No abstract

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.

Rats with lesions restricted to the locus ceruleus were tested for immune inflammatory reactions. In these rats, Arthus and delayed skin hypersensitivity reactions to bovine serum albumin and old tuberculin were suppressed. The ablation of locus ceruleus completely inhibited the development of clinical signs of experimental allergic encephalomyelitis, markedly diminished the occurrence and intensity of lesions in the central nervous system, and significantly reduced the production of antibody against the rat brain myelin basic protein. These results establish a link between the locus ceruleus and immune inflammatory reactions in the rat.

Earlier research had demonstrated that lesions placed in different brain structures may alter the immune responsiveness. Norepinephrine is one of neurotransmitters which plays a role in immune reactions, and the locus ceruleus represents the largest group of norepinephrine-containing neurons in the brain. The present study concerns, therefore, the relationship between the locus ceruleus and humoral immune reactions. For this purpose, rats with electrolytically induced lesions in locus ceruleus were used in the study. Locus ceruleus-lesioned animals showed a decreased ability to produce hemolysin-releasing cells, hemagglutinins, and antibodies to bovine serum albumin. In brain-lesioned rats, thymus tended to the smaller in size, and there was a depletion of CD4+ helper/inducer lymphocyte population in the peripheral blood.

The present study was performed to investigate and compare the effect of acetylcholinesterase inhibitor, physostigmine (0.045, 0.060 and 0.075 mg/kg sc, 30 min before the tests) and Ca-antagonist, verapamil (1.0, 2.5, 5.0 and 10.0 mg/kg sc, 30 min before the tests), on two-way active avoidance (AA) learning (acquisition and performance) in nucleus basalis magnocellularis (NBM)-lesioned rats. Bilateral electrolytic lesions of NBM induced significant decrease of acquisition and performance of AA responses in rats. Physostigmine (0.060 mg/kg) significantly improved only acquisition of AA, while verapamil (2.5 and 5.0 mg/kg) significantly improved both type of AA behavior in NBM-lesioned rats. These results suggest that altered calcium homeostasis might play significant role in pathogenesis of experimental induced Alzheimer's disease (AD) and that administration of calcium antagonist such as verapamil might successfully ameliorate disturbances of learning and memory appeared after lesions of NBM.