A thermal injury-induced circulating factor(s) compromises intestinal cell morphology, proliferation, and migration

• Published in: American journal of physiology: Gastrointestinal and liver physiology Vol. 277; no. 1; pp. G175 - G182
• Main Authors: Varedi, M, Greeley, Jr, G H, Herndon, D N, Englander, E W
• Format: Journal Article
• Language: English
• Published: United States 01.07.1999
• Subjects: Animals; Blood Physiological Phenomena; Burns - blood; Cell Division - physiology; Cell Line; Cell Movement - physiology; Intestinal Mucosa - pathology; Intestine, Small - pathology; Intestine, Small - physiopathology; Male; Rats; Rats, Sprague-Dawley
• ISSN: 0002-9513; 0193-1857; 1522-1547
• DOI: 10.1152/ajpgi.1999.277.1.G175

The effects of a 60% body surface area thermal injury in rats on the morphology and proliferation of the epithelium of the small intestine and the in vitro effects of serum collected from scalded rats on intestinal epithelial cells were investigated. Scald injury caused significant reductions in duodenal villus width and crypt dimensions, villus enterocytes changed in shape from columnar to cuboidal, and the number of goblet cells decreased. The proportion of bromodeoxyuridine-labeled S phase cells in crypts was also diminished. In vitro, incubation of intestinal epithelial cells (IEC-6) with scalded rat serum (SRS) collected at either 12 or 24 h after injury caused a disruption in the integrity of the confluent culture and induced the appearance of large denuded areas. SRS also decreased DNA synthesis and delayed wound closure in an in vitro wound-healing model. The thermal injury-induced changes in intestinal mucosal morphology and epithelial cell growth characteristics described in this study may underlie, in part, the mechanism(s) involved in the diminished absorption of nutrients, increased intestinal permeability, and sepsis in patients with thermal injury.