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Title:   Author  item
                                            Choi, Kangitem
                                            Lillehoj, Hyunitem
                                            Zarlenga, Dante
  Submitted to: Veterinary Immunology and Immunopathology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 9/4/1999
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary: Avian coccidiosis is caused by several different species of Eimeria parasites.  Infection with coccidia causes severe intestinal damages and poor nutrient absorption.  Although coccidiosis is currently managed by drug theraphy, high incidence of drug resistant  Eimeria field strains urges the development of a novel control strategy against coccidiosis.  However, the development of novel control strategy for coccidiosis is hampered by our lack of understanding of the immunobiology of parasite- host interactions.  In this paper, ARS scientists characterized the local host immune responses which control protective immunity to Eimeria.  These scientists showed for the first time that Eimeria parasites activate the intestinal T lymphocytes to produce immunologically active factors such as interferon-gamma and TGF-alpha.  The production of these factors by intestinal lymphocytes is an important feature of the local host immunity.  These findings will increase our understanding of host innate immunity against intestinal intracellular parasites such as Eimeria and aid the development of new control strategies for coccidiosis by the poultry industry.
                                Technical Abstract: Inbred chickens SC (B2B2) and TK (B15B21) display different levels of susceptibility to Eimeria acervulina infection. 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-primary (pi) and secondary (si) infections in SC relative to TK chickens during the later stages of infections. 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, interferon-gamma (IFN-g) mRNA expression in caecal tonsils and splenic lymphocytes was 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 strains, particularly following pi. TGF-alpha 4 mRNA levels generally increased in lymphocytes from the caecal tonsils, spleen and duodenum from both 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.


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