Abstract Shigella flexneri, an enteroinvasive Gram-negative bacterium, is responsible for the worldwide endemic form of bacillary dysentery. The host response to primary infection is characterized by the induction of an acute inflammation, which is accompanied by polymorphonuclear cell (PMN) infiltration, resulting in massive destruction of the colonic mucosa. However, PMN play a major role in the recovery from primary infection, by restricting the bacterial infection at the intestinal mucosa. In this study, we assessed the roles for T and NK cells in the control of primary S. flexneri infection, using an alymphoid mouse strain (Rag°γc°) devoid of B, T, and NK cells. Using the mouse pulmonary model of Shigella infection, we showed that alymphoid Rag°γc° mice were highly susceptible to S. flexneri infection in comparison with wild-type (wt) mice. Whereas PMN recruitment upon infection was similar, macrophage recruitment and production of proinflammatory cytokines were significantly decreased in Rag°γc° mice compared with wt mice. Upon selective engraftment of Rag°γc° mice with polyclonal αβ T cells, but not with αβ T cells from IFN-γ°, S. flexneri infection could be subsequently controlled. Rag° mice devoid of B and T cells but harboring NK cells could control infection. Local IFN-γ production by T and NK cells recruited to the lung was demonstrated in S. flexneri-infected wt mice. These data demonstrate that both αβ T cells and NK cells contribute to the early control of S. flexneri infection through amplification of an inflammatory response. This cellular lymphocyte redundancy assures IFN-γ production, which is central to innate immunity against Shigella infection.

Le-Barillec, K., Magalhaes, J. G., Corcuff, E., Thuizat, A., Sansonetti, P. J., Phalipon, A., & Di Santo, J. P. (2005). Roles for T and NK Cells in the Innate Immune Response to Shigella flexneri. The Journal of Immunology, 175(3), 1735–1740.