Title

Host inflammatory response and vaccine-mediated immune protection against Mycoplasma gallisepticum infection in chickens

Date of Completion

January 2006

Keywords

Agriculture, Animal Pathology

Degree

Ph.D.

Abstract

Mycoplasma gallisepticum infection in chickens leads to inflammation primarily of the trachea, air sacs and lungs. Several killed and live-attenuated vaccines have been developed to control this pathogen. However, the mechanisms of immune protection in vaccinated chickens have not been elucidated. Also, the roles of chemokines, cytokines and molecules critical for innate and acquired immunity during M. gallisepticum infection have not been investigated. This research focuses on evaluating the potential correlates of immune protection in chickens vaccinated with M. gallisepticum strain GT5. This research also characterizes the host inflammatory response with respect to cellular infiltrates as well as chemokine and cytokine gene expression during M. gallisepticum infection. The studies described emphasize the importance of locally-induced, rapid and vigorous humoral immune response that can prevent attachment and colonization by the mycoplasma, leading to the development of mild lesions with few, discrete, subepithelial lymphocytic infiltrates. Sham-vaccinated chickens following challenge with pathogenic M. gallisepticum strain Rlow, develop thickening of the tracheal mucosa due to infiltrates of heterophils, macrophages, lymphocytes and IgA+ and IgG + plasma cells along with persistence of mycoplasma. There was up-regulation of genes encoding chemokines, CCL19, CXCL13, lymphotactin, RANTES, MIP-1β, MIP-2, CXCL-14 and lymphocyte-chemotactic factor, IL-16, in M. gallisepticum -infected chickens. The mRNA levels of IFN-γ, IL-10, TLR's 1, 2 and 4, granzyme A, NK lysin, fas and caspases 3 and 8 were also higher in M. gallisepticum-infected chickens. Expression of CCL20, IL-8 and IL-12p40 genes was down-regulated while there were no significant changes in the expression of pro-inflammatory cytokines. These results further our understanding of the pathogenic process of M. gallisepticum infection in chickens. ^