RESUMEN
Cystic echinococcosis (CE) is an infectious disease caused by the larvae of parasite Echinococcus granulosus (E. granulosus). To successfully establish an infection, parasite release some substances and molecules that can modulate host immune functions, stimulating a strong anti-inflammatory reaction to carry favor to host and to reserve self-survival in the host. The literature was reviewed using MEDLINE, and an open access search for immunology of hydatidosis was performed. Accumulating data from animal experiments and human studies provided us with exciting insights into the mechanisms involved that affect all parts of immunity. In this review we used the existing scientific data and discuss how these findings assisted with a better understanding of the immunology of E. granulosus infection in man. The aim of this study is to point the several facts that challenge immune and autoimmune responses to protect E. granulosus from elimination and to minimize host severe pathology. Understanding the immune mechanisms of E. granulosus infection in an intermediate human host will provide, we believe, a more useful treatment with immunomodulating molecules and possibly better protection from parasitic infections. Besides that, the diagnosis of CE has improved due to the application of a new molecular tool for parasite identification by using of new recombinant antigens and immunogenic peptides. More studies for the better understanding of the mechanisms of parasite immune evasion is necessary. It will enable a novel approach in protection, detection and improving of the host inflammatory responses. In contrast, according to the "hygiene hypothesis", clinical applications that decrease the incidence of infection in developed countries and recently in developing countries are at the origin of the increasing incidence of both allergic and autoimmune diseases. Thus, an understanding of the immune mechanisms of E. granulosus infection is extremely important.
RESUMEN
Experimental autoimmune encephalomyelitis (EAE) is characterized by appearance of anti-myelin autoantibodies in the blood and with the increased expression of MHC (major histocompatibility complex) class I and II antigens in the brain tissue. Although there is an evidence of possible linkage between influenza vaccination and development of autoimmune processes, the precise mechanisms of action of this vaccine on EAE-induction is still unclear. In this study, effects of influenza vaccine on clinical sign, antimyelin antibody titer in the blood by ELISA test and expression of MHC class I and II molecules immunohistochemistry were examined in the brain of C57BL mice with EAE. EAE was induced by MOG 35-55 protein in 16 of 32 mice. Influenza split vaccine was administered to eight MOG-induced EAE mice and to eight previously nontreated mice. A significant increase of anti-influenza antibody was detected in vaccinated mice compared to nontreated mice. Also, significant increase of antimyelin antibodies was detected in mice with EAE compared to vaccinated group without EAE and control group, respectively. In EAE-influenza vaccinated mice, a mild but not significant increase of antimyelin antibodies was detected, compared to EAE mice. High expression of MHC-II and mild expression of MHC-I were detected in the brain of mice with EAE. No expressions were detected in vaccinated and normal intact brains. Similar staining was found between EAE-vaccinated and EAE group in both MHC-I and MHC-II expression. The results obtained show that influenza vaccine has no significant influence on EAE induction and severity of autoimmune processes.
Asunto(s)
Autoinmunidad/inmunología , Encefalomielitis Autoinmune Experimental/inmunología , Vacunas contra la Influenza/inmunología , Animales , Autoanticuerpos/sangre , Autoinmunidad/efectos de los fármacos , Encéfalo/inmunología , Encefalomielitis Autoinmune Experimental/tratamiento farmacológico , Femenino , Vacunas contra la Influenza/uso terapéutico , Complejo Mayor de Histocompatibilidad/inmunología , Ratones , Vaina de Mielina/inmunología , Glicoproteína Mielina-Oligodendrócito/inmunología , Vacunas de Productos Inactivados/inmunología , Vacunas de Productos Inactivados/uso terapéuticoRESUMEN
First, the latest scientific and clinical reports will be evaluated to separate the wheat from the chaff, that is, good data versus merely anecdotal evidence. Thus, the famous (infamous) Stromboli Cocktail will be brought up to date. Second, longevity statistics will be reviewed: Why do the most scientifically advanced countries have such low (comparatively) life expectancies? Scientific knowledge expands exponentially each decade, whereas there have been no significant advances in our knowledge, government, economics, politics, anti-corruption, and so forth since the dawn of history. What can we expect in the future? Will the human species outlive the cockroach? Can we expect to get closer to that theoretical asymptote of 120 years of human life? Will this ceiling ever be lifted? Finally, we offer two vital challenges to scientists of today.
Asunto(s)
Envejecimiento/fisiología , Longevidad/fisiología , Neoplasias/mortalidad , Animales , Infección Hospitalaria/mortalidad , Humanos , Enfermedad Iatrogénica/epidemiología , Estados Unidos/epidemiologíaRESUMEN
In the central nervous system (CNS) microglia are crucial for the defense of the brain against invading microorganisms, formation of tumors, and damage following trauma. However, uncontrolled activation of these cells may have deleterious outcomes through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) and CD3 molecules, among others. Both can be expressed on the glia cells before cytokine release and may facilitate an autoimmune inflammatory reaction in the brain. Round microglial cells among the pyramidal cells of the hippocampus with increased expression of CD32+ (FcγIIa) and near the site of injection of aluminum were detected immunohistochemically and indicate microglial activation at the site of aluminum injury. ICAM-1+ immunoreactivity significantly increased in the hippocampus and in the choroids plexus, indicating increased inflammation in the brain as well as increased CD3ξ+ expression in the hippocampus and non-MHC-restricted T cytotoxicity after aluminum injection. The pattern of expression of CD32+ (FcγIIa receptor) near the site of aluminum injection indicates that microglia may play a phagocytic role at the site of aluminum-induced excitotoxicity in the brain. Significant expression of ICAM-1+ and CD3ξ+ immunoreactive cells with the clusters of ICAM-1+ in the choroid plexus suggests a consequently neurotoxic autoimmune reaction induced by microglial hyperactivation in the injured brain.
Asunto(s)
Compuestos de Aluminio/toxicidad , Autoinmunidad/efectos de los fármacos , Encéfalo/efectos de los fármacos , Complejo CD3/metabolismo , Cloruros/toxicidad , Encefalitis , Molécula 1 de Adhesión Intercelular/metabolismo , Microglía/efectos de los fármacos , Síndromes de Neurotoxicidad/etiología , Receptores de IgG/metabolismo , Envejecimiento/inmunología , Envejecimiento/patología , Cloruro de Aluminio , Animales , Encéfalo/inmunología , Encéfalo/patología , Movimiento Celular/efectos de los fármacos , Plexo Coroideo/efectos de los fármacos , Plexo Coroideo/inmunología , Plexo Coroideo/patología , Citotoxicidad Inmunológica/efectos de los fármacos , Encefalitis/inducido químicamente , Encefalitis/inmunología , Encefalitis/patología , Hipocampo/efectos de los fármacos , Hipocampo/inmunología , Hipocampo/patología , Humanos , Inmunohistoquímica , Mediadores de Inflamación/metabolismo , Microglía/inmunología , Microglía/patología , Síndromes de Neurotoxicidad/inmunología , Síndromes de Neurotoxicidad/patología , Fagocitosis , Ratas , Linfocitos T/efectos de los fármacos , Linfocitos T/inmunologíaRESUMEN
The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs--seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulus mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination.
Asunto(s)
Autoinmunidad/inmunología , Encéfalo/inmunología , Animales , Astrocitos/inmunología , Enfermedades Autoinmunes Desmielinizantes SNC/enzimología , Enfermedades Autoinmunes Desmielinizantes SNC/inmunología , Humanos , Oligodendroglía/inmunología , Péptido Hidrolasas/metabolismo , VirulenciaRESUMEN
The neural cell adhesion molecules (NCAMs), and vascular cell adhesion molecules (VCAMs) that regulate cell-to-extracellular matrix adhesion, and matrix metalloproteinases (MMPs), modulating the extracellular matrix (ECM), are considered to play an important role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE). Clinical signs appearance and significant increases of MMP-2 expression in CA1 and CA3 subdomains of the hippocampus and around the central canal of the cervical spinal cord, with the clusters of VCAM-1(+) immunoreactive cells localized in the choroid plexus epithelium and hypothalamo-hypophyses portal vessel system indicate an inflammation in acute EAE. Decreased NCAM-1 expression in CA1 and CA3 fields of the hippocampus, and in a lesser degree in the basal ganglia, limbic structure and cervical spinal cord, support the concept that the demyelinating neuroinflammatory damage in an autoimmune brain affect synaptic organization of the brain, altering the balance between extracellular proteases and cell adhesion molecules which appears to be critical for both the brain plasticity and autoimmune processes.
