Interleukin-1β secretion induced by mucosa-associated gut commensal bacteria promotes intestinal barrier repair

Wu, Wan-Jung; Kim, Myunghoo; Chang, Lin-Chun; Assié, Adrien; Saldana-Morales, Fatima B.; Zegarra-Ruiz, Daniel F.; Norwood, Kendra; Samuel, Buck S.; Diehl, Gretchen E.

doi:10.1080/19490976.2021.2014772

Cited by 28 publications

(20 citation statements)

References 83 publications

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“…In vitro studies of intestinal segments excised from patients with IBD showed a remarkable increase in IL-1 β expression [ 34 ]. The similar damaging effect of IL-1 β on intestinal mucosal cells may work in combination with other cytokines to cause mucosal damage in IBD [ 35 ]. Furthermore, TNF- α and IL-l β are potent inducers of IL-6 [ 36 ].…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, TNF- α and IL-l β are potent inducers of IL-6 [ 36 ]. Increased IL-6 mRNA expression may be associated with the upregulation of STAT3 signaling, accelerating the conversion of CD4+T cells into Th17 cells [ 35 ]. The activation of proinflammatory chemokines such as CCL2 and CXCL-1 is also responsible for the aggravation of colitis, attributed to adjustments to the transportation of leukocytes [ 37 ].…”

Section: Resultsmentioning

confidence: 99%

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Dietary Supplement of Amomum villosum Lour. Polysaccharide Attenuates Ulcerative Colitis in BALB/c Mice

Luo

Zeng

Guan

et al. 2022

Foods

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Amomum villosum Lour. (A. villosum), a comestible medicinal plant, has been traditionally used in China to treat diarrhea, stomach fullness, and abdominal distension. Polysaccharide, the main chemical component of A. villosum, has been shown to possess potential antioxidant and glycosidase inhibitory activities; however, whether it has anticolitis activity is unknown. The aim of this research was to evaluate the anticolitis effects of A. villosum polysaccharide (AVLP) in BALB/c mice. The results showed that AVLP administration significantly reversed body weight loss, colon shortening and colon weight gain and decreased the levels of proinflammatory cytokines and chemokines in colitis mice (p < 0.05). AVLP administration also maintained intestinal barrier function by the upregulation of ZO-1 protein expression (p < 0.05). In addition, high-throughput sequencing analysis showed that AVLP possessed a great regulatory effect on the growth of Adlercreutzia, Clostridium, Streptococcus, Parabacteroides, Helicobacter, Odoribacter, and Alistipes (p < 0.05, LDA score > 2). The correlation analysis revealed that the protective effects against colitis of AVLP were highly correlated with intestinal bacterium regulation. These results suggest that AVLP intake could serve as a prospective nutritional strategy for inflammatory bowel diseases.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Dietary Supplement of Amomum villosum Lour. Polysaccharide Attenuates Ulcerative Colitis in BALB/c Mice

Luo

Zeng

Guan

et al. 2022

Foods

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“…However, the reason for this is not completely clear. We speculate it might be derived from multiple factors, because the intestinal epithelial barrier is strongly associated with ENS, the intestinal microbiome and their metabolites [10,45], whose anomalies have been found or reported in ALS [19,34,44]. The intestinal mucus barrier prevents its host from harmful stimuli invasions and contributes to intestinal homeostasis.…”

Section: Discussionmentioning

confidence: 97%

Neuroprotective effect of a multi strain probiotic mixture in SOD1G93A mice Through reducing SOD1 aggregation and targeting the microbe-gut-brain axis

