These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Endogenous IL-1 is required for neutrophil recruitment and macrophage activation during murine listeriosis.
    Author: Rogers HW, Tripp CS, Schreiber RD, Unanue ER.
    Journal: J Immunol; 1994 Sep 01; 153(5):2093-101. PubMed ID: 8051414.
    Abstract:
    By using a mixture of neutralizing mAbs to IL-1 alpha, IL-1 beta, and to the type I IL-1R, we previously documented a regulatory role for IL-1 in the development of anti-Listeria responses in mice. Both normal C.B-17 and severe combined immunodeficiency (SCID) mice injected with this mixture of Abs exhibit decreased resistance to Listeria. In this study, we demonstrate that the neutralization of IL-1 activity in SCID mice results in a major defect in neutrophil migration to the peritoneum, in response to Listeria infection. Moreover, anti-IL-1 treatment also inhibits Listeria-induced peripheral blood leukocytosis at all time points examined. We also show that mice injected with anti-IL-1 Abs failed to elaborate class II MHC-positive peritoneal macrophages in vivo at any time during Listeria infection. Even though peritoneal macrophages from anti-IL-1-treated Listeria-infected mice are not activated to express MHC class II molecules, IFN-gamma production in vivo is normal. Moreover, the macrophages are unresponsive to IFN-gamma in vitro, as assayed by MHC class II expression, even when rIL-1 is added. rIL-1 also is unable to increase the expression of IFN-gamma-induced surface class II MHC molecules on resident peritoneal macrophages in vitro. These results indicate that endogenously produced IL-1 plays an important role in Listeria-dependent neutrophil migration, increase in blood leukocyte number, generation of MHC class II-positive macrophages in vivo, and macrophage responsiveness to IFN-gamma.
    [Abstract] [Full Text] [Related] [New Search]