title: Both innate and acquired immunity to Listeria monocytogenes infection are increased in IL-10-deficient mice.
abstract: IL-10-deficient mice were highly resistant to Listeria monocytogenes during the course of infection. An increased innate immunity was suggested by reduced bacterial burdens (as much as 50-fold) early (days 2 and 3) in the infection, as compared with control mice. In addition, in vitro stimulation of both IL-10-deficient peritoneal exudate cells and spleen cells with heat-killed Listeria resulted in a dramatically enhanced proinflammatory cytokine response (e.g., IL-12, IFN-gamma, TNF-alpha, IL-1alpha, and IL-6). During later stages of a primary Listeria infection, the reduced bacterial burden in the infected organs of IL-10-deficient mice was accompanied by decreased tissue damage and earlier clearance of the pathogen, as well as a stronger Th1 polarization. The absence of IL-10 did not influence membrane-bound factors that stimulate Th cell responses, demonstrated by the finding of normal MHC class II, B7.1, and B7.2 surface expression on F4/80+ macrophages in vivo. IL-10-deficient mice were also more resistant to a secondary infection, accompanied by an enhanced Th1 response. The results presented in this work demonstrate that the absence of IL-10 augments innate and acquired immunity during primary and secondary L. monocytogenes infection by up-regulating proinflammatory type 1 cytokine responses. The resulting protective Th1 responses lead to an effective reduction of bacterial growth and tissue destruction and to an earlier clearance of the bacteria. The physiologic role of IL-10 during L. monocytogenes infection studies is discussed and compared with pathogenic infections that induce a more systemic cytokine response in IL-10-deficient mice.
authors.affiliation: Max Planck Institute for Immunobiology, Freiburg, Germany.
authors.forename: W J
authors.initials: WJ
authors.lastname: Dai
authors.forename: G
authors.initials: G
authors.lastname: Köhler
authors.forename: F
authors.initials: F
authors.lastname: Brombacher
mesh_terms: D000818:Animals; D018122:B7-1 Antigen / Q000096:biosynthesis; D002908:Chronic Disease; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D007110:Immunity, Active; D007113:Immunity, Innate; D007117:Immunization, Secondary; D018836:Inflammation Mediators / Q000378:metabolism; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000172:deficiency*; D018664:Interleukin-12 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D007964:Leukocytosis / Q000150:complications; D008088:Listeriosis / Q000209:etiology / Q000235:genetics* / Q000276:immunology*; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009504:Neutrophils / Q000473:pathology; D018417:Th1 Cells / Q000378:metabolism
chemical_list: D018122:B7-1 Antigen; D000949:Histocompatibility Antigens Class II; D018836:Inflammation Mediators; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma