Changes in local IFN-gamma and TGF-beta4 mRNA expression and intraepithelial lymphocytes following Eimeria acervulina infection.

Inbred chickens SC (B2B2) and TK (B15B21) display different levels of susceptibility to Eimeria acervulina infection. Following primary and secondary infections, SC chickens showed significantly lower oocyst production compared to TK chickens. Both strains produce significantly fewer oocysts during secondary infection (si) indicating that a protective host immune response had developed subsequent to primary infection (pi). To elucidate the immunologic differences between SC and TK chickens that may account for their different levels of disease susceptibility, cellular and molecular parameters of intestinal immunity were compared. CD4 T-lymphocytes increased significantly and more rapidly post-pi and si in SC relative to TK chickens during the later stages of infections. However, later during the infections, CD4 cells were higher in TK compared to SC chickens. Although the percentage of CD8 lymphocytes increased in both strains after pi, following si the percentage of these cells continued to increase in SC chickens but showed a marked decrease in TK chickens. Contrary to the effects on CD4 cells, the percentage of TCR1 cells was higher in TK chickens early after pi while the same cell subset was higher in SC chickens later following infection. The percentages of TCR2 cells were significantly higher in both strains following pi. At the molecular level, IFN-gamma mRNA expression in caecal tonsils and splenic lymphocytes was generally higher in SC compared to TK chickens following E. acervulina infection, while intraepithelial lymphocytes from the duodenum demonstrated reduced levels of this cytokine in both the strains, particularly following pi. TGF-beta4 mRNA levels generally increased in lymphocytes from the caecal tonsils, spleen and duodenum from both the strains. These differences in lymphocyte subpopulations and cytokine mRNA expression between SC and TK chickens following E. acervulina infection indicate a complex genetic control of the native immune response to coccidiosis.