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Updated: Aug 8, 2026

Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
The macrophage scavenger receptor SR-AI/II and lung defense against pneumococci and particles
Mohamed S Arredouani1, Zhiping Yang, Amy Imrich
1Physiology Program, 665 Huntington Avenue, SPH-II, Room 221, Boston, MA 02115, USA.
Abstract:
The class A macrophage scavenger receptor SR-AI/II is implicated as a pattern recognition receptor for innate immunity, but its functional role in lung defense has not been studied. We used mice genetically deficient in SR-AI/II and their wild-type C57BL/6 counterparts to investigate the contribution of this receptor to defense against pneumococcal infection and inhaled particles. SR-AI/II deficiency caused impaired phagocytosis of fluorescent bacteria in vivo, diminished clearance of live bacteria from the lungs, and substantially increased pneumonic inflammation. Survival studies also showed increased mortality in SR-AI/II-deficient mice with pneumococcal lung infection. Similarly, after challenge of the airways with TiO(2) particles, SR-AI/II-deficient mice showed increased proinflammatory cytokine levels in lung lavage fluid and a more pronounced neutrophilic inflammation. The data indicate that the lung macrophage class A scavenger receptor SR-AI/II contributes to innate defense against bacteria and inhaled particles.
Insights
The scavenger receptor SR-AI/II is crucial for lung defense against bacteria and inhaled particles. Its absence impairs bacterial clearance and increases inflammation and mortality in mice.
Area of Science:
- Immunology
- Innate Immunity
- Pulmonary Defense
Background:
- Class A macrophage scavenger receptors (SR-AI/II) are pattern recognition receptors involved in innate immunity.
- The specific role of SR-AI/II in lung defense against pathogens and particles remains largely uncharacterized.
Purpose of the Study:
- To investigate the contribution of SR-AI/II to innate lung defense against Streptococcus pneumoniae infection and inhaled titanium dioxide (TiO2) particles.
Main Methods:
- Utilized SR-AI/II-deficient mice and wild-type C57BL/6 controls.
- Assessed bacterial phagocytosis, clearance, lung inflammation, and survival following pneumococcal challenge.
- Evaluated inflammatory responses and cytokine levels in lung lavage fluid after TiO2 particle exposure.
Main Results:
- SR-AI/II deficiency led to impaired in vivo bacterial phagocytosis and reduced clearance of live bacteria from the lungs.
- Mice lacking SR-AI/II exhibited significantly increased pneumonic inflammation and mortality after pneumococcal infection.
- Airway challenge with TiO2 particles in SR-AI/II-deficient mice resulted in elevated proinflammatory cytokines and heightened neutrophilic inflammation.
Conclusions:
- The macrophage scavenger receptor SR-AI/II plays a significant role in the innate immune defense of the lungs.
- SR-AI/II is essential for effective clearance of bacteria and inhaled particles, and for controlling inflammatory responses in the lung.
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