• Ali El Solh, Jahan Porhomayon, and Krsitie Szarpa.
• Western 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. Electronic address:solh@buffalo.edu.
• Obes Res Clin Pract. 2009 Nov 1; 3 (4): 203-7.

UnlabelledBackgroundRecent 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.ObjectivesTo assess whether obesity per se impairs the proinflammatory and antimicrobial functions of alveolar macrophages (AM).MethodsSix 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.ResultsThe 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.ConclusionOur 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.� Published by Elsevier Ltd on behalf of Asia Oceania Assoc. for the Study of Obesity.

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