| First Author | Cusumano V | Year | 2004 |
| Journal | Infect Immun | Volume | 72 |
| Issue | 1 | Pages | 295-300 |
| PubMed ID | 14688108 | Mgi Jnum | J:87832 |
| Mgi Id | MGI:3028309 | Doi | 10.1128/IAI.72.1.295-300.2004 |
| Citation | Cusumano V, et al. (2004) Interleukin-18 is an essential element in host resistance to experimental group B streptococcal disease in neonates. Infect Immun 72(1):295-300 |
| abstractText | 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. |
