Abstract
Abstract Alterations in the composition of intestinal commensal bacteria in humans are associated with enhanced susceptibility to multiple inflammatory diseases suggesting that signals derived from commensal bacteria may influence the development and/or function of the immune system. Supporting this, germ-free or gnotobiotic mice exhibit reduced numbers of lymphocytes in the intestinal intraepithelial compartment. However, whether alterations in the acquisition or composition of commensal bacteria influence immunity to infection remains poorly defined. To test this, mice housed under conventional or gnotobiotic conditions were infected i.p. with Lymphocytic Choriomeningitis Virus (LCMV). At day 7 post-infection, gnotobiotic mice exhibited a significant reduction in the frequency and number of LCMV-specific CD8+ T cells in multiple tissues including the spleen and intraepithelial compartment. Furthermore, LCMV-specific CD8+ T cells from gnotobiotic mice were less capable of producing IFN-γ following LCMV peptide stimulation. In addition, at day 36 post-infection, when conventionally-housed mice have established a LCMV-specific CD8+ memory T cell population, gnotobiotic mice had a significantly impaired population of LCMV-specific CD8+ memory T cells. Diminished LCMV-specific CD8+ effector and memory T cell responses were not the result of inherent defects in gnotobiotic mice as oral administration of a cocktail of antibiotics to conventionally-housed mice also displayed a defective LCMV-specific CD8+ T cell response following infection. Collectively, these data suggest an integral role of commensal bacteria in influencing virus specific CD8+ T cell effector and memory responses.
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