Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

The potential role of intestinal intraepithelial lymphocytes (i-IELs) in th e generation of host protective immunity after helminth infection was inves tigated using the Trichinzella spiralis (Owen, 1835)/mouse model. In this s tudy we found a significant rise of TCR gamma delta(+) i-IELs (P < 0.001) c oncurrent with the jejunal goblet cells (GC) hyperplasia in T. spiralis-inf ected C57BL mice on day 4 p.i. However, no direct relationship between the kinetics of the increase in TCR gamma delta(+) i-IELs and T. spiralis expul sion was observed in infected mice. Taken together, these results implicate that gamma delta i-IELs probably perform a unique functions related to the regulation of the GC proliferation accompanying T. spiralis gut infection. As is known, these TCR gamma delta(+) i-IELs may release mediators or grow th factors that in turn influence GC differentiation With the use of dexame thason (DEX), a potent anti-inflammatory agent which also induces apoptotic cell death in i-IELs, we have confirmed that the expulsion of T. spiralis from the mouse gut is accompanied by an inflammatory response. Indeed, the GC are clearly involved in these phenomena, apparently under the regulation by TCR gamma delta(+) i-IEL-mediated responses, since DEX abrogated GC pro liferation in T. spiralis-infected C57BL mice and subsequently augmented ad ult worm burden. Our data also show that the rejection of adult worms start s concurrently with a significant increase in TCR alpha beta(+) and CD8(+) i-IELs (P < 0.05 and P less than or equal to 0.01, respectively), namely by day 7 p.i. At the same time, CD4(+) cells significantly decreased (P < 0.0 5) in the intestinal epithelium of T. spiralis-infected, vs uninfected mice . These results may indicate that the TCR alpha beta(+) and CD8+ i-IELs act as effectors of anti-T. spiralis defence reactions. The implications of th ese findings for the potential role of intestinal intraepithelial CD8(+) an d TCR alpha beta(+) cells in the pathogenesis of the intestinal lesions dur ing T. spiralis gut infection are discussed.