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Intracellular Bacterial Infection-Induced IFN- Is Critically but Not Solely Dependent on Toll-Like Receptor 4-Myeloid Differentiation Factor 88-IFN--STAT1 Signaling¹

Microbiology and Tumorbiology Center, Karolinska Institute, Stockholm, Sweden

Infection of murine bone marrow-derived macrophages (BMM) with Chlamydia pneumoniae induces IFN--dependent IFN- secretion that leads to control of the intracellular bacterial growth. Enhanced growth of C. pneumoniae in Toll-like receptor (TLR) 4^–/– and myeloid differentiation factor (MyD) 88^–/– (but not TLR2^–/–, TLR6^–/–, or TLR9^–/–) BMM is shown in this study. Reduced accumulation of IFN- and IFN- mRNA was also observed in TLR4^–/–- and MyD88^–/–-infected cells. IL-1R and IL-18R signaling did not account for differences between MyD88^–/– and wild-type BMM. Surprisingly, infection-induced NF-B activation as well as TNF-, IL-1, or IL-6 mRNA expression were all normal in TLR4^–/– and MyD88^–/– cells. Phosphorylation of the transcription factor STAT1 during bacterial infection is IFN- dependent, and necessary for increased IFN- mRNA accumulation and chlamydial growth control. Signaling through common cytokine receptor -chain and RNA-dependent protein kinase both mediated IFN--dependent enhancement of IFN- mRNA levels. Accumulation of IFN- mRNA and control of C. pneumoniae growth required NF-B activation. Such NF-B activation was independent of IFN-, STAT1, and RNA-dependent protein kinase. In summary, C. pneumoniae-induced IFN- expression in BMM is controlled by a TLR4-MyD88-IFN--STAT1-dependent pathway, as well as by a TLR4-independent pathway leading to NF-B activation.

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The JI 2004 172: 5811-5812. [Full Text]  

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