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* Department of Immunology and
Central Core Facility, Microscopy, Max-Planck Institute for Infection Biology, Berlin, Germany; and
Department of Bacteriology, Nara Medical University, Nara, Japan
LFA-1 (CD11a/CD18) plays a crucial role in various inflammatory responses. In this study, we show that LFA-1-/- mice are far more resistant to Listeria monocytogenes infection than LFA-1+/- mice. Consistent with this, we found the following: 1) the numbers of granulocytes infiltrating the liver were markedly higher in LFA-1-/- mice than in LFA-1+/- mice, 2) increased antilisterial resistance in LFA-1-/- mice was abrogated by depletion of granulocytes, and 3) the numbers of granulocytes in peripheral blood, and the serum levels of both G-CSF and IL-17 were higher in LFA-1-/- mice than in LFA-1+/- mice. Neither spontaneous apoptosis nor survival of granulocytes from LFA-1-/- mice were affected by physiological concentrations of G-CSF. Our data suggest regulatory effects of LFA-1 on G-CSF and IL-17 secretion, and as a corollary on neutrophilia. Consequently, we conclude that increased resistance of LFA-1-/- mice to listeriosis is due to neutrophilia facilitating liver infiltration by granulocytes promptly after L. monocytogenes infection, although it is LFA-1 independent.
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