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Rapid Chromatin Remodeling of Toll-Like Receptor 2 Promoter During Infection of Macrophages with Mycobacterium avium¹

Tianyi Wang^*, William P. Lafuse, Kiyoshi Takeda, Shizuo Akira and Bruce S. Zwilling^2,*,

^* Department of Microbiology, College of Biological Sciences, and Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine and Public Health, Ohio State University, Columbus, OH 43210; and Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

We have previously reported that NF-B and stimulating factor 1 elements within the proximal mouse Toll-like receptor 2 (TLR2) promoter region are required for the transcriptional activation of TLR2 expression following infection with Mycobacterium avium. In the present study, we found that a rapid increase in both DNase I sensitivity and restriction enzyme accessibility at the TLR2 promoter region occurred following infection with M. avium. Increase in restriction enzyme accessibility at the TLR2 promoter region covering the NF-B and stimulating factor 1 elements was associated with the induction of TLR2 expression at the mRNA level. Furthermore, the increase in restriction enzyme accessibility at the TLR2 promoter region did not appear to result from binding of NF-B, but rather depended on a TLR2-myeloid differentiation factor 88 signaling pathway. Together our results indicate that chromatin remodeling occurs at TLR2 promoter region following infection with M. avium, allowing the access of transcription factors to initiate the transcription of TLR2.

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