| When the integrity of the intestinal epithelium is compromised, such as during infection by pathogenic organisms, intestinal epithelial cells (IECs) respond with the production of proinflammatory cytokines and chemoattractant cytokines or chemokines, which then attract and activate specific subsets of leukocytes. During chronic inflammation, the panel of IEC chemokines produced likely represents the net effect of a plethora of mediators present in the milieu, including cytokines from activated T lymphocytes (e.g. interferon (IFN)-gamma and interleukin (IL)-4), proinflammatory cytokines from activated macrophages and non-hematopoietic cells (e.g. IL-1beta) and products from luminal bacteria (e.g. lipopolysaccharide (LPS)).;In this study, we treated IEC-18 cells with IFN-gamma, IL-4, IL-1beta and LPS and measured their effect on production of IL-1alpha, two CC chemokines (monocyte chemoattractant protein (MCP)-1 and eotaxin) and a CXC chemokine (macrophage inflammatory protein (MIP)-2).;This study implicates the IEC as being a central component of the intestinal cytokine network, whereby it responds to numerous cytokine stimuli and bacterial products with increased proinflammatory cytokine and chemokine expression that may influence further cytokine expression by leukocytes. (Abstract shortened by UMI.). |
