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Endogenous Interleukin‐4 Does Not Suppress the Resistance Against a Primary or a Secondary Listeria monocytogenes Infection in Mice
Author(s) -
J.N. Samsom,
A Annema,
Jan A. M. Langermans,
R. van Furth
Publication year - 1998
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1998.00314.x
Subject(s) - listeria monocytogenes , spleen , listeria , immune system , antibody , biology , microbiology and biotechnology , cytokine , immunology , toxoplasma gondii , monoclonal antibody , interferon gamma , bacteria , genetics
Interleukin‐4 (IL‐4), a cytokine produced by T‐helper 2 (Th2) cells, can inhibit the development of T‐helper 1 (Th1) cells, which results in a decreased release of cytokines by the latter. As interferon‐γ (IFN‐γ), produced by Th1 cells, is involved in the resistance against a Listeria monocytogenes infection, the role of endogenously formed IL‐4 during a Listeria infection in mice was investigated. Neutralization of endogenously formed cytokines by subcutaneously injected alginate‐encapsulated monoclonal antibody (MoAb)‐forming cells results in high antibody titres in the circulation over a long time period. The aim of the present study was to re‐evaluate the effect of neutralization of IL‐4 during a primary Listeria infection and to investigate the role of IL‐4 during a secondary infection in mice using encapsulated MoAb‐forming cells. During the course of a primary infection in mice given anti‐IL‐4 antibody‐forming cells (anti‐IL‐4‐FC), the number of Listeria found in the liver and spleen was comparable to that found in control mice given anti‐β‐galactosidase antibody‐forming cells (anti‐β‐gal‐FC). Activation of macrophages measured by inhibition of Toxoplasma gondii proliferation and the release of reactive nitrogen intermediates (RNI) was not affected by anti‐IL‐4‐FC treatment during infection. Furthermore, during a secondary L. monocytogenes infection the number of bacteria in the liver and spleen of anti‐IL‐4‐treated immune mice was comparable to anti‐β‐gal‐FC‐treated, control, immune mice. The concentration of IFN‐γ in plasma of anti‐IL‐4‐treated immune mice was similar to that of control immune mice. Taken together, these findings demonstrate that neutralization of endogenously formed IL‐4 does not affect resistance to a primary or a secondary L. monocytogenes infection in mice.