title: Interleukin-4 and listeriosis.
abstract: Experimental infection of mice with Listeria monocytogenes (L. monocytogenes) has served as an appropriate model for analyzing Th1-cell-driven immune responses. Generally, Th2 responses are absent and IL-4 is not detectable. Here, we describe experimental settings under which IL-4 is detectable in listeriosis. Our data suggest that IL-4 is rapidly produced after infection. This prompt IL-4 burst seems to stimulate chemokine responses and, therefore, may participate in the regulation of the early antilisterial host response. Soon thereafter, IL-4 production wanes. At least partially this seems to be caused by downregulation of IL-4-producing CD4+ NK1+ TCR alpha beta int lymphocytes by IL-12. In the absence of IFN-gamma responsiveness, IL-4 production is demonstrable during acquired immunity against L monocytogenes, and this elevated IL-4 production apparently contributes to disease exacerbation. In conclusion, the data are consistent with a detrimental role of IL-4 in listeriosis and active control of IL-4 synthesis by the antilisterial immune response. The rapid, but transient, IL-4 burst in listeriosis probably contributes to host defense without impairing development of the acquired T-cell response because of its shortness.
authors.affiliation: Department of Immunology, University of Ulm, Germany. Stefan.Kaufmann@Medizin.Uni-Uhn.De
authors.forename: S H
authors.initials: SH
authors.lastname: Kaufmann
authors.forename: M
authors.initials: M
authors.lastname: Emoto
authors.forename: G
authors.initials: G
authors.lastname: Szalay
authors.forename: J
authors.initials: J
authors.lastname: Barsig
authors.forename: I E
authors.initials: IE
authors.lastname: Flesch
mesh_terms: D000818:Animals; D015847:Interleukin-4 / Q000096:biosynthesis*; D008088:Listeriosis / Q000276:immunology*; D051379:Mice; D018448:Models, Immunological; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D015847:Interleukin-4