• Seija Sipola, Tero I Ala-Kokko, Jouko J Laurila, Juha Saarnio, Pasi Ohtonen, Hannu Syrjälä, and Tuomo J Karttunen.
• Division of Intensive Care Medicine, Department of Anesthesiology, University Hospital of Oulu, Oulu, Finland - seija.sipola@ppshp.f.
• Minerva Anestesiol. 2017 Oct 1; 83 (10): 1017-1025.

BackgroundAbnormal permeability and extensive epithelial injury are characteristic of colon wall damage complicating critical illness, such as sepsis, and associated with mortality. To assess mechanisms of such colon epithelial disruption, we studied expression of markers of innate immunity and intercellular junctions in patients with critical illness.MethodsEmergency colectomy samples from 38 intensive care unit patients with sepsis, fulminant C. difficile colitis, or colon ischemia were studied. Expression of tight junction proteins (claudin‑1, claudin‑2, occludin) and Toll-like receptors (TLRs) (TLR2, TLR4, TLR5, and TLR9) was studied in samples representing histologically verified damaged segments of the colon, and compared with normal colon (N.=28).ResultsAs compared with normal epithelium, histologically damaged samples showed decreased claudin‑1 (P=0.002) expression. Expression of TLR2, TLR4, and TLR5 was similar in patients and controls, but TLR9 expression was up-regulated in the histologically damaged region (P=0.03). The expression of other markers (claudin‑1, claudin‑2, occludin, TLR2,TLR4, TLR5 and TLR9) did not differ between survivors and non-survivors.ConclusionsDown-regulation of claudin‑1 and up-regulation of TLR9 suggest that epithelial barrier dysfunction and innate immunity activation are involved in the pathogenesis of colon epithelial injury in patients with critical illness.

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