The global obesity epidemic combined with yearly influenza outbreaks and potential for a pandemic makes it crucial to determine how protection from influenza differs in an obese host. In contrast to a vaccine antibody response which recognizes surface proteins, memory T cells generated during a primary infection target internal viral proteins and are protective against heterologous strains. As our prior work demonstrated that obese mice have an impaired primary response to influenza virus infection, we hypothesized that obese mice would also have an impaired memory response to a secondary influenza infection. To test this hypothesis, obese and lean mice were infected with influenza X‐31. At 31 days post infection, mice were challenged with a lethal dose of a different strain, influenza A/PR/8. While lean mice were protected from lethal infection, obese mice had 25% mortality, increased lung pathology and virus titers, reduced antiviral cytokine expression, and decreased and delayed adaptive immune cytokine expression following secondary challenge. These results indicate that memory response to influenza in obese mice is significantly altered and ineffective and obesity may hinder the generation or function of these protective cells. These results suggest obese populations are at risk for impaired immune memory response, which has significant public health implications for current vaccination protocols.
Grant Funding Source
DK56350