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Title:   Author  item
                                            Lillehoj, Hyunitem
                                            Lee, Sung Eunitem
                                            DALLOUL, RAMI - BA VST SYitem
                                            LILLEHOJ, ERIC - UNIVERSITY OF MARYLAND
  Submitted to: Veterinary Immunology and Immunopathology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 3/2/2007
                                    Publication  Date: 5/2/2007
                                    Citation: Hong, Y.H., Lillehoj, H.S., Lee, S., Dalloul, R.A., Lillehoj, E. 2007. Analysis of chicken cytokine and chemokine gene expression following Eimeria acervulina and Eimeria tenella infections. Veterinary Immunology and Immunopathology. 114:220-223.Interpretive Summary: Coccidiosis is the major parasitic disease of poultry which cost industry over $1.2 billion annual loss.  Current control methods need to be improved due to high cost involved. Ability to develop a novel method for coccidiosis control will require comprehensive understanding of protective immunity against avian coccidiosis. In this paper, ARS scientists, in collaboration with scientists at the University of Maryland, investigated various host immune factors which are secreted by host lymphocytes in response to coccidia parasites. The molecular and cellular analysis of immune related changes in the intestine demonstared complex interaction of host-parasite interaction. Identification of effector molecules involved in protective immune response against coccidia parasites will lead to the development of logical control strategy against avian coccidiosis and will lessen the economic loss due to this infection.
                                Technical Abstract: The expression levels of mRNAs encoding a panel of 28 chicken cytokines and chemokines were quantified in intestinal lymphocytes following E. acervulina and E. tenella primary and secondary infections.  Compared with uninfected controls, transcripts of the pro-inflammatory cytokines IFN-', IL-1', IL-6, and IL-17 were increased up to 2,020-fold following primary infection.  By contrast, following secondary infection by either microorganism, pro-inflammatory mRNAs levels were relatively unchanged (< 20-fold).  Transcripts encoding the Th1 and Th1 regulatory cytokines IFN-g, IL-2, IL-10, IL-12, IL-15, IL-16, and IL-18 were uniformly increased 14- to 2471-fold after E. acervulina primary infection, but either unchanged (IL-15, IL-16, IL-18), increased (IFN-g, IL-10, IL-12), or decreased (IL-2) following E. tenella primary infection.  Following secondary infections, Th1 cytokine mRNA levels were relatively unchanged, with the exception of IL-12 which was increased 1.5 x 105-fold after E. acervulina and decreased 5.1 x 104-fold after E. tenella infection.  Transcripts for the Th2 or Th2 regulatory cytokines IL-3 and GM-CSF were increased up to 327-fold following primary or secondary infection with both parasites, while IL-4 and IL-13 mRNAs were decreased 25- to 2 x 105-fold after primary or secondary infections. The dynamics of chicken chemokine expression revealed modest changes (< 100-fold) following primary or secondary infections except for lymphotactin. When lymphocyte subpopulations were similarly analyzed, IFN-g, IL-2, IL-3, IL-15, and MIF were most highly increased in TCR2+ cells following E. acervulina infection, while TCR1+ cells only expressed high levels of IL-16 following E. tenella infection.  In contrast, CD4+ cells only expressed highest levels of IL-10 after E. acervulina infection, whereas these cells produced abundant transcripts for IFN-g, IL-3, and IL-15, and MIF after E. tenella infection.  We conclude that coccidiosis induces a diverse and robust primary cytokine/chemokine response, but a more subdued secondary response.


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