INTERLEUKIN-4 AND LISTERIOSIS

Experimental infection of mice with Listeria monocytogenes (L. monocyt ogenes) has served as an appropriate model for analyzing Th1-cell-driv en immune responses. Generally, Th2 responses are absent and IL-4 is n ot 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 ch emokine responses and, therefore, may participate in the regulation of the early antilisterial host response. Soon thereafter, IL-4 producti on 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 de monstrable during acquired immunity against L. monocytogenes, and this elevated IL-4 production apparently contributes to disease exacerbati on. In conclusion, the data are consistent with a detrimental role of IL-4 in listeriosis and active control of IL-4 synthesis by the antili sterial immune response. The rapid, but transient, IL-4 burst in liste riosis probably contributes to host defense without impairing developm ent of the acquired T-cell response because of its shortness.