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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #182003
Title: BACTERIAL CPG-DNA AND VIRAL DOUBLE-STRANDED RNA SYNERGIZE INNATE IMMUNE RESPONSES IN MONOCYTES FROM NEONATAL CHICKENS

Author
item He, Louis
item Genovese, Kenneth - Ken
item Kogut, Michael - Mike

Submitted to: International Cytokine Society Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 7/8/2005
Publication Date: 10/20/2005
Citation: He, H., Genovese, K.J., Kogut, M.H. 2005. Bacterial CpG-DNA and viral double-stranded RNA synergize innate immune responses in monocytes from neonatal chickens [abstract]. Cell Research. 15(Suppl. 10):249.

Interpretive Summary:

Technical Abstract: Toll-like receptors (TLRs) recognize microbial components and initiate innate immune responses that control microbial infections. Nitric oxide (NO) is generated in immune cells, such as monocytes and macrophages, in response to microbial stimulation and is involved in pathogenesis and control of both bacterial and viral infections. We have investigated the innate immune response of chicken monocytes to bacterial CpG-motif containing oligodeoxydinucleotide (CpG-ODN) and the analog of viral double-stranded RNA, poly I:C, by measuring the induction of NO synthesis. Our results show ligands poly I:C and CpG-ODN of the TLR3 and TLR9, respectively, synergized the induction of NO in chicken monocytes, indicating a synergistic interaction between TLR3 and TLR9. When stimulated separately, CpG-ODN was able to induce certain quantities of NO in the chicken monocytes; whereas, poly I:C stimulated very little NO production in the chicken monocytes. In combination, CpG-ODN and poly I:C synergize the effect on NO synthesis, inducing significantly higher levels of NO in chicken monocytes. The control ODN (without the CpG motif) did not stimulate NO production and had no synergistic effect when combined with poly I:C. Our results suggest that the combination of bacterial and viral infections may induce significantly greater inflammatory immune responses in the host.