| Autor: |
Ingrid Chou Koo, Ohol, Yamini M., Ping Wu, Morisaki, J. Hiroshi, Cox, Jeffery S., Brown, Eric J. |
| Předmět: |
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| Zdroj: |
Proceedings of the National Academy of Sciences of the United States of America; 1/15/2008, Vol. 105 Issue 2, p710-715, 6p, 5 Graphs |
| Abstrakt: |
The pathogenic mycobacteria that cause tuberculosis (TB) and TB-like diseases in humans and animals elude sterilizing immunity by residing within an intracellular niche in host macrophages, where they are protected from microbicidal attack. Recent studies have emphasized microbial mechanisms for evasion of host defense; less is known about mycobactericidal mechanisms that remain intact during initial infection. To better understand macrophage mechanisms for restricting mycobacteria growth, we examined Mycobacterium marinum infection of Drosophila 52 cells. Among ≈1,000 host genes examined by RNAi depletion, the lysosomal enzyme β-hexosaminidase was identified as an important factor in the control of mycobacterial infection. The importance of β-hexosaminidase for restricting mycobacterial growth during mammalian infections was confirmed in macrophages from β-hexosaminidase knockout mice. p-Hexosaminidase was characterized as a peptidoglycan hydrolase that surprisingly exerts its mycobactericidal effect at the macrophage plasma membrane during mycobacteria-induced secretion of lysosomes. Thus, secretion of lysosomal enzymes is a mycobactericidal mechanism that may have a more general role in host defense. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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