Article
Inhibition of toll-like receptor 2 (TLR-2)-mediated response in human alveolar epithelial cells by mycolic acids and Mycobacterium tuberculosis mce1 operon mutant
Registro en:
SEQUEIRA, Patricia C.; SENARATNE, Ryan H. ; RILEY, Lee W. Inhibition of toll-like receptor 2 (TLR-2)-mediated response in human alveolar epithelial cells by mycolic acids and Mycobacterium tuberculosis mce1 operon mutant. Pathogens and Disease, v.70, n.2, p.132-140, 2014.
2049-632X
10.1111/2049-632X.12110
Autor
Sequeira, Patricia C
Senaratne, Ryan H
Riley, Lee W
Resumen
In human lungs, the earliest encounter of Mycobacterium tuberculosis, the agent
of tuberculosis, involves alveolar epithelial cells. Droplets expectorated by a
patient with tuberculosis are likely to contain a mixed population of M. tuberculosis
cells in different physiologic and metabolic states from the lung lesions of the
patient. Here, we compared the chemokine expression patterns of human
epithelial cell line A549 and RAW 264.7 macrophage cells infected with wild-type
M. tuberculosis H37Rv against patterns induced by a mutant that accumulates
free mycolic acids in its cell wall (Dmce1). We also examined the effect of free
mycolic acids on toll-like receptor-2 (TLR-2). Wild-type M. tuberculosis induced
significantly higher levels of IL-8, MCP-1, RANTES, and IP-10 in both cell types
than did Dmce. Free mycolic acids reduced the ability of the mammalian cells to
respond to a TLR-2 agonist in a dose-dependent manner. These observations
suggest that differences in mycolic acid abundance in the M. tuberculosis cell wall
can affect TLR-2-mediated pro-inflammatory response in both epithelial and
macrophage cells. The final fate of a new infection may be ultimately determined
by the proportion of M. tuberculosis cells expressing free mycolates in the infecting
inoculum population.
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