Submitted to: Western Poultry Disease Conference
Publication Type: Proceedings
Publication Acceptance Date: February 14, 2006
Publication Date: March 5, 2006
Citation: Kapczynski, D.R., Holt, P.S. 2006. Highly virulent exotic Newcastle disease virus stimulates differential cytokine gene expression in chicken splenocytes from low virulent lasota strain. Proceedings of the 55th Western Poultry Disease Conference. p. 91. Interpretive Summary: The immune system can be divided into two functional components, the innate and adaptive, that differ in their mechanism of pathogen recognition. The innate immune response is responsible for detecting invading microorganisms during the initial stages of infection, which is a crucial determinant of disease resistance or susceptibility. Toll-like receptor (TLR) family members are responsible for recognizing the presence of invading microorganisms through pathogen-associated molecular patterns and initiation of immune responses. Recently, several chicken TLR’s have been identified, including TLR7, which is reported to be involved with recognition of ribonucleic acid components characteristic of viral genomes (e.g. ssRNA). In this study, the innate immune response induced by highly virulent exotic Newcastle disease virus (ENDV) from the 2002-03 California outbreak was compared to the low virulent Newcastle disease virus (NDV) LaSota vaccine strain following in vitro infection of chicken splenocytes. Using real-time RT-PCR, both pathotypes of NDV induced cytokine gene expression, however, ENDV induced higher levels of gene expression of IL-1 beta, IL-6, interferon (IFN)-alpha and IFN-upsilon. The addition of chloroquine abrogated cytokine induction in ENDV-infected splenocytes indicating endosomal maturation is important for downstream cytokine pathway signaling. Using a LaSota virosome model, increased cytokine gene expression was determined to be dependent on the presence of viral RNA. These findings support the role of avian TLR7 in recognition of ssRNA and suggest differences in innate immune response between different pathotypes of NDV.
Technical Abstract: Not required.