Xin

Liu

et al. 2022

Preprint

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Amyotrophic lateral sclerosis is a devastating neurodegenerative disease characterized by the formation of intracellular protein aggregations and the selective loss of motor neurons. Inflammatory response imbalance was considered to be a risk factor and disease-modifier and involved in the regulation of abnormal protein aggregation in ALS disease. The “microbiota-gut-brain axis” is a bidirectional communication system, which has been shown play some regulatory role in neuroinflammation and abnormal protein aggregation of neurodegenerative disorders. But whether probiotics can exert effects on ALS disease through “microbiota-gut-brain axis” is not clear. In our present study, we first report on superoxide dismutase 1-positive aggregates in intestinal myenteric neurons of SOD1G93A mice. This phenomenon was accompanied by structural disorder of myenteric neurons and enteric glial cells, impaired barrier function and overactivated pro-inflammatory response in intestine. This pathological change is different in colon and ileum, suggesting that it may be related to the difference of microbiota in their lumen. Oral administration of a multi-strain probiotic mixture containing Lactobacillus acidophilus, Bifidobacterium longum and Enterococcus faecalis not only improved the gut barrier function and pro-inflammatory response of spinal cord and intestine but also reduced aberrant SOD1 aggregation in myenteric neurons and spinal cord. This effect is accompanied by the alteration of gut microbiota composition and the increased level of short-chain fatty acids. Together, these findings might imply a potential benefit of microbiota-gut-brain axis axis-based therapy in ALS.

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“…Mice were treated with a single dose of 20 mg/mL streptomycin (MilliporeSigma, S9137-25G) by per os (P.O.) with 1 g/1 L ampicillin (Fisher BioReagent, Thermo Fisher Scientific; BP176025) in drinking water for 2 weeks ( 76 ). Mice were switched to autoclaved water for 2 days before transplant of PBS-resuspended cecal content from mice fed HFD or LFD for 7 days.…”

Section: Methodsmentioning

confidence: 99%

“…Mice were treated with a single dose of 20 mg/ml streptomycin (Sigma, S9137-25G) by per os (P.O.) with 1g/1L ampicillin (Fisher BioReagent, BP176025) in drinking water for 2 weeks (76).…”

Section: Cecal Microbiota Transplantmentioning

confidence: 99%

Acute high-fat diet impairs macrophage-supported intestinal damage resolution

Hill¹,

Kim²,

Zegarra-Ruiz³

et al. 2023

JCI Insight

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Chronic exposure to high-fat diets (HFD) worsens intestinal disease pathology, but acute effects of HFD in tissue damage remain unclear. Here, we used short-term HFD feeding in a model of intestinal injury and found sustained damage with increased cecal dead neutrophil accumulation, along with dietary lipid accumulation. Neutrophil depletion rescued enhanced pathology.Macrophages from HFD treated mice showed reduced capacity to engulf dead neutrophils.Macrophage clearance of dead neutrophils activates critical barrier repair and anti-inflammatory pathways including IL10, which was lost after acute HFD feeding and intestinal injury. IL10 overexpression restored intestinal repair after HFD feeding and intestinal injury. Macrophage exposure to lipids from the HFD prevented tethering and uptake of apoptotic cells and Il10 induction. Milk fat globule-EGF factor-8 (MFGE8) is a bridging molecule that facilitates macrophage uptake of dead cells. MFGE8 also facilitates lipid uptake, and we demonstrate that dietary lipids interfere with MFGE8-mediated macrophage apoptotic neutrophil uptake and subsequent Il10 production. Our findings demonstrate that HFD promotes intestinal pathology by interfering with macrophage clearance of dead neutrophils, leading to unresolved tissue damage.

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Interleukin-1β secretion induced by mucosa-associated gut commensal bacteria promotes intestinal barrier repair

Cited by 28 publications

References 83 publications

Dietary Supplement of Amomum villosum Lour. Polysaccharide Attenuates Ulcerative Colitis in BALB/c Mice

Dietary Supplement of Amomum villosum Lour. Polysaccharide Attenuates Ulcerative Colitis in BALB/c Mice

Neuroprotective effect of a multi strain probiotic mixture in SOD1G93A mice Through reducing SOD1 aggregation and targeting the microbe-gut-brain axis

Acute high-fat diet impairs macrophage-supported intestinal damage resolution

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