitration and the corresponding downstream anti-inflammatory actions of NO2-CLA were recapitulated in a mouse peritonitis model where NO2-CLA administration decreased pro-inflammatory cytokines and inhibited leukocyte recruitment. Taken together, our results demonstrate that the formation of NO2-CLA has the potential to function as an adaptive response capable of not only modulating inflammation amplitude but also protecting neighboring tissues via the expression of Nrf2-dependent genes.

Asunto(s)

Inmunoconjugados/metabolismo , Inflamación/metabolismo , Ácidos Linoleicos Conjugados/metabolismo , Óxido Nítrico/metabolismo , Animales , Modelos Animales de Enfermedad , Humanos , Inmunoconjugados/inmunología , Inflamación/inducido químicamente , Inflamación/inmunología , Inflamación/patología , Ácidos Linoleicos Conjugados/inmunología , Ácidos Linoleicos Conjugados/farmacología , Ratones , FN-kappa B/metabolismo , Óxido Nítrico/química , Óxido Nítrico/inmunología , Transducción de Señal

RESUMEN

BACKGROUND: Cross-sectional epidemiological studies have demonstrated that farm milk from traditional farm settings possesses allergoprotective properties. Up to now, it has not been clarified which milk ingredient is responsible for protection against allergic diseases. As farm milk is rich in conjugated linoleic acids (CLA), it is hypothesized that this n-3 polyunsaturated fatty acid family contributes to the allergoprotective capacity of farm milk. We aim to prove this hypothesis in a murine model of allergic airway inflammation. METHODS: To prove the bioavailability and allergoprotective capacity of milk-associated CLA in a standardized protocol, milk batches that differed significantly in terms of their CLA content were spray dried and incorporated into a basic diet by substituting the regular sunflower fat fraction. Initially, the milk CLA uptake from the diet was monitored via measurement of the CLA content in plasma and erythrocyte membranes obtained from supplemented mice. To determine whether a milk CLA-enriched diet possesses allergoprotective properties, female Balb/c mice were fed the milk CLA-enriched diet ahead of sensitization and a challenge with ovalbumin (OVA) and the parameters of airway inflammation and eisosanoid pattern were measured. RESULTS: In animals, supplementation with a diet rich in milk CLA resulted in elevated CLA levels in plasma and erythrocyte membranes, indicating bioavailability of milk fatty acids. Though membrane-associated phospholipid patterns were affected by supplementation with milk CLA, this application neither reduced the hallmarks of allergic airway inflammation in sensitized and OVA-challenged mice nor modified the eiconsanoid pattern in the bronchoalveolar lavage fluid of these animals. CONCLUSION: Milk-associated CLA was not capable of preventing murine allergic airway inflammation in an animal model of OVA-induced allergic airway inflammation.

Asunto(s)

Asma/inmunología , Ácidos Linoleicos Conjugados/inmunología , Leche/inmunología , Animales , Disponibilidad Biológica , Modelos Animales de Enfermedad , Femenino , Ácidos Linoleicos Conjugados/farmacocinética , Ratones , Ratones Endogámicos BALB C , Leche/química

