Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages

Infection and Immunity - Tập 69 Số 3 - Trang 1477-1482 - 2001
Matthew Hirschfeld1, Janis J. Weis1, Vladimir Y. Toshchakov2, C A Salkowski2, Michael J. Cody2, Dawn Ward3, Nilofer Qureshi4,5, Suzanne M. Michalek3, Stefanie N. Vogel2
1Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland
2<!--label omitted: 2-->Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, Maryland2;
3; and Department of Animal Health and Biomedical Sciences, University of Wisconsin at Madison, Madison, Wisconsin
4<!--label omitted: 4-->Department of Animal Health and Biomedical Sciences, University of Wisconsin at Madison, Madison, Wisconsin4
5Department of Microbi-ology and Immunology, USUHS, 4301 Jones Bridge Road, Bethesda, MD 20814.

Tóm tắt

ABSTRACTLipopolysaccharide (LPS) derived from the periodontal pathogenPorphyromonas gingivalishas been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation ofP. gingivalisLPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants. More importantly, TLR2 stimulation by thisP. gingivalisLPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages byEscherichia coliLPS. These data suggest that (i)P. gingivalisLPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively. Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.

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Infection and Immunity

Tập 69 Số 3

1477-1482

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