These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: IL-23 neutralization protects mice from Gram-negative endotoxic shock.
    Author: Belladonna ML, Vacca C, Volpi C, Giampietri A, Fioretti MC, Puccetti P, Grohmann U, Campanile F.
    Journal: Cytokine; 2006 May; 34(3-4):161-9. PubMed ID: 16759878.
    Abstract:
    Excessive production of proinflammatory cytokines, including TNF-alpha, IL-1, IL-6, IL-12, and IFN-gamma is thought to contribute significantly to lethality in septic shock syndromes. IL-23 is a heterodimeric cytokine that combines the p40 subunit of IL-12 with a specific p19 subunit. Similar to IL-12, IL-23 is considered to be a key immunoregulator in the response to pathogenic organisms but its contribution to Gram-negative endotoxic shock is as yet unclear. Using an established shock model with Pseudomonas aeruginosa, we found early and sustained expression of IL-23 p19 transcripts in the spleens of mice undergoing lethal challenge with the bacterium. Administration of p19-neutralizing antibody reduced mortality in a dose-dependent fashion. Survival in P. aeruginosa-challenged mice was associated with a dramatic decrease in circulating levels of the pathogenetic cytokines, TNF-alpha and IFN-gamma. Hence, IL-23 may represent a new therapeutic target in Gram-negative endotoxic shock.
    [Abstract] [Full Text] [Related] [New Search]