Studies from Technical University of Munich yield new information about chlamydia
2007 NOV 22 -- "Chlamydia pneumoniae, an intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule myeloid differentiation factor-88 ( MyD88) play a critical role in inducing immunity against this microorganism and are crucial for survival," investigators in Munich, Germany report. "To explore the influence of MyD88 on induction of immune responses in vivo on a genome- wide level, wildtype ( WT) or MyD88 (-/-) mice were infected with C. pneumoniae on anesthesia, and the pulmonary transcriptome was analyzed 3 days later by microarrays. We found that the infection caused pulmonary cellular infiltration in WT but not MyD88 (-/-) mice. Furthermore, it induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88 (-/-) mice. This cluster contains primarily genes encoding for chemokines and cytokines like MIP- 1 alpha, MIP- 2, MIP- 1 gamma, MCP- 1, TNF, and KC and other immune effector molecules like immunoresponsive gene-1 and TLR2. Arginase was highly induced after C. pneumoniae infection and was MyD88 dependent. Genes induced by interferons were abundant in a cluster of 102 genes that were only partially MyD88 dependent. Also, lcn2 ( lipocalin- 2) and timp1 were represented within this cluster. Interestingly, a set of 37 genes including sprrla was induced more strongly in MyD88 (-/-) mice, and most of them are involved in the regulation of cellular replication," wrote N. Rodriguez and colleagues, Technical University of Munich. The researchers concluded: "In summary, ex vivo analysis of the pulmonary transcriptome on infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses and identified MyD88-independentgenes involved in cellular replication." Rodriguez and colleagues published their study in Physiological Genomics (MyD88-dependent changes in the pulmonary transcriptome after infection with Chlamydia pneumoniae. Physiological Genomics, 2007;30(2):134-145). For additional information, contact T. Miethke, Technical University of Munich, Institute Med Microbiology Immunology & Hyg, Trogerstr 30, D-81675 Munich, Germany. The publisher of the journal Physiological Genomics can be contacted at: American Physiological Society, 9650 Rockville Pike, Bethesda, MD 20814, USA. Keywords: Germany, Munich, Chlamydia Trachomatis, Gynecology, Infectious Disease, Sexually Transmitted Disease, Women's Health's, Technical University of Munich. This article was prepared by Women's Health Weekly editors from staff and other reports. Copyright 2007, Women's Health Weekly via NewsRx.com.
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