title: No Impairment in host defense against Streptococcus pneumoniae in obese CPEfat/fat mice.
abstract: In the US and globally, dramatic increases in the prevalence of adult and childhood obesity have been reported during the last 30 years. In addition to cardiovascular disease, type II diabetes, and liver disease, obesity has recently been recognized as an important risk factor for influenza pneumonia. During the influenza pandemic of 2009, obese individuals experienced a greater severity of illness from the H1N1 virus. In addition, obese mice have also been shown to exhibit increased lethality and aberrant pulmonary inflammatory responses following influenza infection. In contrast to influenza, the impact of obesity on bacterial pneumonia in human patients is controversial. In this report, we compared the responses of lean WT and obese CPE(fat/fat) mice following an intratracheal infection with Streptococcus pneumoniae, the leading cause of community-acquired pneumonia. At 16 weeks of age, CPE(fat/fat) mice develop severe obesity, hyperglycemia, elevated serum triglycerides and leptin, and increased blood neutrophil counts. There were no differences between lean WT and obese CPE(fat/fat) mice in survival or lung and spleen bacterial burdens following intratracheal infection with S. pneumoniae. Besides a modest increase in TNF-α levels and increased peripheral blood neutrophil counts in CPE(fat/fat) mice, there were not differences in lung or serum cytokines after infection. These results suggest that obesity, accompanied by hyperglycemia and modestly elevated triglycerides, at least in the case of CPE(fat/fat) mice, does not impair innate immunity against pneumococcal pneumonia.
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan, United States of America; Graduate Program in Immunology, University of Michigan, Ann Arbor, Michigan, United States of America.
authors.forename: Peter
authors.initials: P
authors.lastname: Mancuso
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan, United States of America.
authors.forename: Edmund
authors.initials: E
authors.lastname: O Brien
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan, United States of America.
authors.forename: Joseph
authors.initials: J
authors.lastname: Prano
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan, United States of America.
authors.forename: Deepti
authors.initials: D
authors.lastname: Goel
authors.affiliation: Division of Infectious Diseases, Department of Medicine, Vanderbilt University, Nashville, Tennessee, United States of America.
authors.forename: David M
authors.initials: DM
authors.lastname: Aronoff
mesh_terms: D000818:Animals; D001835:Body Weight; D002268:Carboxypeptidases / Q000378:metabolism; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D051379:Mice; D008820:Mice, Obese; D009765:Obesity / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology*; D013296:Streptococcus pneumoniae / Q000502:physiology*
chemical_list: D002268:Carboxypeptidases