Asunto(s)
Antígeno CD56/metabolismo , Encefalomielitis Autoinmune Experimental/metabolismo , Metaloproteinasa 2 de la Matriz/metabolismo , Plasticidad Neuronal/fisiología , Molécula 1 de Adhesión Celular Vascular/metabolismo , Animales , Sistema Nervioso Central/inmunología , Sistema Nervioso Central/metabolismo , Sistema Nervioso Central/patología , Encefalomielitis Autoinmune Experimental/inmunología , Encefalomielitis Autoinmune Experimental/patología , Femenino , Inmunización Pasiva , Inmunohistoquímica , Masculino , Proteínas de la Mielina , Glicoproteína Asociada a Mielina/inmunología , Glicoproteína Mielina-Oligodendrócito , Ratas , Ratas EndogámicasRESUMEN
This article reports here on the influence of the static magnetic fields (MFs), locally applied to the brain area, on Na, K-ATPase activity in the rat with lesioned nucleus basalis magnocellularis (NBM) by intracerebral injection of 5 microl, 1% AlCl3 into the nucleus. Two AKMA micromagnets (M) flux density of 60 miliTesla, 5 mm in diameter, were bilaterally implanted with "N" polarity facing down to the cranial bones in the vicinity of the pineal gland (PG), immediately after the lesioning of NBM, during the same operation procedure. Ten days after the lesions of NBM, Na, K-ATPase activity on the erythrocyte membranes in the peripheral blood, measured spectrophotometrically, was completely inhibited. Magnetic stimulation (60 mT) of the brain during the 10 days significantly increased Na, K-ATPase activity on the erythrocyte membranes of rats with lesioned NBM. This results suggests that altered by lesions Na, K-ATPase activity in an experimental model of Alzheimer's disease might be ameliorated by magnetic stimulation of the brain.
Asunto(s)
Compuestos de Aluminio/farmacología , Núcleo Basal de Meynert/efectos de los fármacos , Encéfalo/efectos de los fármacos , Cloruros/farmacología , Magnetismo , ATPasa Intercambiadora de Sodio-Potasio/metabolismo , Cloruro de Aluminio , Animales , Núcleo Basal de Meynert/metabolismo , Encéfalo/enzimología , Encéfalo/efectos de la radiación , Membrana Eritrocítica/efectos de los fármacos , Membrana Eritrocítica/enzimología , Membrana Eritrocítica/efectos de la radiación , Ratas , Ratas WistarRESUMEN
The ultimate goal of this report is to learn how to manipulate the level of memory T cells for more effective treatment of such neurological diseases as multiple sclerosis (MS), where certain T cell subsets recognize self-antigens as opposed to pathogen antigens, and Alzheimer's disease (AD). Brain lesions (electrolitically, by kainic acid, with AlCl, and with 6-OHDA); stimulations (electrical, magnetic, or pharmacological); or restoration of some neurological functions (thermoregulatory and behavioral) by fetal graft allotransplantations in bilaterally lesioned anterior hypothalamic area (AHA-immune regulation) and nucleus basalis magnocellularis (NBM-experimental AD) in our studies were designed to reproduce immune and cognitive deficits induced by lesions of these brain structures. To localize memory traces in the immune system and in the brain we used ethanol and drugs such as kainic acid and 6-OHDA, which have been used very effectively to produce temporary lesions in the brain. Rats showed no learning and memory ability as well as inhibition of immune reactions.
Asunto(s)
Envejecimiento/fisiología , Encéfalo/fisiología , Memoria Inmunológica/fisiología , Memoria/fisiología , Plasticidad Neuronal/fisiología , Enfermedad de Alzheimer/inmunología , Enfermedad de Alzheimer/fisiopatología , Animales , Autoanticuerpos/metabolismo , Conducta/fisiología , Encéfalo/anatomía & histología , Trastornos del Conocimiento/metabolismo , Encefalomielitis Autoinmune Experimental/inmunología , Magnetismo , Red Nerviosa , Ratas , Linfocitos T/inmunología , TrasplantesRESUMEN
Recent data of our group have shown that bilateral electrolytic lesions of the nucleus basalis magnocellularis (NBM) in rats reduced the escape behavior deficit that occurs in the learned helplessness test. The present study was done to establish the effect of intracerebral neural transplantation on the change in escape behavior of NBM-lesioned adult male Wistar rats in the learned helplessness test. At 2 days (NBM-ET) or 10 days (NBM-DT) after bilateral electrolytic NBM-lesions, small fragments of fetal frontal cortex (18th day of gestation) were allotransplanted into the lesioned NBM. Ten days after neural transplantation, the learned helplessness test was performed. The number of shocks that animals received before making an escape response was significantly reduced in NBM-lesioned rats (p < .001, compared to intact control and sham-operated rats). In comparison to NBM-lesioned and sham-ET rats, the NBM-ET rats showed a marked (p < .001) increase in the number of shocks delivered before the animal made such an escape response. On the other hand, NBM-DT rats did not show this increase. These results indicate that neural transplantation performed at an early time after lesioning of NBM reversed the effect of this lesion in rats exposed to learned helplessness test.