Research Report
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World J Gastroenterol. Apr 21, 2014; 20(15): 4345-4352
Published online Apr 21, 2014. doi: 10.3748/wjg.v20.i15.4345
Hepcidin expression in colon during trinitrobenzene sulfonic acid-induced colitis in rats
Érica Martins Ferreira Gotardo, Gilberto de Almeida Ribeiro, Thayane Rodrigues Leite Clemente, Camila Henrique Moscato, Renata Bortolin Guerra Tomé, Thalita Rocha, José Pedrazzoli Jr, Marcelo Lima Ribeiro, Alessandra Gambero
Érica Martins Ferreira Gotardo, Gilberto de Almeida Ribeiro, Thayane Rodrigues Leite Clemente, Camila Henrique Moscato, Renata Bortolin Guerra Tomé, Thalita Rocha, José Pedrazzoli Jr, Marcelo Lima Ribeiro, Alessandra Gambero, Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Bragança Paulista, SP 12916-900, Brazil
Author contributions: Gotardo EMF and Ribeiro GA contributed equally to this work; Gotardo EMF, Ribeiro GA, Clemente TRL, Moscato CH and Tomé RBG performed the experiments; Rocha T and Pedrazzoli Jr J analyzed the data and wrote the manuscript; Ribeiro ML and Gambero A designed the experiments, analyzed the data and wrote the manuscript.
Supported by The Fundação de Amparo à Pesquisa do Estado de São Paulo, No. FAPESP 2010/02991-6
Correspondence to: Alessandra Gambero, PhD, Clinical Pharmacology and Gastroenterology Unit, São Francisco University Medical School, Av. São Francisco de Assis 218, Bragança Paulista, SP 12916-900, Brazil. alessandra.gambero@usf.edu.br
Telephone: +55-11-24548 8982 Fax: +55-11-2454 8974
Received: October 22, 2013
Revised: December 18, 2013
Accepted: January 19, 2014
Published online: April 21, 2014
Core Tip

Core tip: Hepcidin is an endogenous peptide with weak antimicrobial properties that regulates changes in iron metabolism during inflammation. However, infection-associated cytokines, pathogen-derived molecules or whole pathogens can induce hepcidin synthesis as part of the host response to infection. This is the first study to describe that colitis induces hepcidin expression in colons associated with the Interleukin-6/Stat-3 signaling pathways and local iron sequestration. This finding suggests a host response to infection because reducing the iron available to pathogens is an important antimicrobial mechanism. However, we could not exclude the possibility that hepcidin expression contributes to increased local inflammation by stimulating pro-inflammatory macrophages.