Both innate and acquired immunity to Listeria monocytogenes infection are increased in IL-10-deficient mice

Citations Over TimeTop 10% of 1997 papers

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.

Related Papers

• → Impact of aging on innate immunity(1998)162 cited
• → Aging and antimicrobial immunity. Impaired production of mediator T cells as a basis for the decreased resistance of senescent mice to listeriosis.(1981)44 cited
• → A defective Th1 response of the spleen in the initial phase may explain why splenectomy helps prevent aListeriainfection(2005)13 cited
• → Impaired function of immune reactivity to Listeria monocytogenes in diet-fed mice(1984)9 cited
• → INFLUENCE OF ROUTE OF INFECTION AND OTHER FACTORS ON GROWTH AND DISTRIBUTION OFLISTERIA MONOCYTOGENESIN ORGANS OF MICE(1963)5 cited