Dose-dependent early recruitment of intestinal intraepithelial gamma deltaT cells following experimental Trichinella spiralis gut infection

Citation
M. Dominis-kramaric et al., Dose-dependent early recruitment of intestinal intraepithelial gamma deltaT cells following experimental Trichinella spiralis gut infection, HELMINTHOL, 37(4), 2000, pp. 187-193
Citations number
33
Categorie Soggetti
Animal Sciences
Journal title
HELMINTHOLOGIA
ISSN journal
04406605 → ACNP
Volume
37
Issue
4
Year of publication
2000
Pages
187 - 193
Database
ISI
SICI code
0440-6605(200011)37:4<187:DEROII>2.0.ZU;2-W
Abstract
Since the expulsion of Trichinella spiralis worms is a dose-dependent effec t, to assess whether or not intestinal intraepithelial lymphocytes (i-IELs) , particularly gamma delta T cells, respond comparably to different sized T . spiralis infection, we used C57BL mice, orally infected with two doses, 5 0 or 400 viable T. spiralis muscle larvae (L-1). In the present study we found that the appearance of gamma delta T cells pr eceded that of alpha beta T cells among i-IELs of infected mice. The propor tion of gamma delta T cells increased promptly (on day 1 p. i.) and signifi cantly (P < 0.005) in the gut epithelium of mice infected with 400 L-1 T. s piralis larvae, but not in mice infected with 50 L-1 larvae, compared with uninfected mice. These data indicate that <gamma>delta T cell responses var ied in a dose-dependent manner. In spite of their rapid increase, no correl ation between kinetics of gamma delta nor alpha beta T cells in i-IELs and T. spiralis worm expulsion was observed in mice infected with either 400 (b ecause of a rapid decrease in the i-IEL population in gut epithelium early after activation, by day 7 p. i.) or 50 L-1 larvae (since no statistically significant rise in the proportion of gamma delta or alpha beta T cells was observed during the course of infection). All-together, our results sugges t that both T. spiralis infection levels probably elicit immunodepression b y interference with the first line defence of T cell function thereby influ encing the outcome of experimental T. spiralis gut infection.