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The subtle villi abnormalities could trigger mechanisms of tissue damage such as the alteration in the mucosa barrier dysfunction and systemic translocation of bacteria and their products [25].
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During sepsis, the most frequent complication within the gastrointestinal tract is mucosal barrier dysfunction.
It is reported that intestinal epithelial apoptosis contributes to mucosal barrier dysfunction [9] [11].
Intestinal mucosa barrier (IMB) dysfunction results in many notorious diseases for which there are currently few effective treatments.
Supporting perfusion of the intestinal mucosa could ameliorate barrier dysfunction.
Early intestinal microcirculatory dysfunction has been observed even in normotensive sepsis [ 9] and it may lead to complications such as altered intestinal motility [ 10], mucosa barrier disruption, bacterial translocation [ 11], and multiple organ dysfunction syndrome [ 12].
In addition to activating pro-inflammatory events, intestinal barrier dysfunction initiates immunoregulatory processes.
The current studies highlight the critical requirement for AhR-Nrf2 in protecting from barrier dysfunction.
This is the first in vivo analysis of physiologically relevant barrier dysfunction and consequent immunoregulation.
Thaiss, C. A. et al. Hyperglycemia drives intestinal barrier dysfunction and risk for enteric infection.
UroA/UAS03 failed to repair TNBS-induced barrier dysfunction and colitis in Nrf2−/− mice (Fig. 7).
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