RESUMEN

BACKGROUND: Oxidized linoleic acid metabolites (OLAMs) are a class of endogenous agonists to the transient receptor potential V1 (TRPV1) receptor. Although TRPV1 mediates inflammatory heat hyperalgesia, it is not known if the OLAMs contribute to the peripheral activation of this receptor during tissue inflammation. In the present study, we evaluated whether the OLAM system is activated during inflammation and whether cytochrome P450 enzymes mediate OLAM contributions to heat hyperalgesia using the complete Freund's adjuvant (CFA) model of inflammation. RESULTS: Our results demonstrate that the intraplantar (ipl) injection of anti-OLAM antibodies significantly reversed CFA-induced heat hyperalgesia. Moreover, application of lipid extracts from inflamed rat skin to cultured sensory neurons triggered a significant release of iCGRP that is blocked by co-treatment with I-RTX, a TRPV1 antagonist. To determine the role of CYP enzymes in mediating OLAM effects, we used a broad spectrum CYP inhibitor, ketoconazole. Pretreatment with ketoconazole inhibited the release of TRPV1 agonists in lipid extracts from inflamed skin and significantly reversed CFA-induced heat hyperalgesia by a peripheral mechanism of action. Moreover, the ipl injection of linoleic acid to rats 24 hr after CFA evoked spontaneous nocifensive behaviors that were significantly reduced by capsazepine, by knockout of the TRPV1 gene, or by pretreatment with either anti-OLAM antibodies or ketoconazole. CONCLUSIONS: Taken together, our data suggests that OLAMs contribute to inflammatory nociception in the periphery and that cytochrome P450 enzymes play a crucial role in mediating OLAM contributions to inflammatory heat hyperalgesia.

Asunto(s)

Inhibidores Enzimáticos del Citocromo P-450 , Inhibidores Enzimáticos/farmacología , Inflamación/tratamiento farmacológico , Cetoconazol/farmacología , Ácido Linoleico/metabolismo , Dolor/tratamiento farmacológico , Animales , Anticuerpos/farmacología , Conducta Animal/efectos de los fármacos , Sistema Enzimático del Citocromo P-450/metabolismo , Adyuvante de Freund , Calor , Hiperalgesia/tratamiento farmacológico , Hiperalgesia/patología , Inflamación/complicaciones , Inflamación/patología , Ácidos Linoleicos/inmunología , Ácidos Linoleicos Conjugados/inmunología , Ratones , Ratones Endogámicos C57BL , Nocicepción/efectos de los fármacos , Oxidación-Reducción/efectos de los fármacos , Dolor/complicaciones , Dolor/patología , Ratas , Ratas Sprague-Dawley , Canales Catiónicos TRPV/agonistas , Canales Catiónicos TRPV/metabolismo

RESUMEN

Supplementation with a mixture of trans-10, cis-12 (t10,c12) and cis-9, trans-11 (c9,t11) isomers of conjugated linoleic acid (CLA), or t10,c12 CLA alone, reduces body weight and fat deposition in animals and some humans. However, these anti-obesity actions of t10,c12 CLA are routinely accompanied by increased markers of inflammation and insulin resistance. Thus, we examined the extent to which blocking c-Jun NH2-terminal kinase (JNK) signaling using the JNK inhibitor SP600125 attenuated markers of inflammation and insulin resistance in primary human adipocytes treated with t10,c12 CLA. SP600125 attenuated t10,c12 CLA-mediated phosphorylation of cJun and increased protein levels of activating transcription factor (ATF) 3, two downstream targets of JNK. SP600125 attenuated t10,c12 CLA-mediated induction of inflammatory genes, including interleukin (IL)-6, IL-8, IL-1ß, ATF3, monocyte chemoattractant protein (MCP)-1, and cyclooxygenase-2. Consistent with these data, SP600125 prevented t10,c12 CLA-mediated secretion of IL-8, IL-6, and MCP-1. SP600125 prevented t10,c12 CLA suppression of lipogenic genes including peroxisome proliferator activated receptor gamma, liver X receptor, sterol regulatory element binding protein, acetyl-CoA carboxylase, and stearoyl-CoA desaturase. Additionally, SP600125 blocked t10,c12 CLA-mediated induction of suppressor of cytokine synthesis-3 and suppression of adiponectin and insulin-dependent glucose transporter 4 mRNA levels. Collectively, these data suggest that JNK signaling plays an important role in t10,c12 CLA-mediated regulation of inflammatory and lipogenic gene expression in primary cultures of human adipocytes.

