{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T11:00:15Z","timestamp":1787742015184,"version":"build-2784847793"},"reference-count":55,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2021,1,15]],"date-time":"2021-01-15T00:00:00Z","timestamp":1610668800000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Gut ischemia and hypoxia post severe burn leads to breakdown of intestinal epithelial barrier and enteric bacterial translocation (EBT), resulting in serious complications, such as systemic inflammatory response syndrome, sepsis and multiple organ failure. Cystic fibrosis transmembrane conductance regulator (CFTR) is known to be downregulated by hypoxia and modulate junctional complexes, which are crucial structures maintaining the intestinal barrier. This study aimed to investigate whether CFTR plays a role in both regulating the intestinal barrier and mediating EBT post severe burn, as well as the signaling pathways involved in these processes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>An in vitro Caco-2 cell model subjected to hypoxic injury and an in vivo mouse model with a 30% total body surface area full-thickness dermal burn were established. DF 508 mice (mice with F508del CFTR gene mutation) were used as an in vivo model to further demonstrate the role of CFTR in maintaining normal intestinal barrier function. QRT-PCR, western blot, ELISA, TER assay and immunofluorescence staining were used to detect the expression and localization of CFTR and tight junction proteins, as well as the function of tight junctions.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Our data indicated that, in Caco-2 cells, the hypoxia condition significantly reduced CFTR expression; activated extracellular signal-regulated kinase and nuclear factor-\u03baB signaling; elevated secretion of inflammatory factors (tumor necrosis factor-\u03b1, interleukin-1\u03b2 and interleukin-8); downregulated zonula occludens-1, occludin and E-cadherin expression; decreased transepithelial electrical resistance values; and led to a cellular mislocation of ZO-1. More importantly, knockdown of CFTR caused similar alterations. The upregulation of inflammatory factors and downregulation of tight junction proteins (ZO-1 and occludin) induced by knockdown of CFTR could be reversed by specific extracellular signal-regulated kinase or nuclear factor-\u03baB inhibition. In support of the in vitro data, exuberant secretion of pro-inflammatory mediators and EBT was observed in the intestine of severely burnt mice in vivo. EBT occurred in DF508 mice (mice with the F508del\u2002CFTR\u2002gene\u2002mutation), accompanied by augmented tumor necrosis factor-\u03b1, interleukin-1\u03b2 and interleukin-8 levels in the ileum compared to wildtype mice. In addition, vitamin D3 was shown to protect the intestinal epithelial barrier from hypoxic injury.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Collectively, the present study illustrated that CFTR and downstream signaling were critical in modulating the intestinal epithelial junction and EBT post severe burn.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/burnst\/tkaa042","type":"journal-article","created":{"date-parts":[[2021,1,13]],"date-time":"2021-01-13T16:15:46Z","timestamp":1610554546000},"source":"Crossref","is-referenced-by-count":7,"title":["Molecular mechanism mediating enteric bacterial translocation after severe burn: the role of cystic fibrosis transmembrane conductance regulator"],"prefix":"10.1093","volume":"9","author":[{"given":"Xinzhu","family":"Liu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Proteomics Disease, Institute of Burn Research, Southwest Hospital (the First Affiliated Hospital), Third Military Medical University (Army Military Medical University), Gao Tan Yan Street, Chongqing 400038, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Proteomics Disease, Institute of Burn Research, Southwest Hospital (the First Affiliated Hospital), Third Military Medical University (Army Military Medical University), Gao Tan Yan Street, Chongqing 400038, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"You","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Proteomics Disease, Institute of Burn Research, Southwest Hospital (the First Affiliated Hospital), Third Military Medical University (Army Military Medical University), Gao Tan Yan Street, Chongqing 400038, China"},{"name":"Department of Burn and Plastic Surgery, No. 958 Hospital of Army, Southwest Hospital, Third Military Medical University (Army Military Medical University), Jian Xin Dong Street, Chongqing 400020, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuan","family":"Peng","sequence":"additional","affiliation":[{"name":"Department of Plastic and Reconstructive Surgery, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Zhi Zao Ju Road, Shanghai 200011, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yajie","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Proteomics Disease, Institute of Burn Research, Southwest Hospital (the First Affiliated Hospital), Third Military Medical University (Army Military Medical University), Gao Tan Yan Street, Chongqing 400038, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zichen","family":"Yang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Proteomics Disease, Institute of Burn Research, Southwest Hospital (the First Affiliated Hospital), Third Military Medical University (Army Military Medical University), Gao Tan Yan Street, Chongqing 400038, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yixin","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Plastic and Reconstructive Surgery, Shanghai Ninth People\u2019s Hospital, Shanghai Jiao Tong University School of Medicine, Zhi Zao Ju Road, Shanghai 200011, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Key Laboratory for Proteomics Disease, Institute of Burn Research, Southwest Hospital (the First Affiliated Hospital), Third Military Medical University (Army Military Medical University), Gao Tan Yan Street, Chongqing 400038, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,1,15]]},"reference":[{"key":"2021042310351456800_ref1","doi-asserted-by":"crossref","first-page":"6","DOI":"10.1128\/IAI.43.1.6-10.1984","article-title":"Bacterial translocation from the gastrointestinal tracts of rats receiving thermal injury","volume":"43","author":"Maejima","year":"1984","journal-title":"Infect Immun"},{"key":"2021042310351456800_ref2","doi-asserted-by":"crossref","first-page":"524","DOI":"10.1097\/00006534-199209000-00032","article-title":"The role of the gastrointestinal tract in the development of burn sepsis","volume":"90","author":"Epstein","year":"1992","journal-title":"Plast 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