Radiographic and histopathological study of gastrointestinal dysmotility in lipopolysaccharide‐induced sepsis in the rat

Abstract

BackgroundSepsis is a highly incident condition in which a cascade of proinflammatory cytokines is involved. One of its most frequent consequences is ileus, which can increase mortality. Animal models such as that induced by systemic administration of lipopolysaccharide (LPS) are useful to deeply evaluate this condition. The effects of sepsis on the gastrointestinal (GI) tract have been explored but, to our knowledge, in vivo studies showing the motor and histopathological consequences of endotoxemia in an integrated way are lacking. Our aim was to study in rats the effects of sepsis on GI motility, using radiographic methods, and to assess histological damage in several organs.MethodsMale rats were intraperitoneally injected with saline or E. coli LPS at 0.1, 1, or 5 mg kg−1. Barium sulfate was intragastrically administered, and X‐rays were performed 0–24 h afterwards. Several organs were collected for organography, histopathology, and immunohistochemistry studies.Key ResultsAll LPS doses caused gastroparesia, whereas changes in intestinal motility were dose‐and time‐dependent, with an initial phase of hypermotility followed by paralytic ileus. Lung, liver, stomach, ileum, and colon (but not spleen or kidneys) were damaged, and density of neutrophils and activated M2 macrophages and expression of cyclooxygenase 2 were increased in the colon 24 h after LPS 5 mg kg−1.Conclusions and InferencesUsing radiographic, noninvasive methods for the first time, we show that systemic LPS causes dose‐, time‐, and organ‐dependent GI motor effects. Sepsis‐induced GI dysmotility is a complex condition whose management needs to take its time‐dependent changes into account.

Galactooligosaccharide Mediates NF-κB Pathway to Improve Intestinal Barrier Function and Intestinal Microbiota

“…Intestinal damage arises from the destruction of tight junctions at intestinal barriers, permitting lipopolysaccharide (LPS) entry into the blood and causing adverse downstream reactions [1,2]. These include increased mucosal permeability, mucosal inflammation, anemia and malabsorption, protein loss, ileal dysfunction, diarrhea, mucosal ulceration, strictures due to diaphragm disease, and active bleeding and perforation [3].…”