Asunto(s)

Adipocitos/efectos de los fármacos , Antracenos/farmacología , Proteínas Quinasas JNK Activadas por Mitógenos/antagonistas & inhibidores , Ácidos Linoleicos Conjugados/inmunología , Factor de Transcripción Activador 3/inmunología , Adipocitos/inmunología , Adulto , Células Cultivadas , Femenino , Regulación de la Expresión Génica/efectos de los fármacos , Humanos , Inflamación/tratamiento farmacológico , Resistencia a la Insulina , Lipogénesis/efectos de los fármacos , Persona de Mediana Edad , Transducción de Señal/efectos de los fármacos , Adulto Joven

RESUMEN

Immune function (response to concanavalin A, cytokine production, and lymphocyte profiles) and blood chemistry variables were measured in growing-finishing pigs (Yorkshire/Landrace/Duroc dam × Hampshire sire) fed varying percentages of CLA (0, 0.12, 0.25, 0.50, and 1.0%). Blood was collected at 0, 14, 28, 42, and 56 d on feed (DOF). Total white blood cell (WBC) count increased (P < 0.01) linearly to 42 DOF. No differences (P = 0.53) were observed for WBC across CLA treatment. Nitric oxide was greater (P < 0.01) for the 1.0% CLA treatment compared with all other treatments. Flow cytometry using fluorescent labeled monoclonal antibodies to the CD4, CD8, double-positive CD4/CD8, and CD2 surface markers was used to determine lymphocyte subpopulations. Supplementation of CLA had no effect (P = 0.61) on lymphocyte subpopulation cell distribution. Most blood chemistry variables were within the normal metabolic range for pigs. A decrease was observed over DOF for P (P < 0.01) and K (P < 0.05). Additionally, Na and Cl concentrations increased (P < 0.05) from 14 to 28 DOF and decreased over the remainder of the trial. Electrolyte balance was not different (P = 0.38) across CLA treatments and was likely explained by no differences in feed intake among the CLA treatment groups. Blood lipid variables indicated that total cholesterol (P < 0.001), triglycerides (P < 0.001), high-density lipoproteins (P < 0.001), and low-density lipoproteins (P < 0.01) increased as the amount of CLA in the diet increased, but none of the results from these treatments exceeded the normal range of acceptability. These results suggested that CLA was safe when fed to growing-finishing pigs and had little effect on their immune function and blood chemistry variables.

Asunto(s)

Concanavalina A/inmunología , Citocinas/inmunología , Inmunidad Innata/inmunología , Ácidos Linoleicos Conjugados/inmunología , Porcinos/inmunología , Animales , Análisis Químico de la Sangre/veterinaria , Citocinas/análisis , Femenino , Citometría de Flujo/veterinaria , Inmunofenotipificación/veterinaria , Recuento de Leucocitos/veterinaria , Estudios Longitudinales , Masculino , Distribución Aleatoria , Porcinos/sangre

RESUMEN

Conjugated linoleic acid (CLA) has been reported to exert beneficial physiological effects on body composition and the immune system. However, little information is available on the influence of CLA on immune function during early life periods. The present study evaluates the effect of feeding an 80:20 mixture of cis-9, trans-11- and trans-10, cis-12-CLA isomers during gestation and suckling on the systemic immune response of weaned Wistar rats. Pups received dietary CLA from dams through the placental barrier and during suckling by breast milk (group A) or by oral administration (group B). Pups from group C only received CLA during suckling by oral administration. Group D constituted the reference group. Milk from dams fed the CLA diet had a high content of CLA and higher IgA and IgG concentrations than rats fed the standard diet. The plasma of pups from groups A, B and C showed six, twelve and nine times higher content of the cis-9, trans-11-CLA isomer than that of the group D pups. Rats from group A exhibited higher serum IgG concentrations than rats from the rest of the groups (22.14 (SEM 2.14) v. about 5 mg/ml; P < 0.05), whereas rats from groups A and B showed approximately 2-fold higher splenocyte IgM production than rats from groups C and D. However, CLA supplementation did not influence significantly the splenocyte proliferative response or cytokine secretion. Supplementation during gestation and suckling with an 80:20 cis-9, trans-11-trans-10, cis-12 CLA mix enhances the production of the main in vivo and in vitro Ig isotypes in Wistar rats.

