{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T05:54:12Z","timestamp":1791352452368,"version":"4.3.1"},"reference-count":44,"publisher":"BMJ","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"accepted":{"date-parts":[[2010,10,25]]},"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Enteric glial cells (EGCs) are important regulators of intestinal epithelial barrier (IEB) functions. EGC-derived\n                      <jats:italic>S<\/jats:italic>\n                      -nitrosoglutathione (GSNO) has been shown to regulate IEB permeability. Whether EGCs and GSNO protect the IEB during infectious insult by pathogens such as\n                      <jats:italic>Shigella flexneri<\/jats:italic>\n                      is not known.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      <jats:italic>S flexneri<\/jats:italic>\n                      effects were characterised using in vitro coculture models of Caco-2 cells and EGCs (or GSNO), ex vivo human colonic mucosa, and in vivo ligated rabbit intestinal loops. The effect of EGCs on\n                      <jats:italic>S flexneri<\/jats:italic>\n                      -induced changes in the invasion area and the inflammatory response were analysed by combining immunohistochemical, ELISA and PCR methods. Expression of small G-proteins was analysed by western blot. Expression of ZO-1 and localisation of bacteria were analysed by fluorescence microscopy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      EGCs significantly reduced barrier lesions and inflammatory response induced by\n                      <jats:italic>S flexneri<\/jats:italic>\n                      in Caco-2 monolayers. The EGC-mediated effects were reproduced by GSNO, but not by reduced glutathione, and pharmacological inhibition of pathways involved in GSNO synthesis reduced EGC protecting effects. Furthermore, expression of Cdc42 and phospho-PAK in Caco-2 monolayers was significantly reduced in the presence of EGCs or GSNO. In addition, changes in ZO-1 expression and distribution induced by\n                      <jats:italic>S flexneri<\/jats:italic>\n                      were prevented by EGCs and GSNO. Finally, GSNO reduced\n                      <jats:italic>S flexneri<\/jats:italic>\n                      -induced lesions of the IEB in human mucosal colonic explants and in a rabbit model of shigellosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These results highlight a major protective function of EGCs and GSNO in the IEB against\n                      <jats:italic>S flexneri<\/jats:italic>\n                      attack. Consequently, this study lays the scientific basis for using GSNO to reduce barrier susceptibility to infectious or inflammatory challenge.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gut.2010.229237","type":"journal-article","created":{"date-parts":[[2010,12,7]],"date-time":"2010-12-07T22:51:26Z","timestamp":1291762286000},"page":"473-484","source":"Crossref","is-referenced-by-count":101,"title":["Enteric glia protect against\n                    <i>Shigella flexneri<\/i>\n                    invasion in intestinal epithelial cells: a role for\n                    <i>S<\/i>\n                    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