The Immune Response to the Parasitic Nematode Trichinella and the Ways to Escape it. From Experimental Studies to Implications for Human Infection

Abstract

The review describes different aspects of the host immune response to Trichinella, not only at the intestinal level on which most of the studies have focused until now, but also in the muscles which represent the final target of host invasion. The role of antibodies, T cells, mast cells, eosinophils and neutrophils, respectively, in immune reaction to this nematode is considered, in the light of the recent data derived from experimental models, both "in vivo" and more recently "in vitro" and when available, from clinical observations. A section is also devoted to the principal escape mechanisms from host immune responses, described in Trichinella, which are in part common to other parasites, in part peculiar. Two groups of mechanisms are described: antigen-dependent, such as anatomic seclusion, antigen stage-specificity, shedding and renewal and molecular mimicry, and those directly affecting the host immune response. Of the latter, some act at central level like immune suppression, polyclonal activation and eosinophilia induction, others interfere with effector functions as in the case of host leukocyte modification, immune complex accumulation, blocking antibody production or complement assembly blocking. The antigenic composition of the different stages is the subject of another section which has the aim to give an overview of the principal antigens described up to now, without giving too many biochemical details, but just illustrating the candidates for possible vaccines. Finally, the perspectives for vaccination are described. Most of the results described are derived from the experimental studies, but their implications in human infection are relevant.

Trichinella spiralis infection rapidly induces lung inflammatory response

“…Upon arrival at the lungs, the parasite encounters a reactive organ that acts as a retention and parasite destruction site. Only those larvae capable of avoiding this response will achieve muscle invasion (Gansmüller et al 1987;Bruschi 2002). Thus, during T. spiralis infection, not only an effector mechanism directed toward adult worms in the intestine is developed, but also our results suggest an effector mechanism directed against the migrant stage in the lung.…”

Protein change of intestinal epithelial cells induced in vitro by Trichinella spiralis infective larvae

“…During their invasion and development, parasites encounter hostile host environment and immune defenses; therefore, they produce numerous molecules as survival strategies against these adverse changes (Bruschi 2002;Dzik 2006). Better understanding of these molecules would help elucidate the mechanism of parasite invasion and survival in the host and identify possible targets for vaccine development.…”

Type 1 Fimbrial Adhesin FimH Elicits an Immune Response That Enhances Cell Adhesion of Escherichia coli

“…Whether or not antibody shedding happens in vivo and has a physiological impact, such as immune evasion, remains to be determined. Antibody shedding is a known phenomenon in parasitic nematodes that are able to slough off antibodies against their surface coat, but this involves complete shedding of the surface antigen and takes many hours of growth (10). To our knowledge, our study is the first to report the phenomenon of antibody shedding mediated by a conformational switch of the protein antigen.…”