Asunto(s)

Suplementos Dietéticos , Inmunoglobulinas/biosíntesis , Ácidos Linoleicos Conjugados/inmunología , Fenómenos Fisiologicos de la Nutrición Prenatal/inmunología , Animales , Animales Lactantes , Proliferación Celular , Células Cultivadas , Citocinas/biosíntesis , Dieta , Femenino , Inmunoglobulinas/sangre , Ácidos Linoleicos Conjugados/sangre , Activación de Linfocitos/inmunología , Intercambio Materno-Fetal/inmunología , Leche/metabolismo , Embarazo , Ratas , Ratas Wistar , Bazo/inmunología , Aumento de Peso/inmunología

RESUMEN

Animal studies suggest that conjugated linoleic acid (CLA) may modulate the immune response, while studies in healthy human subjects have shown little effect and results are controversial. However, the effects of CLA may be more prominent in situations of immune imbalance, such as allergy. We studied the effects of the natural CLA isomer, cis-9, trans-11-CLA, on allergy symptoms and immunological parameters in subjects with birch pollen allergy. In a randomised, placebo-controlled study, forty subjects (20-46 years) with diagnosed birch pollen allergy received 2 g CLA/d in capsules, which contained 65.3 % cis-9, trans-11-CLA and 8.5 % trans-10, cis-12-CLA (n 20), or placebo (high-oleic acid sunflower-seed oil) (n 20) for 12 weeks. The supplementation began 8 weeks before the birch pollen season and continued throughout the season. Allergy symptoms and use of medication were recorded daily. Lymphocyte subsets, cytokine production, immunoglobulins, C-reactive protein, lipid and glucose metabolism and lipid peroxidation were assessed before and after supplementation. The CLA group reported a better overall feeling of wellbeing (P < 0.05) and less sneezing (P < 0.05) during the pollen season. CLA supplementation decreased the in vitro production of TNF-alpha (P < 0.01), interferon-gamma (P < 0.05) and IL-5 (P < 0.05). Total plasma IgE and birch-specific IgE concentrations did not differ between groups, whereas plasma IgA (P < 0.05), granulocyte macrophage colony-stimulating factor (P < 0.05) and eosinophil-derived neurotoxin (P < 0.05) concentrations were lower after CLA supplementation. Urinary excretion of 8-iso-PGF2alpha, a major F2-isoprostane (P < 0.01), and 15-keto-dihydro-PGF2alpha, a primary PGF2alpha metabolite (P < 0.05), increased in the CLA group. The results suggest that cis-9, trans-11-CLA has modest anti-inflammatory effects in allergic subjects.

Asunto(s)

Betula/inmunología , Suplementos Dietéticos , Ácidos Linoleicos Conjugados/uso terapéutico , Polen/inmunología , Rinitis Alérgica Estacional/prevención & control , Adulto , Recuento de Células Sanguíneas , Glucemia/metabolismo , Células Cultivadas , Citocinas/biosíntesis , Femenino , Humanos , Inmunoglobulinas/sangre , Mediadores de Inflamación/metabolismo , Ácidos Linoleicos Conjugados/inmunología , Peroxidación de Lípido/efectos de los fármacos , Lípidos/sangre , Subgrupos Linfocitarios/efectos de los fármacos , Subgrupos Linfocitarios/inmunología , Masculino , Persona de Mediana Edad , Cooperación del Paciente , Rinitis Alérgica Estacional/sangre , Rinitis Alérgica Estacional/inmunología , Índice de Severidad de la Enfermedad , Estornudo/inmunología , Adulto Joven

