|Sudeep, Perumbakkam -|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: February 10, 2013
Publication Date: February 10, 2013
Citation: Sudeep, P., Hunt, H.D., Cheng, H.H. 2013. Does resistance to Marek’s disease select for specific gut microflora that play a role in influencing the host immune response. Meeting Abstract. Keystone Symposia Conference, The Gut Microbiome: The Effector/Regulator Immune Network, February 10-15, 2013, Taos, New Mexico. Technical Abstract: Marek’s disease (MD) is an economically important neoplastic disease of chickens caused by the Marek’s disease virus (MDV), a naturally occurring oncogenic alphaherpesvirus. Experimental inbred chicken lines 63 and 72 are known to be MD resistant and susceptible, respectively. In this study, we characterized chicken immune cells over time in response to MDV challenge in both the above mentioned lines, as well as profiled for microbial species in the chicken ceca. Day-old control and MDV-infected (2,000 pfu Md5 strain) chicks were housed in separate isolators. Invasive sampling was performed on 5 individual birds from each treatment (20 total) every 7 days. Splenic cells and DNA from ceca samples were isolated to elucidate changes to the immune system and gut flora, respectively. Based on flow cytometry, MD resistant birds differed from susceptible ones for the following characteristics: (1) a delayed increase in CD4+ cells following MDV infection (21 vs. 14 dpi in the susceptible birds), (2) Cytotoxic T lymphocytes (CTL) population was reduced in MDV-infected birds compared to uninfected with a greater reduction in line 6, and (3) Only MD resistant birds showed an increase in CD8a/a cells in response to MDV infection. These results suggest CD4+ cells are activated in response to infection and CTL levels show immune evasive function induced by the virus to escape recognition. CD8a/a activity is recognition of monomorphic antigens like bacterial lipids, and these cells were present in higher levels in infected resistance compared to susceptible birds at 21 and 28 dpi suggesting a protective role for MD pathogenesis. Further mining of the both the microbial and immunological data is presently being undertaken to understand spatial and temporal changes to the microbial community to infection and immune response.