Inflammatory response of porcine epithelial IPEC J2 cells to enterotoxigenic E. coli infection is modulated by zinc supplementation
| Autor: | Marie-Anne Shaw, H. M. Miller, Hannah R. Sargeant |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
Swine
Immunology Gene Expression chemistry.chemical_element Zinc Biology medicine.disease_cause Cell Line Microbiology chemistry.chemical_compound In vivo Heat shock protein Enterotoxigenic Escherichia coli medicine Animals Immunologic Factors Molecular Biology Pathogen Escherichia coli Infections Oligonucleotide Array Sequence Analysis Inflammation Innate immune system Reverse Transcriptase Polymerase Chain Reaction NF-kappa B Epithelial Cells NF-κB Gene Expression Regulation chemistry Cell culture Zinc Oxide |
| Zdroj: | Molecular Immunology. 48:2113-2121 |
| ISSN: | 0161-5890 |
| DOI: | 10.1016/j.molimm.2011.07.002 |
| Popis: | Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhoea in pigs and humans. The duration and severity of diarrhoea can be controlled using zinc supplementation, typically pharmacological levels of zinc oxide in pigs. In this study, IPEC J2 cells were used as an in vitro model of intestinal ETEC infection, with separate and simultaneous zinc treatment. Genomic analysis identified increased expression of a variety of innate immune response genes (NF-κB targets) in response to ETEC exposure, and several stress response genes in response to zinc exposure, provided as ZnO. Expression of genes involved in the innate immune response was reduced when cells were simultaneously exposed to ZnO, and it is suggested that ZnO treatment inhibits the induction of NF-κB in response to pathogens, possibly through up-regulated heat shock proteins. A similar response in vivo with consequent down-regulation in the inflammatory response would reduce further pathogen invasion, maintain normal gut function and maintain growth. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect