[The organ pathology in the acute stage of tissue helminthiases: the role of eosinophilia of the blood and tissues, blood immunoglobulins E and G4 and immune response-inducing factors].
The pathogenesis of organic lesions in the early phase of tissue-dwelling helminthic infections has been analyzed and discussed by taking into account the previous findings [8, 9, 12], the results of current clinical and immunological studies [10, 11, 60] in the light of a fundamental literature data review. The products secreted by invasive helminthic larvae and the substances expressed onto their cuticula tegument surface mimic nonspecific [34, 43] and specific [21, 28, 33, 42] modulators of host inflammatory processes or induce the latter directly [37, 30, 42, 70]. The development of severe visceral pathology at the very early stage of human toxocariasis [60] is associated with unbalanced overproduction of these modulators and directly acting substances by a zoonotic agent. Some of these substances provoke organic and systemic pathology in the nearest day-hours after massive human invasion with sylvatic Trichinella spiralis strains or with Paragonimus westermani ichunensis larvae with a fatal end in 2-2.5 weeks [8, 14]. Parasitic enzymes that mimic the host proteins [73, 42], perhaps recently revealed [30] parasitic myogenic proteins, human tissue epitopes normally unexpressed [71], i.e. autoantigens from the impaired tissues [16] have been regarded as the factors leading to immunopathological/autoimmunological processes [21, 73]. Experimental allergic myocarditis (EAM) with endo-, pericardial, and valvular damages was reproduced in the guinea pigs immunized with T. spiralis somatic antigen and myocardial tissue homogenate (without BCG) in lanoline and mineral oil [8]. The development of trichinellosis-induced EAM with its pathomorphological characteristics revealed the existence of a Th1-variant of myocarditis in trichinosis similar to that of myosin-induced myocarditis [69] and confirmed the unfavourable effect of Th1 population stimulated in tissue-dwelling helminthic infections [62, 66, 70]. Visceral pathology in 22 patients at the acute stage of trichinosis, Opisthorchis felineus infection and in the early phase of toxocariasis coincided with serum IgG4 hyperproduction, competitive with serum IgE production, or with hypereosinophilia in IL-4-independent allergic reaction [60]. The absence of visceral pathology in the examined patients with high blood eosinophilia and serum IgE content (without elevated IgG4 levels) confirmed the protective functions of these parameters of immune responses in helminthic infections. However, there were individual variations of responses in terms of these parameters: high levels of all 3 parameters in three patients and IL-4-independent allergic reaction in 4 patients, only 6 of them had no visceral pathology. These substantial individual variations of immune responses at the early stage of disease seem to reflect the susceptibility to infections [71].
Ozeretskovskaia
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D000208:Acute Disease; D000917:Antibody Formation; D000937:Antigen-Antibody Reactions / Q000276:immunology*; D004802:Eosinophilia / Q000276:immunology* / Q000473:pathology*; D006373:Helminthiasis / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D007111:Immunity, Cellular; D007073:Immunoglobulin E / Q000097:blood*; D007074:Immunoglobulin G / Q000097:blood*
D007074:Immunoglobulin G; D007073:Immunoglobulin E