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Legionella pneumophila and Interleukin-12 Production: In Vitro Infection Model, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555817985/9781555812300_Chap22-1.gif /docserver/preview/fulltext/10.1128/9781555817985/9781555812300_Chap22-2.gifAbstract:
Interleukin-12 (IL-12), one of the key cytokines in regulating the development of Th1 response, is a heterodimeric cytokine composed of two disulfide-linked p35 and p40 subunits. Both subunits have to be expressed within the same cell to produce biologically active p70 heterodimer. The production of IL-12 by monocytes/macrophages is induced by exposing responsive cells to a variety of microbial products such as lipopolysaccharide (LPS). The suppression of IL-12 by Legionella pneumophila infection may be occurring at the level of gene transcription. The analysis of the steady-state levels of IL-12 p35 and IL-12 p40 mRNA determined by reverse transcriptase-PCR (RT-PCR) showed that L. pneumophila infection induced the suppression of mRNA accumulation for the IL-12 p40 gene in response to LPS stimulation, but not the IL-12 p35 gene, which was constitutive in all macrophages treated. L. pneumophila infection induced production of MCP-1 protein and up-regulated the LPS-induced production of MCP-1 protein regardless of the virulence of L. pneumophila and its viability in the macrophages. The experimental mouse infection with L. pneumophila resulted in certain levels of IL-12. Since IL-12 production is regulated by multiple mechanisms, including cytokines produced by other cells, it can be speculated that the suppressed IL-12 by infection may be overcome by other systems in vivo, such as the host defense system.