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Long Term Chronic Pseudomonas aeruginosa Airway Infection in Mice
Published on: March 17, 2014
SP-A preserves airway homeostasis during Mycoplasma pneumoniae infection in mice
Julie G Ledford1, Hisatsugu Goto, Erin N Potts
1Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.
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.
Insights
Surfactant protein-A (SP-A) is crucial for lung defense against Mycoplasma pneumoniae (Mp) infection. Lacking SP-A exacerbates inflammation and lung dysfunction, highlighting SP-A's protective role.
Area of Science:
- Pulmonary immunology
- Host-pathogen interactions
- Respiratory medicine
Background:
- The lung's defense mechanisms maintain homeostasis against environmental irritants and pathogens.
- Surfactant protein-A (SP-A) is a key component of pulmonary host defense, modulating inflammatory and infectious responses.
- SP-A exhibits bacteriostatic effects on Mycoplasma pneumoniae (Mp) by binding to its surface.
Purpose of the Study:
- To investigate the role of SP-A in acute pulmonary infection with Mycoplasma pneumoniae.
- To assess the impact of SP-A deficiency on biologic and physiologic responses to Mp infection.
Main Methods:
- Utilized SP-A deficient (SP-A(-/-)) mice and wild-type littermates for infection studies.
- Administered Mycoplasma pneumoniae to induce acute pulmonary infection.
- Pharmacologically inhibited TNF-alpha to evaluate its role in Mp-induced responses.
Main Results:
- SP-A(-/-) mice exhibited significantly greater inflammation and cellular infiltration during Mp infection compared to wild-type mice.
- Physiologic lung functions, including airway hyperresponsiveness and lung compliance, were more severely impaired in SP-A(-/-) mice.
- Pharmacologic inhibition of TNF-alpha attenuated both biologic and physiologic changes induced by Mp infection.
Conclusions:
- SP-A is essential for maintaining lung homeostasis and effective host defense against Mycoplasma pneumoniae.
- SP-A limits inflammatory cell recruitment and curbs excessive TNF-alpha responses during Mp infection.
- Targeting SP-A or TNF-alpha may offer therapeutic strategies for pulmonary infections.
