Submitted to: World Veterinary Poultry Association
Publication Type: Abstract only
Publication Acceptance Date: 4/6/2007
Publication Date: 9/9/2007
Citation: Kapczynski, D.R., Pantin Jackwood, M.J. 2007. Innate immune responses to avian influenza differ between chickens and ducks [abstract]. 15th World Veterinary Poultry Congress, September 13-16, 2007, Beijing, China. p. 135. Interpretive Summary:
Technical Abstract: Introduction: Avian influenza (AI) remains a constant economic threat to commercial poultry production throughout the world. Influenza viruses can occur naturally among wild bird species, including aquatic waterfowl, without causing significant morbidity or mortality. Conversely, commercial poultry are highly susceptible to significant morbidity and mortality following infection. Previous research in our laboratory has demonstrated differences in pathogenicity between chickens and ducks to various highly pathogenic AI (HPAI) viruses. The reasons for the differences in pathogenicity are unclear and ill defined but may involve the host immune response. The major function of an immune response is to recognize and eliminate infection. The immune system of vertebrates is made up of two functional elements, the innate and adaptive, which contrast by their time of response and mechanisms of pathogen recognition. The early reactions of the innate immune system use germ-line encoded receptors which recognize evolutionarily conserved molecular markers of infectious microbes. The later adaptive immune responses use highly specific antigen receptors on T (cellular immunity) and B-lymphocytes (humoral immunity) that are generated by random processes by gene rearrangement. Because most birds will succumb to HPAI infection before the adaptive immune response can be mobilized, it is the innate immune response which appears as a crucial determinant of disease resistance or susceptibility. These studies were designed to examine the role of the innate immune response in protection from disease by measuring cytokine expression with RRT-PCR immediately following infection. Materials and Methods: In the first set of experiments, splenocytes were isolated from chickens and ducks and infected in vitro with high and low pathogenic AI (H5N2) isolates from the 1983 U.S. outbreak in Pennsylvania. After 6 hours post-inoculation (h.p.i.), RNA was isolated and tested for cytokine induction or suppression by RRT-PCR. The second set of experiments examined the cytokine expression in vivo from chickens and ducks in lung and spleen tissue at 48 h.p.i. following exposure to H5N1 HPAI isolates from Southeast Asia. Results: Following in vitro stimulation both species induced interferon-alpha, however, both IL-2 and IL-4 expression was reduced in chickens compared to ducks. In vivo, innate responses differed between chickens and ducks, as well as different HPAI isolates. In general, cytokine expression in chickens was suppressed following H5N1 infection compared to controls chickens and ducks. Discussion: Based on the results of these studies, differences in innate immune response may play a role in understanding the pathogenesis of AI viruses in both chickens and ducks. Our studies indicate ducks are able to up-regulate cytokine expression which correlated with protection from disease. In contrast, chickens displayed suppressed innate responses, which correlated with susceptibility to disease. Understanding the mechanisms for cytokine induction and suppression following HPAI infection will provide insights into the molecular interactions of AI within avian species.