Open AccessRole of macrophages in experimental group B streptococcal arthritis
Author(s) -
Puliti Manuela,
Von Hunolstein Christina,
Bistoni Francesco,
Castronari Roberto,
Orefici Graziella,
Tissi Luciana
Publication year - 2002
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1046/j.1462-5822.2002.00223.x
Subject(s) - arthritis , septic arthritis , proinflammatory cytokine , immunology , population , biology , etoposide , group b , group a , monocyte , cytokine , macrophage , interleukin 10 , medicine , inflammation , chemotherapy , biochemistry , environmental health , in vitro
Summary Septic arthritis is a clinical manifestation of group B Streptococcus (GBS) infection in both neonates and adults. Because macrophages are known to participate in tissue injury, the role of this cell population in GBS‐induced arthritis was investigated. Mice were rendered monocytopenic by administration of etoposide, a drug that selectively depletes the monocyte/macrophage population and then injected with GBS (1 × 10 7 colony‐forming units per mouse). Appearance of arthritis, mortality, GBS growth in the organs, and local and systemic cytokine production were examined. Etoposide‐treated mice had a significantly less severe arthritis than control animals. Histopathological analysis of the joints confirmed clinical observations. Decreased joint levels of the proinflammatory cytokines interleukin 1 (IL‐1) beta and IL‐6 accompanied the less severe development of arthritis in monocytopenic mice. In contrast, mortality was increased in the etoposide‐treated mice compared with controls. Monocytopenic mice exhibited elevated bacterial load in the blood and kidneys at all time points exam‐ined. These results indicate that lack of macrophages leads to less severe joint lesions, but also results in impaired clearance of bacteria, and consequent enhancement of mortality rates.