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The Journal of Immunology, 2004, 173: 4040-4049.
Copyright © 2004 by The American Association of Immunologists

IL-12p40 and IL-18 Modulate Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection1

Shan-Ze Wang2,*, Yi-Xiao Bao2,*, Cynthia L. Rosenberger*, Yohannes Tesfaigzi*, James M. Stark{dagger} and Kevin S. Harrod3,*

* Asthma and Pulmonary Immunology Program, Lovelace Respiratory Research Institute, Albuquerque, NM 87108; and {dagger} Pediatric Pulmonary and Critical Care Medicine, Health Science Center, Houston Medical School, University of Texas, Houston, TX 77030

Respiratory syncytial virus-induced bronchiolitis has been linked to the development of allergy and atopic asthma. IL-12 and possibly IL-18 are central mediators orchestrating Th1 and/or Th2 immune responses to infection. To determine a possible role for IL-12 in regulating the immune response to acute respiratory syncytial virus infection, IL-12p40 gene-targeted (IL-12p40–/–) and wild-type mice were intratracheally infected with respiratory syncytial virus, and lung inflammatory and immune responses were assessed. Lung inflammation and mucus production were increased in the airways of IL-12p40–/– mice as compared with those of wild-type mice, concurrent with increased levels of the Th2 effector cytokines IL-5 and IL-13. Respiratory syncytial virus clearance and levels of Th1 effector cytokine IFN-{gamma} were not altered. Interestingly, IL-18, another mediator of IFN-{gamma} production, was significantly increased in the lungs of IL-12p40–/– mice early during the course of infection. Abrogation of IL-18-mediated signaling in IL-12p40–/– mice further enhanced Th2 immune response and mucus production in the airways during respiratory syncytial virus infection but failed to modulate IFN-{gamma} production or viral clearance. These findings implicate a role for IL-12 and IL-18 in modulating respiratory syncytial virus-induced airway inflammation distinct from that of viral clearance.




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