• J. Mol. Med. · Sep 2017

    Cathelicidin-deficient mice exhibit increased survival and upregulation of key inflammatory response genes following cecal ligation and puncture.

    • Patricia Severino, Suely Kubo Ariga, Hermes Vieira Barbeiro, Thais Martins de Lima, Elisangela de Paula Silva, Denise Frediani Barbeiro, Machado Marcel Cerqueira César MCC Departamento de Emergências Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Victor Nizet, and Pinheiro da Silva Fabiano F http://orcid.org/0000-0003-2673-2202 Departamento de Emergências Clínicas, Faculdade de Medicina da Universidade de São Pa.
    • Instituto Israelita de Ensino e Pesquisa, Hospital Israelita Albert Einstein, São Paulo, Brazil.
    • J. Mol. Med. 2017 Sep 1; 95 (9): 995-1003.

    AbstractAntimicrobial peptides possess a myriad of molecular properties including bacterial killing and the regulation of many aspects of innate immunity. Cathelicidins are a group of antimicrobial peptides widely investigated by the scientific community. Many studies have focused on the bactericidal and pro-inflammatory roles of cathelicidins. Because the role of endogenous cathelicidin expression remains obscure in deep-seated systemic infections, we induced sepsis in cathelicidin knockout and wild-type (WT) mice by cecal ligation and puncture, performing transcriptome screening by DNA microarray in conjunction with other immunologic assays. Cathelicidin-deficient mice showed increased survival compared to WT mice in this established experimental model of polymicrobial sepsis, in association with upregulation of certain key inflammatory response genes. Therefore, cathelicidins can exert both pro- and anti-inflammatory activities depending on the disease and cellular context.

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