Liver cystic echinococcosis and human host immune and autoimmune follow-up: A review

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

Morphological changes in lymph nodes and spleen upon EAE induction in C57BL/6 mic

Myelin oligodendrocyte glycoprotein (MOG) is a protein widely used in the induction of experimental autoimmune encephalomyelitis (EAE) for studying human multiple sclerosis (MS). In C57BL/6 female mice aged eight weeks, we administered subcutaneously MOG35-55 peptide in CFA (complete Freund's adjuvant) along with pertussis vaccine injected intraperitoneally. We observed the sign of flaccid tail as early as thirteen days post-immunization in five of twelve animals. Hematoxylin and eosin staining of paraffin-embedded sections of lymph nodes and spleen revealed the presence of germinal centers in the immunized animals. In the control group of animals, lymphoid follicles without germinal centers were observed. Immunohistochemical staining of spleen sections revealed an expression of MHC II molecules in the EAE-induced group. We would like to point out that even though the clinical signs are mild, the morphological changes are apparent in the lymph nodes and spleen of MOG35-55-immunized mice

Magnetic brain stimulation and immune response in the rat with lesioned brain structures

Rats with electrolytic anterior hypothalamic lesions showed a suppressed Arthus reaction, delayed skin hypersensitivity, and antibody production at 7, 14 and 21 days after immunization with bovine serum albumin (BSA) in complete Freund's adjuvant (CFA). However, magnetic treatment of the brain of rats with anterior hypothalamic or caudate nucleus lesions increased both humoral and cellular sensitivity reactions. These data indicate that magnetic stimulation of the brain is capable of modulating immune functions

The neuronal and immune memory systems as supervisors of neural plasticity and aging of the brain - From phenomenology to coding of information

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

Ethanol consumption affecting some brain proteins and cortical plasticity might disturb the neural networks of long-term memory

The objective of this study is to investigate whether chronic ethanol consumption include brain damage expressed as; an increase of antibody titer to S-100 and synaptic membrane proteins, additioning of lateral ventricles volume and increasing within the brain cortex in the rats. After six months of ethanol consumption rats wer tested for antibody titer to S-100, neuron specific enolase (NSE), 14-3-2 and synaptic membrane proteins. In this rat's diameter of anterior, medial and posterior cortical areas and diameter of lateral ventricles were measured after histological examination. Ethanol consumption significantly increases antibody titer to V-100 and synaptic membranes, decrease antibody titer to 14-3-2 protein and do not affect antibody to NSE in peripheral blood of these animals. Additional volume of lateral right and left ventricles indicate that brain atrophy appears after six months of ethanol consumption. Increased diameter of anterior cortical area but not medial and posterior cortical area indicate morphological changes in the brain cortical tissue in prefrontal, and frontal cortical areas that art, responsible for attention memory and associative long-term memory in this part of the brain. Of course, all of these morpho-functional changes in the cortex find some depth structures of the brain might disturb the function of neural networks for abovementioned types of memory in the brain

Aluminum excytotoxicity and neuroautotoimmunity: The role of the brain expression of CD32+ (FcγRIIa), ICAM-1+ and CD3ε in aging

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 [1]. However, uncontrolled activation of these cells may have deleterious outcomes [2] through activation of Fcγ and the complement 3 receptors and the induction of an adaptive immune reaction [3]. Proteins contributing to this reaction are the intercellular adhesion molecule-1 (ICAM-1) [3] 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 CD3ε+ 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 CD3ε + 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

Aging, cancer, and longevity: The uncertain road

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

Magnetic stimulation of the brain increase Na+, K+-atpase activity decreased by injection of alcl(3) into nucleus basalis magnocellularis of rats

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 mu l, 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

Role of inactivated influenza vaccine in regulation of autoimmune processes in experimental autoimmune encephalomyelitis

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