CHRONICITY IN STRONGYLOIDES-STERCORALIS INFECTIONS - DICHOTOMY OF THEPROTECTIVE IMMUNE-RESPONSE TO INFECTIVE AND AUTOINFECTIVE LARVAE IN AMOUSE MODEL

Citation
Ra. Brigandi et al., CHRONICITY IN STRONGYLOIDES-STERCORALIS INFECTIONS - DICHOTOMY OF THEPROTECTIVE IMMUNE-RESPONSE TO INFECTIVE AND AUTOINFECTIVE LARVAE IN AMOUSE MODEL, The American journal of tropical medicine and hygiene, 56(6), 1997, pp. 640-646
Citations number
33
Categorie Soggetti
Public, Environmental & Occupation Heath","Tropical Medicine
ISSN journal
00029637
Volume
56
Issue
6
Year of publication
1997
Pages
640 - 646
Database
ISI
SICI code
0002-9637(1997)56:6<640:CISI-D>2.0.ZU;2-H
Abstract
Strongyloidiasis is an intestinal disease that can last for decades du e to the occurrence of autoinfective larvae (L3a) in an infected perso n, which contribute to the maintenance of the population of adult worm s in the intestine. The goal of the present study was to determine if L3a are susceptible to the protective immunity that targets the infect ive stage of the worm, the third-stage larvae (L3). Mice immunized and challenged with Strongyloides stercoralis L3 kill more than 90% of ch allenge larvae contained within diffusion chambers. The L3 do not rema in antigenically static in mice, however, but undergo some degree of a ntigenic change before they are killed, becoming host-activated larvae (L3+). The L3/L3+ are killed in this model system by the combined eff ects of both parasite-specific IgM and eosinophils. Mice immunized wit h L3 were able to hill L3/L3+, but did not kill L3a, in challenge infe ctions. Eosinophils were, however, present in diffusion chambers conta ining L3a, and IgM bound to the surface of L3a. We hypothesized that d ifferential IgM recognition of soluble L3a, L3, and L3+ antigens is th e reason why the immune response generated against L3 could not kill L 3a. Many common antigens on L3, L3+, and L3a were recognized by serum from mice immunized with L3, as determined by immunoblotting. However, several unique L3, L3+, and L3a antigens were also recognized by immu ne serum, thus indicating that antigen recognition with IgM antibodies is different between the L3, L3+, and L3a stages. This difference in antigen recognition could explain why L3a are able to evade the immune response that targets L3/L3+ in chronically infected hosts.