IL-9 Protects Mice from Gram-Negative Bacterial Shock: Suppression of TNF-α, IL-12, and IFN-γ, and Induction of IL-10
Author(s) -
Ursula Grohmann,
Jacques Van Snick,
Franca Campanile,
Silvia Silla,
Antonio Giampietri,
Carmine Vacca,
JeanChristophe Renauld,
Maria C. Fioretti,
Paolo Puccetti
Publication year - 2000
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.164.8.4197
Subject(s) - cytokine , immunology , septic shock , tumor necrosis factor alpha , pseudomonas aeruginosa , inflammation , interleukin 10 , interleukin 4 , interleukin , biology , medicine , sepsis , bacteria , genetics
IL-9 is a T cell-derived cytokine that, similar to the Th2 cytokines IL-4 and IL-10, has been implicated in the response to parasitic infections, allergy, and inflammatory processes. Because both IL-4 and IL-10 can confer protection to mice from septic shock, we investigated whether IL-9 may also be capable of conferring resistance on recipients of an otherwise lethal challenge with Pseudomonas aeruginosa. Prophylactic injections of rIL-9 appeared to be most effective in preventing the onset of a lethal shock, according to a pattern that was both dose dependent and time dependent. The protective effect of IL-9 was correlated with marked decreases in the production of the inflammatory mediators TNF-alpha, IL-12, and IFN-gamma, as well as the induction of the anti-inflammatory cytokine IL-10. Sustained levels of IL-9-specific transcripts could be detected in the spleens of mice recovering from sublethal P. aeruginosa infection. Therefore, IL-9 may be protective in septic shock via a rather unique mechanism involving a complex modulation of inflammatory and anti-inflammatory mediators.
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