|Rothwell, Lisa - INST FOR ANIMAL HEALTH|
|Kaiser, Pete - INST FOR ANIMAL HEALTH|
Submitted to: Congress International Society Develop Comparative Immunology
Publication Type: Abstract Only
Publication Acceptance Date: July 1, 2003
Publication Date: N/A
Technical Abstract: Internalization of pathogens by phagocytic cells starts the innate immune response, which in turn regulates the acquired response. Phagocytes express a variety of receptors that are involved in recognition of pathogens including: (1) pathogen recognition receptors (PRRs) that recognize conserved motifs, (2) complement recptors that recognize complement-opsonized pathogens, and (3) Fc receptors that recognize antibody-opsonized pathogens. Recognition of microbes is accompanied by inducing multiple cell processes including the production of pro- and anti-inflammatory cytokines and chemokines. The objective of the present experiments was to use probes to known avian pro- and anti-inflammatory cytokines and TaqMan technology to ascertain cytokine gene expression in avian heterophils following phagocytosis with either nonopsonized Salmonella enteritidis (SE), serum opsonized SE, or IgG-opsonized SE. Expression of IL-6 and IL-8, considered in mammals as a pro-inflammatory chemokine, were upregulated following exposure to the nonopsonized or the opsonized SE. However, mRNA expression for IL-18 and IFN-gamma were down-regulated while the expression of mRNA for the anti-inflammatory cytokine TGF-beta4 was upregulated. Interestingly, IL-1beta mRNA expression was upregulated only in heterophils that phagocytized the nonopsonized SE; whereas both serum-opsonized and IgG-opsonized SE induced a down-regulation of IL-1beta mRNA. These results suggest that signaling interactions initiated by receptor recognition of the microbe surface differentially regulates the induction of inflammatory cytokines in avian heterophils. PRRs on heterophils appear to be, initially, better able to induce a proinflammatory response to SE.