RESUMEN

A naturally occurring fatty acid, conjugated linoleic acid (CLA), reduces immune-induced TNF and inducible cyclooxygenase (COX-2) expression; key mediators of inflammation in rheumatoid arthritis (RA). On the basis of previous work, it was hypothesized that dietary CLA would act as an anti-inflammatory agent in select animal models of RA. In the collagen antibody-induced arthritis (CAIA) model, mice fed CLA (mixed isomers of c9, t11, and t10, c12-CLA) for 3 wk before anticollagen antibody injection had reduced lipopolysaccharide-induced plasma TNF levels and had arthritic scores that were 60% of mice fed corn oil (CO). In the collagen-induced arthritis (CIA) model, mice fed mixed isomers of CLA for 21 days before immunization had lower IgG(1) titers, earlier signs of joint inflammation, but similar arthritis scores compared with CO fed mice during the remaining 70-day post-injection period. Beginning on day 80 to 133, CLA-fed mice had arthritic scores 70% that of the CO-fed mice. In a second CIA experiment, CLA was fed only after the booster injection. Plasma IgG(1) levels were not reduced and arthritis onset was delayed 4 days in CLA-fed mice compared with the CO-fed mice. Peak arthritis score was similar between CLA and CO-fed mice from day 35 to 56. Because CLA reduced inflammation in the CAIA model, delayed onset of arthritis in the CIA model (CIA experiment 2) and reduced arthritis score after day 80 in the CIA model (CIA experiment 1), we concluded that dietary CLA exhibited anti-inflammatory activity that was dependent on antibody.

Asunto(s)

Artritis Reumatoide/dietoterapia , Artritis Reumatoide/inmunología , Ácidos Linoleicos Conjugados/inmunología , Ácidos Linoleicos Conjugados/farmacología , Alimentación Animal , Animales , Artritis Experimental/dietoterapia , Artritis Experimental/inmunología , Artritis Experimental/patología , Artritis Reumatoide/patología , Autoanticuerpos/sangre , Ciclooxigenasa 2/metabolismo , Grasas de la Dieta/inmunología , Grasas de la Dieta/farmacología , Modelos Animales de Enfermedad , Inmunoglobulina G/sangre , Lipopolisacáridos/inmunología , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Endogámicos DBA , Factor de Necrosis Tumoral alfa/metabolismo

RESUMEN

PURPOSE OF REVIEW: This review critically evaluates studies investigating the effects of conjugated linoleic acid on human health, including effects on body composition, blood lipids, liver metabolism, insulin sensitivity and immune function. It focuses mainly on human intervention studies, but includes some reference to animal and cellular studies which provide insight into potential molecular mechanisms of action of conjugated linoleic acid. RECENT FINDINGS: Human studies continue to report inconsistent effects of conjugated linoleic acid on human health. Some of these reports are based on overinterpretation of marginal effects of supplementation. Recent data suggest that the effects of the substance may be isomer dependent and that cis-9,trans-11 and trans-10,cis-12 conjugated linoleic acids have opposing effects on blood lipids and on metabolism in adipocytes and hepatic cells. SUMMARY: Claims that conjugated linoleic acid is beneficial for health remain as yet unconvincing. Human studies investigating the effects of conjugated linoleic acid supplements have tended to use mixtures of isomers and have been inconsistent. More recent studies have attempted to use relatively pure preparations of single isomers and these studies suggest that the effects of conjugated linoleic acid may be isomer-specific. These recent data suggest a relative detrimental effect of trans-10,cis-12 conjugated linoleic acid on blood lipids. There appears to be little effect of conjugated linoleic acid on immune function and the effects on insulin sensitivity remain unclear.

Asunto(s)

Insulina/metabolismo , Ácidos Linoleicos Conjugados/fisiología , Metabolismo de los Lípidos/efectos de los fármacos , Obesidad/metabolismo , Composición Corporal/efectos de los fármacos , Suplementos Dietéticos , Medicina Basada en la Evidencia , Humanos , Resistencia a la Insulina , Isomerismo , Ácidos Linoleicos Conjugados/química , Ácidos Linoleicos Conjugados/inmunología , Metabolismo de los Lípidos/fisiología , Lípidos/sangre

