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Infection and Immunity, January 2004, p. 295-300, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.295-300.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Interleukin-18 Is an Essential Element in Host Resistance to Experimental Group B Streptococcal Disease in Neonates

Vitaliano Cusumano,1 Angelina Midiri,1 Valentina Valeria Cusumano,2 Antonella Bellantoni,1 Giuseppe De Sossi,1 Giuseppe Teti,1 Concetta Beninati,1 and Giuseppe Mancuso1*

Department of Pathology and Experimental Microbiology, Medical School, University of Messina, Messina, Italy I-98125,1 VII Department of Infectious Diseases, Cotugno Hospital, Naples, Italy I-801312

Received 4 August 2003/ Returned for modification 27 September 2003/ Accepted 13 October 2003

Previous studies demonstrated that interleukin-12 (IL-12)-dependent gamma interferon (IFN-{gamma}) responses have a major role in restricting in vivo bacterial growth during infection of mice with group B streptococci (GBS), important human pathogens. Like IL-12, IL-18 is a potent IFN-{gamma} inducer. The role of IL-18 in experimental GBS infection was investigated here. Significant elevations of IL-18 levels over baseline values were detected in plasma samples from neonatal mice rendered septic with GBS. Neutralization of IL-18 significantly increased mortality and bacterial burden (P < 0.05). In contrast, administration of recombinant IL-18 (rIL-18) before or after GBS challenge remarkably improved survival and decreased blood colony counts, in association with increased IFN-{gamma} production by spleen cells. The beneficial effects of rIL-18 were counteracted by administration of neutralizing anti-IFN-{gamma} monoclonal antibodies, indicating that the effects of IL-18 were mediated by IFN-{gamma}. Finally, low rIL-18 doses that had no effect of their own on bacterial burden could act in synergy with rIL-12 to protect neonatal mice during GBS infection. Collectively, our data indicate that IL-18 responses have an important role in host defenses against GBS and that rIL-18 may be useful in alternative strategies to treat neonatal GBS disease.

* Corresponding author. Mailing address: Policlinico Universitario, Via C. Valeria, 1, I-98125 Messina, Italy. Phone: 39-090-221-3317. Fax: 39-090-221-3312. E-mail: mancuso{at}depem.org.

Editor: J. T. Barbieri

Infection and Immunity, January 2004, p. 295-300, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.295-300.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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