SP-A preserves airway homeostasis during Mycoplasma pneumoniae infection in mice
- PMID: 19494306
- PMCID: PMC3656438
- DOI: 10.4049/jimmunol.0900452
SP-A preserves airway homeostasis during Mycoplasma pneumoniae infection in mice
Erratum in
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Correction: SP-A Preserves Airway Homeostasis during Mycoplasma pneumoniae Infection in Mice.J Immunol. 2015 Sep 15;195(6):2917-8. doi: 10.4049/jimmunol.1501597. J Immunol. 2015. PMID: 26342104 No abstract available.
Abstract
The lung is constantly challenged during normal breathing by a myriad of environmental irritants and infectious insults. Pulmonary host defense mechanisms maintain homeostasis between inhibition/clearance of pathogens and regulation of inflammatory responses that could injure the airway epithelium. One component of this defense mechanism, surfactant protein-A (SP-A), exerts multifunctional roles in mediating host responses to inflammatory and infectious agents. SP-A has a bacteriostatic effect on Mycoplasma pneumoniae (Mp), which occurs by binding surface disaturated phosphatidylglycerols. SP-A can also bind the Mp membrane protein, MPN372. In this study, we investigated the role of SP-A during acute phase pulmonary infection with Mp using mice deficient in SP-A. Biologic responses, inflammation, and cellular infiltration, were much greater in Mp infected SP-A(-/-) mice than wild-type mice. Likewise, physiologic responses (airway hyperresponsiveness and lung compliance) to Mp infection were more severely affected in SP-A(-/-) mice. Both Mp-induced biologic and physiologic changes were attenuated by pharmacologic inhibition of TNF-alpha. Our findings demonstrate that SP-A is vital to preserving lung homeostasis and host defense to this clinically relevant strain of Mp by curtailing inflammatory cell recruitment and limiting an overzealous TNF-alpha response.
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Comment in
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Findings of Research Misconduct.Fed Regist. 2019 Nov 7;84(216):60097-60098. Fed Regist. 2019. PMID: 37547121 Free PMC article. No abstract available.
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