RESUMEN

Conjugated linoleic acid (CLA) is a collective term for a mixture of positional and geometric isomers of conjugated dienoic derivatives of linoleic acid. CLA has received considerable attention as a result of animal experiments that report anti-carcinogenic, anti-atherogenic and anti-diabetic properties, and modulation of body composition and immune function. Several studies of CLA supplementation in human subjects have now been published, but in contrast to animal studies there has been marked variation between reports on the health-related outcomes. The consensus from seventeen published studies in human subjects is that CLA does not affect body weight or body composition. Some detrimental effects of the trans-10,cis-12 CLA isomer have also been reported in terms of altered blood lipid composition and impaired insulin sensitivity. Finally, CLA has only limited effects on immune functions in man. However, there have been reports of some interesting isomer-specific effects of CLA on the blood lipid profile, but not on immune function. These isomer-specific effects need further investigation. Until more is known, CLA supplementation in man should be considered with caution.

Asunto(s)

Resistencia a la Insulina , Ácidos Linoleicos Conjugados/inmunología , Ácidos Linoleicos Conjugados/metabolismo , Lípidos/sangre , Obesidad/metabolismo , Animales , Composición Corporal , Humanos

RESUMEN

BACKGROUND & AIMS: The molecular targets for the protective actions of conjugated linoleic acid (CLA) on experimental inflammatory bowel disease (IBD) are unknown. We used a loss-of-function approach to investigate whether CLA ameliorated colitis through a peroxisome proliferator-activated receptor gamma (PPAR gamma)-dependent mechanism. METHODS: The expression of PPAR gamma, delta, and their target genes in the colon of mice fed control or CLA-supplemented diets was assayed after a 7-day dextran sodium sulfate (DSS) challenge by quantitative real-time polymerase chain reaction (PCR). Additionally, nuclear factor-kappa B (NF-kappaB) p65 activation was quantified in the colon. To determine the involvement of PPAR gamma in the mechanism of action of CLA directly, specific deletions of PPAR gamma in the colon were performed in mice by using the Cre-lox recombination system. Colonic PPAR gamma null mice and wild-type littermates were fed either a CLA-supplemented or a control diet for 42 days and challenged with 2.5% DSS. The therapeutic efficacy of CLA also was examined by using the CD4 + CD45RB hi transfer colitis model. RESULTS: CLA induced PPAR gamma and delta, transcriptionally modulated PPAR gamma and delta-responsive gene clusters involved in lipid metabolism (uncoupling protein [UCP]1, UCP3, PPAR gamma coactivator 1alpha [PGC-1alpha], and CD36) and epithelial cell maturation (Gob-4 and Keratin 20). Additionally, CLA repressed tumor necrosis factor alpha (TNF-alpha) expression and NF-kappaB activation while inducing the immunoregulatory cytokine transforming growth factor beta 1 (TGF-beta 1 ). Clinically, CLA ameliorated DSS- and CD4 + -induced colitis. Loss of the PPAR gamma gene in the colon abrogated the beneficial effects of CLA in DSS colitis. CONCLUSIONS: Our studies provide molecular evidence in vivo, suggesting that CLA ameliorates colitis through a PPAR gamma-dependent mechanism.

Asunto(s)

Enfermedades Inflamatorias del Intestino/inmunología , Ácidos Linoleicos Conjugados/inmunología , Receptores Citoplasmáticos y Nucleares/biosíntesis , Factores de Transcripción/biosíntesis , Animales , Proteínas Portadoras/inmunología , Regulación de la Expresión Génica/inmunología , Enfermedades Inflamatorias del Intestino/dietoterapia , Ácidos Linoleicos Conjugados/genética , Ratones , Ratones Endogámicos C57BL , Modelos Animales , FN-kappa B/inmunología , Proteínas de Neoplasias/inmunología , Receptores Citoplasmáticos y Nucleares/genética , Receptores Citoplasmáticos y Nucleares/inmunología , Factor de Transcripción ReIA , Factores de Transcripción/genética , Factores de Transcripción/inmunología