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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.

No Impairment in Host Defense against Streptococcus pneumoniae in Obese CPEfat/fat Mice