Enhanced immediate inflammatory response to Streptococcus pneumoniae in the lungs of mice with pulmonary emphysema
Yoshikane Tokairin1, Yoko Shibata, Makoto Sata
1Department of Cardiology, Pulmonology and Nephrology, Yamagata University School of Medicine, Yamagata, Japan.
Background And Objective:
Pulmonary emphysema is associated with frequent respiratory infections but little is known about the reasons for this susceptibility to bacterial infection. We previously demonstrated an impaired inflammatory response to Streptococcus pneumoniae in an experimental emphysema mouse model at 24 h, or longer following bacterial inoculation. Toll-like receptors (TLR) have been recognized as regulators in the inflammatory response. We examined the expression of TLR on alveolar macrophages in experimental emphysema mice and evaluated the immediate inflammatory response of the emphysematous lung to streptococcal infection.
Methods:
Elastase was administered once into mice trachea to induce pulmonary emphysema. Three weeks later, expression of TLR-2 and TLR-4 in the BAL cells was examined by immunostaining. Following the intratracheal inoculation of Streptococcus pneumoniae, pro-inflammatory cytokine concentrations were measured in the BAL fluids of the control and emphysema mice.
Results:
The expression of TLR-2 and TLR-4 was significantly elevated in the alveolar macrophages of emphysema mice. Six hours after infection, neutrophils in the BAL fluid of emphysema mice were significantly increased, and the levels of tumour necrosis factor-alpha, IL-1beta and IL-6 were significantly elevated, compared with the control mice. At 3 h post inoculation, macrophage inflammatory protein-2 levels were significantly elevated.
Conclusions:
The immediate inflammatory response in the emphysematous lung is significantly enhanced in response to streptococcal infection. This may be partly attributed to the increased expression of TLR in the alveolar macrophages of emphysema mice.
Insights
Pulmonary emphysema enhances the immediate inflammatory response to Streptococcus pneumoniae infection, partly due to increased Toll-like receptors (TLR) on alveolar macrophages. This finding sheds light on emphysema-related infection susceptibility.
Area of Science:
- Immunology
- Pulmonology
- Microbiology
Background:
- Pulmonary emphysema increases susceptibility to bacterial respiratory infections.
- The mechanisms behind this heightened susceptibility remain unclear.
- Previous studies showed an impaired inflammatory response in emphysema models.
Purpose of the Study:
- To investigate the role of Toll-like receptors (TLR) in the inflammatory response of emphysema.
- To evaluate the immediate inflammatory response in an experimental emphysema mouse model following Streptococcus pneumoniae infection.
Main Methods:
- Pulmonary emphysema was induced in mice using elastase.
- Toll-like receptor (TLR)-2 and TLR-4 expression on alveolar macrophages was assessed.
- Pro-inflammatory cytokine levels were measured in bronchoalveolar lavage (BAL) fluid after bacterial inoculation.
Main Results:
- Emphysema mice showed significantly elevated expression of TLR-2 and TLR-4 on alveolar macrophages.
- Neutrophil counts and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) were significantly increased in BAL fluid of emphysema mice post-infection.
- Macrophage inflammatory protein-2 levels were also elevated early after infection.
Conclusions:
- The immediate inflammatory response to Streptococcus pneumoniae is enhanced in emphysema.
- Increased expression of TLR on alveolar macrophages likely contributes to this enhanced response in emphysema.
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