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Updated: Apr 27, 2026
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Proinflammatory and phagocytic functions of alveolar macrophages in obesity
Ali El Solh1, Jahan Porhomayon2, Krsitie Szarpa1
1Western New York Respiratory Research Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY, United States.
Background:
Recent epidemiologic investigations have pointed to an increase susceptibility of obese individuals to lower respiratory tract infections. The cellular mechanism responsible for this phenomenon has not been identified.
Objectives:
To assess whether obesity per se impairs the proinflammatory and antimicrobial functions of alveolar macrophages (AM).
Methods:
Six obese (BMI ≥ 30 < 40 kg/m(2)) and six morbidly obese (BMI ≥ 40 kg/m(2)) subjects free of comorbid diseases participated in the study. A control group (BMI < 25 kg/m(2)) matched for age and gender was included. Alveolar macrophages collected by bronchoalveolar lavage were tested for lipopolysaccharide (LPS) stimulated production of TNF-α. Phagocytosis was measured by assessing the degree of ingested opsonized and unopsonized particles. Microbicidal activity was determined by the ability of AM to kill Listeria monocytogenes.
Results:
The percentage of AM in the bronchoalveolar lavage was comparable among the three groups. There was no significant difference of TNF-α levels at baseline and after LPS-stimulated production between obese, morbidly obese, and nonobese subjects. Opsonized and unopsonized phagocytosis and microbicidal activity remained intact and was not affected by increasing BMI.
Conclusion:
Our data suggest that in the absence of underlying comorbidities, the increased frequency of respiratory infections in obesity cannot be explained by impairment of alveolar macrophages. Further work is required to delineate the relationship between obesity and the noncellular aspects of innate immunity.
Insights
Obesity does not impair alveolar macrophage function in individuals without comorbidities. This study found that immune cell functions remain intact, suggesting other factors contribute to increased respiratory infections in obese individuals.
Area of Science:
- Immunology
- Pulmonology
- Obesity research
Background:
- Obesity is linked to increased susceptibility to lower respiratory tract infections.
- The underlying cellular mechanisms for this increased susceptibility remain unclear.
Purpose of the Study:
- To investigate if obesity impairs the proinflammatory and antimicrobial functions of alveolar macrophages (AM).
Main Methods:
- Compared alveolar macrophages from obese, morbidly obese, and nonobese individuals.
- Assessed lipopolysaccharide (LPS)-stimulated TNF-α production.
- Measured phagocytosis and microbicidal activity against Listeria monocytogenes.
Main Results:
- Alveolar macrophage percentages were similar across groups.
- TNF-α production was not significantly different between obese and nonobese subjects.
- Phagocytic and microbicidal activities of AM were unaffected by increasing BMI.
Conclusions:
- Impaired alveolar macrophage function does not explain increased respiratory infections in obesity without comorbidities.
- Further research is needed to explore noncellular innate immunity aspects in obesity.
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