| About 95% of infection takes place in mucosa or through mucosa and thus increasing attention has been paid to mucosal immunity. Intestinal epithelial cell( IEC) not only has barrier function, but also plays a role in regulation of innate and acquired immunity at sensory and effector levels. Among the intestinal epithelial cells (IEC) there are numerous lymphocytes named intraepithelial lymphocytes (IEL), which are the first immune cells to encounter foreign antigens in the mucosal immune system. There are also other kinds of immune cells such as macrophages (MΦ) and dendritic cells underneath the epithelial layer. Studies have indicated that the epithelium is not only associated with immune cells anatomically, but also through complicated "cross-talk" between them under physiological as well as pathological conditions, which involved in the maintaining of the homeostasis between internal and external environment.The co-culture of mucosal immune cells with characterized epithelial cells and the subsequent analysis of epithelial physiology have contributed significantly to our appreciation of immune regulation of epithelial function and of effects of epithelium on immune modulation. So it is fundamental to explore the cross-talk between mucosal immune cells and IEC by establishing a stable two cell co-culture system in vitro of human colonic epithelial cell line Caco-2 with freshly isolated rat intestinal intraepithelial lymphocyte and then three cell co-culture system of Caco-2-IEL-MΦ.In this study, we observed modulatory effect of immune cells on epithelial cells, and vice versa, in response to challenge of Shigella F2a-12 LPS or infected by S. flexneri2a-12 and T32 in vitro and the silencing of IL-8 in Caco-2 by RNAi technique. The results indicated that:1 Modulation of epithelial cells by immune cells1) Modulation of barrier function of epithelial cellsIEL could modulate epithelial barrier function in two-ways: enhancing the barrier in physiological condition, while impairing under the challenging of S.F2a-12 LPS. This function of IEL may mainly mediated by cell-cell contact. The junction-like structure found for the first time between IEL and Caco-2 under TEM may be involved in this modulation.Macrophage could further decrease the barrier function of IEC infected by F2a-12, which would be helpful for the attraction of inflammatory cells such as neutrophils and eliminate the infection as well as further invasion and extension of bacteria.2) Modulation of cytokines secretion of epithelial cellsIEL could affect the secretion of RANTES of epithelial cells; Macrophage could increase the secretion of inflammation cytokines (Eotaxin, Eotaxin-2, GCSF, IFN-Y ,IL-1 P , IL-8, MCP-2, MCSF, MIG) of epithelial cells infected by S. F2a-123) Modulation of CFTR expression of epithelial cellsIEL could increase the expression of CFTR of Caco-2, especially after challenged by LPS, which suggest that CFTR may involved in the cross-talk between IEL-IEC.2 Modulation of immune cells by epithelial cells1) Modulation of EEL viabilityCell-cell contact is vital for the survival of IEL, junction-like structure between IEL-IEC may be the structural basis for the survival of IEL.2) Modulation of immune cell function by cytokinesEpithelial cells could inhibit immune cells to maintain the immune tolerance of epithelium by TGF- P in physiological conditions; They could secrete chemokines and inflammation cytokines (Eotaxin, Eotaxin-2, GCSF, IFN- Y ,IL-1 ￡ , IL-8, MCP-2, MCSF, MIQet al) to attract and activate immune cells when there is an infection; They could feedback regulate the immune response by secretion of IL-10 in case it cause...
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