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Infection and Immunity, September 1999, p. 4545-4550, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Role of Tumor Necrosis Factor Alpha, Interleukin-1beta , and Interleukin-6 in a Mouse Model of Group B Streptococcal Arthritis

Luciana Tissi,1,* Manuela Puliti,1 Roberta Barluzzi,1 Graziella Orefici,2 Christina von Hunolstein,2 and Francesco Bistoni1

Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, 06122 Perugia,1 and Laboratory of Bacteriology and Medical Mycology, Istituto Supiore di Sanità, Rome,2 Italy

Received 24 February 1999/Returned for modification 4 May 1999/Accepted 10 June 1999

Intravenous inoculation of CD1 mice with 107 CFU of type IV group B Streptococcus (GBS IV) results in a high incidence of diffuse septic arthritis. In this study the roles of tumor necrosis factor alpha (TNF-alpha ), interleukin-1beta (IL-1beta ), and IL-6 in articular pathology were evaluated. Cytokine levels were quantified in the serum and joints by enzyme-linked immunosorbent assay in mice injected with GBS IV and tested or not tested with pentoxifylline (PTF), a methylxanthine that affects cytokine production. PTF was administered intraperitoneally at a dose of 1 mg/mouse (50 mg/kg of body weight) 1 h after GBS infection and then at 24-h intervals for 4 days. High levels of IL-1beta and IL-6, but not TNF-alpha , were detected in the joints of mice injected with GBS IV from 5 to 15 days after infection, when articular lesions were most frequent and severe. IL-1beta and IL-6 concentrations in the joints significantly (P < 0.001) exceeded those detected in the serum, confirming a strong local production. PTF treatment resulted in a strong reduction of cytokine production and in a marked decrease in both the incidence and severity of arthritis. Inoculation of exogenous murine recombinant IL-1beta or IL-6 in mice treated with GBS IV plus PTF resulted in an incidence and severity of articular lesions similar to those obtained with inoculation of GBS IV alone. No significant effect was obtained with TNF-alpha administration. These data show a strong involvement of IL-1beta and IL-6, but not TNF-alpha , in the pathogenesis of GBS arthritis.

* Corresponding author. Mailing address: Microbiology Section, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Via del Giochetto, 06122 Perugia, Italy. Phone: 39-075-585-3409. Fax: 39-075-585-3400. E-mail: tissi{at}unipg.it.

Infection and Immunity, September 1999, p. 4545-4550, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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