Mechanisms and regulation of IL-22-mediated intestinal epithelial homeostasis and repair

Patnaude, Lori; Mayo, Martha; Mario, Regina; Wu, Xiaoming; Knight, Heather; Creamer, Kelly; Wilson, Sarah S.; Pivorunas, Valerie; Karman, Jozsef; Phillips, Lucy; Dunstan, Robert W.; Kamath, Rajesh V.; McRae, Bradford L.; Terrillon, Sonia

doi:10.1016/j.lfs.2021.119195

Cited by 47 publications

(96 citation statements)

References 38 publications

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“…In different models of colitis, although IL-22 is considered to be an epithelium-protective cytokine, its role in mediating or preventing ER stress and mucus secretion remains unclear [63,64]. It was recently confirmed that IL-22 induces epithelial stem cell proliferation and glycocalyx-associated mucins at the expense of GCs and MUC2 expression [65]. Together, these studies suggest that the effect of IL-22 on GC-derived mucus production is principally environmental rather than an intrinsic and direct effect.…”

Section: Regulation Of Mucin Production By Immune Mediatorsmentioning

confidence: 99%

Intestinal mucus barrier: a missing piece of the puzzle in food allergy

Parrish

Boudaud

Kuehn

et al. 2022

Trends in Molecular Medicine

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Section: Regulation Of Mucin Production By Immune Mediatorsmentioning

confidence: 99%

Intestinal mucus barrier: a missing piece of the puzzle in food allergy

Parrish

Boudaud

Kuehn

et al. 2022

Trends in Molecular Medicine

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“…Therefore, we focused on exploring the mechanism of A. baumannii OmpA-mediated barrier dysfunction. Inflammatory responses have important roles in the regulation of epithelial barrier function; specifically, inflammatory mediators (e.g., TNF and ILs) induce inflammatory injury and repair of the epithelial barrier (29,30), which may be involved in cytoskeleton dynamics and the regulation of cell-cell junctions (31). Transcriptome profiling revealed that genes related to TNF, cytokine-cytokine receptor interaction, and TLR were significantly upregulated in A. baumannii acute lethal pneumonia (32).…”

Section: Discussionmentioning

confidence: 99%

Acinetobacter baumannii Outer Membrane Protein A Induces Pulmonary Epithelial Barrier Dysfunction and Bacterial Translocation Through The TLR2/IQGAP1 Axis

et al. 2022

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Pulmonary epithelial barrier dysfunction is a critical pathophysiological process in pneumonia and associated invasive infections, such as those caused by Acinetobacter baumannii. However, the mechanisms underlying A. baumannii-induced pulmonary epithelial barrier dysfunction and bacterial translocation remain unclear. In this study, lungs of mice and A549 human epithelial cell monolayers were challenged with the A. baumannii wild-type strain and an outer membrane protein A (ompA) deletion strain. In addition, epithelial cells in culture were treated with purified OmpA protein or transfected with a eukaryotic expression vector encoding ompA (pCMV-ompA). Bacterial translocation across cell monolayers and intrapulmonary burden were measured, barrier function was evaluated in vivo and in vitro; cell migration ability was determined. The specific inhibitors C29 and JSH-23 were used to suppress the activity of Toll-like receptor 2 (TLR2) and of NF-κB, respectively. IQ-GTPase-activating protein 1 (IQGAP1) small interfering RNA was used to knock down endogenous IQGAP1 expression. In this work, we show that OmpA from A. baumannii increased the production of pro-inflammatory cytokines, remodeled the cytoskeleton, and internalized intercellular adherens junctions (AJs); these changes eventually induced pulmonary epithelial barrier dysfunction to promote bacterial translocation. IQGAP1-targeting small interfering RNA and chemical inhibition of TLR2 or NF-κB prevented high permeability of the pulmonary epithelial barrier. TLR2/NF-κB signaling was involved in OmpA-induced inflammation, IQGAP1-mediated OmpA-induced opening of the pulmonary epithelial barrier via cytoskeleton dynamic remodeling, and cellular redistribution of the major AJ protein, E-cadherin. These observations indicate that A. baumannii uses OmpA to overcome epithelial defences and cross the pulmonary epithelial barrier.

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“…In fact, the probiotic Escherichia coli strain Nissle (EcN) and some species of Lactobacilli induced a high expression of human betadefensin-2 in epithelial cells. Similarly, other probiotics, such as Lactobacillus reuteri, can increase the secretion of interleukin-22 (IL-22), which mediate intestinal mucosa repair and defense via AMPs induction (Wehkamp et al, 2004;Gaudino et al, 2021;Patnaude et al, 2021).…”

Section: Probiotics Benefits On Alcoholic Liver Diseasementioning

confidence: 99%

Probiotics-Based Treatment as an Integral Approach for Alcohol Use Disorder in Alcoholic Liver Disease

et al. 2021

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Alcoholic liver disease (ALD) is one of the leading causes of morbidity among adults with alcohol use disorder (AUD) worldwide. Its clinical course ranges from steatosis to alcoholic hepatitis, progressing to more severe forms of liver damage, such as cirrhosis and hepatocellular carcinoma. The pathogenesis of ALD is complex and diverse elements are involved in its development, including environmental factors, genetic predisposition, the immune response, and the gut-liver axis interaction. Chronic alcohol consumption induces changes in gut microbiota that are associated with a loss of intestinal barrier function and inflammatory responses which reinforce a liver damage progression triggered by alcohol. Alcohol metabolites such as acetaldehyde, lipid peroxidation-derived aldehyde malondialdehyde (MDA), and protein-adducts act as liver-damaging hepatotoxins and potentiate systemic inflammation. Additionally, ethanol causes direct damage to the central nervous system (CNS) by crossing the blood-brain barrier (BBB), provoking oxidative stress contributing to neuroinflammation. Overall, these processes have been associated with susceptibility to depression, anxiety, and alcohol craving in ALD. Recent evidence has shown that probiotics can reverse alcohol-induced changes of the microbiota and prevent ALD progression by restoring gut microbial composition. However, the impact of probiotics on alcohol consumption behavior has been less explored. Probiotics have been used to treat various conditions by restoring microbiota and decreasing systemic and CNS inflammation. The results of some studies suggest that probiotics might improve mental function in Alzheimer’s, autism spectrum disorder, and attenuated morphine analgesic tolerance. In this sense, it has been observed that gut microbiota composition alterations, as well as its modulation using probiotics, elicit changes in neurotransmitter signals in the brain, especially in the dopamine reward circuit. Consequently, it is not difficult to imagine that a probiotics-based complementary treatment to ALD might reduce disease progression mediated by lower alcohol consumption. This review aims to present an update of the pathophysiologic mechanism underlying the microbiota-gut-liver-brain axis in ALD, as well as to provide evidence supporting probiotic use as a complementary therapy to address alcohol consumption disorder and its consequences on liver damage.

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Mechanisms and regulation of IL-22-mediated intestinal epithelial homeostasis and repair

Cited by 47 publications

References 38 publications

Intestinal mucus barrier: a missing piece of the puzzle in food allergy

Intestinal mucus barrier: a missing piece of the puzzle in food allergy

Acinetobacter baumannii Outer Membrane Protein A Induces Pulmonary Epithelial Barrier Dysfunction and Bacterial Translocation Through The TLR2/IQGAP1 Axis

Probiotics-Based Treatment as an Integral Approach for Alcohol Use Disorder in Alcoholic Liver Disease

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