Mpn491, a secreted nuclease of Mycoplasma pneumoniae, plays a critical role in evading killing by neutrophil extracellular traps

Neutrophils play an important role in antimicrobial defense as the first line of innate immune system. Recently, the release of neutrophil extracellular traps (NETs) has been identified as a killing mechanism of neutrophils against invading microbes. Mycoplasma pneumoniae, a causative agent of respi...

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Bibliographic Details
Published in:Cellular microbiology 2017-03, Vol.19 (3), p.np-n/a
Main Authors: Yamamoto, Takeshi, Kida, Yutaka, Sakamoto, Yuichi, Kuwano, Koichi
Format: Article
Language:English
Subjects:
Deoxyribonucleases - metabolism
Extracellular Traps - metabolism
Host-Pathogen Interactions
Hydrolysis
Immune Evasion
Magnesium - metabolism
Mycoplasma pneumoniae
Mycoplasma pneumoniae - enzymology
Mycoplasma pneumoniae - immunology
Mycoplasma pneumoniae - pathogenicity
Neutrophils
Neutrophils - immunology
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Summary:Neutrophils play an important role in antimicrobial defense as the first line of innate immune system. Recently, the release of neutrophil extracellular traps (NETs) has been identified as a killing mechanism of neutrophils against invading microbes. Mycoplasma pneumoniae, a causative agent of respiratory infection, has been shown to be resistant to in vitro killing by neutrophils, suggesting that the bacterium might circumvent bactericidal activity of NETs. In this study, we investigated whether M. pneumoniae possesses resistance mechanisms against the NETs‐mediated killing of neutrophils and found that the bacterium degrades the NETs induced upon M. pneumoniae infection. The NETs‐degrading ability of M. pneumoniae required the production of a secreted nuclease, Mpn491, capable of using Mg2+ as a cofactor for its hydrolytic activity. Moreover, the inactivation of the nuclease resulted in increased susceptibility of M. pneumoniae to the NETs‐mediated killing of neutrophils. The results suggest that M. pneumoniae employs Mpn491 as a means for evading the killing mechanism of neutrophils.
ISSN:1462-5814
1462-5822
DOI:10.1111/cmi.12666