The focal complex of epithelial cells provides a signalling platform for interleukin‐8 induction in response to bacterial pathogens. (2nd June 2014)

• Record Type: Journal Article
• Authors: Eucker, Tyson P.; Samuelson, Derrick R.; Hunzicker‐Dunn, Mary; Konkel, Michael E.
• Is Part Of: Cellular microbiology. Volume 16:Number 9(2014:Sep.)
• Page Start: 1441
• Page End: 1455
• Publication Date: 2014-06-02
• Subjects: Microbiology -- Periodicals; Cytology -- Periodicals; Host-parasite relationships -- Periodicals; Microbiology -- Periodicals; Cells -- Periodicals; Microbiologie -- Périodiques; Microbiologie; Relation hôte-parasite; Cytologie; Cellule; Réponse cellulaire; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); 579.05
• DOI: 10.1111/cmi.12305
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>Bacterial pathogens can induce an inflammatory response from epithelial tissues due to secretion of the pro‐inflammatory chemokine interleukin‐8 (IL‐8). Many bacterial pathogens manipulate components of the focal complex (FC) to induce signalling events in host cells. We examined the interaction of several bacterial pathogens with host cells, including <italic>C</italic><italic>ampylobacter jejuni</italic>, to determine if the FC is required for induction of chemokine signalling in response to bacterial pathogens. Our data indicate that secretion of IL‐8 is triggered by <italic>C</italic>. <italic>jejuni</italic>, <italic>H</italic><italic>elicobacter pylori</italic> and <italic>S</italic><italic>almonella enterica</italic> serovar Typhimurium in response to engagement of β<sub>1</sub> integrins. Additionally, we found that the secretion of IL‐8 from <italic>C</italic>. <italic>jejuni</italic> infected epithelial cells requires FAK, Src and paxillin, which in turn are necessary for Erk 1/2 recruitment and activation. Targeting the FC component paxillin with siRNA prevented IL‐8 secretion from cells infected with several bacterial pathogens, including <italic>C</italic>. <italic>jejuni</italic>, <italic>H</italic><italic>elicobacter pylori</italic>, <italic>S</italic><italic>almonella enterica</italic> serovar Typhimurium, <italic>S</italic><italic>taphylococcus aureus</italic>, <italic>P</italic><italic>seudomonas aeruginosa</italic>, and <italic>V</italic><italic>ibrio parahaemolyticus</italic>. Our findings indicate that maximal IL‐8 secretion from epithelial cells in response to bacterial infection is dependent on the FC. Based on the commonality of the host response to bacterial pathogens, we propose that the FC is a signalling platform for an epithelial cell response to pathogenic organisms.</p> </abstract>