Avian gut-associated lymphoid tissues and intestinal immune responses to Eimeria parasites

Abstract

Coccidiosis, an intestinal infection caused by intracellular protozoan parasites belonging to several different species of Eimeria, seriously impairs the growth and feed utilization of livestock and poultry. Host immune responses to coccidial infection are complex. Animals infected with Eimeria spp. produce parasite-specific antibodies in both the circulation and mucosal secretions. However, it appears that antibody-mediated responses play a minor role in protection against coccidiosis. Furthermore, there is increasing evidence that cell-mediated immunity plays a major role in resistance to infection. T lymphocytes appear to respond to coccidial infection through both cytokine production and a direct cytotoxic attack on infected cells. The exact mechanisms by which T cells eliminate the parasites, however, remain unclear. Although limited information is available on the intestinal immune system of chickens, gut lymphoid tissues have evolved specialized features that reflect their role as the first line of defense at mucosal surfaces, including both immunoregulatory cells and effector cells. This review summarizes our current understanding of the avian intestinal immune system and mucosal immune responses to Eimeria spp., providing an overview of the complex cellular and molecular events involved in intestinal immune responses to enteric pathogens.

Immunity in rats against Eimeria separata : oocyst excretion, effects on endogenous stages and local tissue response after primary and challenge infections

“…Using corresponding conditions in Sprague Dawley rats, Marquardt et al (1987) reported a 72±84% protection in challenged animals. These results suggest that primary and secondary E. separata infections are dierently controlled in rats, as already suggested in coccidial infections of mice and chicken (for reviews see Lillehoj and Trout 1996).…”

“…These dierences would ®t the concept that primary Eimeria infections are predominantly controlled by T helper cells whereas cytotoxic T cells may act as eector cells against Eimeria spp. in immune hosts (Rose et al 1988(Rose et al , 1992a; see also Lillehoj and Trout 1996).…”

Porcine Coccidiosis – Investigations on the Cellular Immune Response against Isospora suis

“…The roles of CD4 + and CD8 + T lymphocytes in coccidial infections seem to vary; in E. vermiformis infections in mice, CD4 + T lymphocytes seem to be protective in primary, CD8 + lymphocytes in secondary immune response (Lillehoj and Trout 1996), while in bovine E. bovis infections CD4 + Th1-like cells are predominantly involved in the termination S153 PROTOZOA of primary infections (Hermosilla et al 1999). In primary infections with E. acervulina or E. tenella, on the other hand, CD4 + T cells do not seem play a major role but CD8 + T cells do (Lillehoj and Trout 1996;Swinkels et al 2006). In Cryptosporidum muris infections, CD4 + T cells appear to control the infection and the production of IFN-γ is essential for this control, while CD8 + cells are of minor importance (Culshaw et al 1997).…”

“…Interestingly, this kind of protection cannot be attributed to passive transmission by the colostrum or milk from the sow (Baekbo et al 1994;Stuart and Lindsay 1986;Taylor 1984). From this observation and investigations of other coccidial infections it can now be assumed that resistance to coccidia is mainly based on cellular immune response (e.g., Wakelin and Rose 1990;Lillehoj and Trout 1996;Worliczek et al 2007) and that serum antibodies play only a minor role in the control of the infection. For infections with I. suis, this assumption is supported by the finding that in piglets antigen-specific T cells with the phenotype of T-helper cells (T H cells), cytotoxic T lymphocytes (CTL) and T-cell receptor-γδ positive (TcR-γδ + ) cells can be identified either by production of IFN-γ or proliferation after antigen-specific restimulation in vitro (Worliczek, unpublished results).…”

“…This reaction is further promoted by alterations of adhesion factors on cell surfaces, leading to further accumulation of leukocytes in infected tissues (Hermosilla et al 2006). There is strong evidence that in chicken adaptive cellular immune responses are the most important defence mechanisms against Eimeria infections (reviewed in Lillehoj and Trout 1996). However, this finding cannot be applied for all Eimeria infections in other hosts; e.g., primary infections of mice with E. papillata seem to be controlled primarily by natural killer cells (NK cells) and neutrophils (Schito and Barta 1997), while adaptive responses mediate protection against reinfection (Schito et al 1996).…”