IL-4 Deficiency Decreases Mortality but Increases Severity of Arthritis in Experimental Group BStreptococcusInfection
Author(s) -
Luciana Tissi,
Francesco Bistoni,
Manuela Puliti
Publication year - 2009
Publication title -
mediators of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.37
H-Index - 97
eISSN - 1466-1861
pISSN - 0962-9351
DOI - 10.1155/2009/394021
Subject(s) - arthritis , algorithm , streptococcus agalactiae , sepsis , medicine , chemokine , cytokine , streptococcus , immunology , inflammation , biology , mathematics , bacteria , genetics
IL-4 is an anti-inflammatory cytokine that inhibits the onset and severity in different experimental arthritis models. Group B streptococci (GBS) have been recognized as an ever-growing cause of serious invasive infections in nonpregnant adults. Septic arthritis is a clinical manifestation of GBS infection. To investigate the role of IL-4 in experimental GBS infection, IL-4 deficient or competent mice were inoculated with 1 × 10 7 GBS/mouse. Mortality, appearance of arthritis, GBS growth in the organs, and local and systemic cytokine and chemokine production were examined. IL-4−/− mice showed lower mortality rates but increased severity of arthritis and exhibited a lower microbial load in blood, kidneys, and joints than wt mice. Increased local levels of IL-1 β , IL-6, TNF- α , MIP-1 α , and MIP-2 accompanied the more severe arthritis in IL-4−/− mice. Our results suggest a detrimental role of IL-4 in GBS sepsis, whereas it plays a beneficial effect on GBS-induced arthritis.
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