Fecal Myeloperoxidase as a Biomarker for Inflammatory Bowel Disease

Hansberry, David R.; Shah, Kush C.; Agarwal, Prateek; Agarwal, Nitin

doi:10.7759/cureus.1004

Cited by 80 publications

(74 citation statements)

References 29 publications

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“…Neutrophils often exert pro-inflammatory functions at sites of inflammation ( 71 , 72 ), and a neutrophil-derived protein, myeloperoxidase, is widely used as a marker of colitis severity in IBD ( 73 – 75 ). Therefore, we investigated the cellular mechanisms contributing to elevated numbers of neutrophils in DSS-treated LysMCre;Arnt fl / fl mice.…”

Section: Resultsmentioning

confidence: 99%

Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis

et al. 2018

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Colonic tissues in Inflammatory Bowel Disease (IBD) patients exhibit oxygen deprivation and activation of hypoxia-inducible factor 1α and 2α (HIF-1α and HIF-2α), which mediate cellular adaptation to hypoxic stress. Notably, macrophages and neutrophils accumulate preferentially in hypoxic regions of the inflamed colon, suggesting that myeloid cell functions in colitis are HIF-dependent. By depleting ARNT (the obligate heterodimeric binding partner for both HIFα subunits) in a murine model, we demonstrate here that myeloid HIF signaling promotes the resolution of acute colitis. Specifically, myeloid pan-HIF deficiency exacerbates infiltration of pro-inflammatory neutrophils and Ly6C+ monocytic cells into diseased tissue. Myeloid HIF ablation also hinders macrophage functional conversion to a protective, pro-resolving phenotype, and elevates gut serum amyloid A levels during the resolution phase of colitis. Therefore, myeloid cell HIF signaling is required for efficient resolution of inflammatory damage in colitis, implicating serum amyloid A in this process.

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Section: Resultsmentioning

confidence: 99%

Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis

et al. 2018

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“…In our study, myeloperoxidase (MPO) whose activity is assessed during evaluation of intestinal ischemic injury, was shown to be an enzyme released due to neutrophil activation and is present during the production of free oxygen radicals [15,16]. Various studies have demonstrated that increase in MPO activity as a sign of neutrophil infiltration during mesenteric I/R injury causes endothelia dysfunction and inflammation [17,18].…”

Section: Discussionmentioning

confidence: 76%

The Protective Effect of Spironolactone and Role of the Na /K -ATPase Pump on Intestinal Ischemia/Reperfusion Injury

Akyüz¹,

Uzun²,

Sunamak³

et al. 2018

jrp

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The aim of this study was to evaluate the possible protective effect of spironolactone (SPL) and role of the Na-K ATPase pump on intestinal ischemia/reperfusion injury. In our study, the period of ischemia was established by clamping the mesenteric artery for 45 minunder anesthesia in Wistar albino rats and the animals left for reperfusion at the end of this period were decapitated after one hour. Spironolactone (20 mg kg-1) was administered orally for three days before ischemia, 30 minbefore ischemia. The control group rats were subjected to the Sham operation and administered saline solution. TNF-α and IL-1β levels were measured in the serum samples. Ileal Na+/K+-ATPase, myeloperoxidase (MPO) analysis were performed. Structural injury was assessed histopathologically. Ischemia/reperfusion increased serum TNF-α and IL-1β levels together with MPO activity, whereas these values were maintained at the control group levels through SPL activation. However, ischemia/reperfusion decreased Na+/K+-ATPase activity in ileal tissues; however, these parameters were found to be significantly increased with SPL activation. The protective effect of SPL against ischemia/reperfusion injury by different mechanisms, mainly the activity of the Na+/K+-ATPase pump, suggests that this nontoxic agent may constitute a new clinical therapeutic principle.

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“…S1H, S1I, S1J, and S1K). MPO production is often increased in the colon of IBDs patients [24]. Similarly, DSS drastically elevated the MPO concentration in the colon of mice, but such an elevation was signi cantly dampened by oral EGCG (Fig.…”

Section: Oral But Not Rectal Administration Of Egcg Alleviates Dss-mentioning

confidence: 82%

Oral, but not rectal delivery of epigallocatechin-3-gallate alleviates colitis by regulating the gut microbiota, oxidative stress, inflammation, and barrier integrity

Huang

et al. 2020

Preprint

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Background: Alteration of the gut microbiota may contribute to the development of inflammatory bowel diseases (IBDs). Epigallocatechin-3-gallate (EGCG), a major bioactive constituent of green tea, is known to be beneficial in IBDs alleviation. However, it is unclear whether EGCG attenuates IBDs through direct improvement of gastrointestinal function or indirect alteration of the structure and function of the gut microbiota.Results: We first investigated the therapeutic effects of EGCG on disease severity, oxidative stress, inflammation, barrier function, and gut microbiota in murine colitis model, and further demonstrate it via EGCG pre-supplementation. We revealed that, oral, but not rectal, delivery of EGCG alleviated the severity of colitis through attenuation of anti-oxidative and anti-inflammatory response. Mucin-secreting goblet cell number, barrier function gene expression levels, and the integrity of tight junctions in the colon were also enhanced by oral EGCG. Additionally, we observed distinct EGCG-mediated alternation in the gut microbiome, as highlighted by increased Akkermansia abundance and butyrate production. Furthermore, we revealed that prophylactic oral application of EGCG for 21 days prior to the onset of dextran sodium sulfate (DSS)-induced colitis also ameliorated colonic damage, oxidative stress, and inflammatory response. Prophylactic EGCG significantly enriched Akkermansia, Faecalibaculum, and Bifidobacterium and enhanced acetate, propionate and butyrate production in DSS-treated mice. Moreover, scores of differential microbes, in particular Akkermansia, showed a strong positive correlation with short-chain fatty acids (SCFAs) and antioxidant enzyme levels in both the plasma and colon, but a negative association with inflammatory cytokines and malondialdehyde.Conclusions: EGCG is capable of treating DSS-induced colitis both therapeutically and prophylactically by inducing a pronounced anti-oxidative and anti-inflammatory response. Attenuation of colitis by oral, but not rectal administration of, EGCG suggests an intimate involvement of the gut microbiota. Increased Akkermansia and subsequent protective SCFAs production may be largely responsible for the anti-inflammatory and anti-oxidative function of EGCG, leading to restoration of intestinal epithelial homeostasis of the host. These findings provide novel insights into EGCG-mediated remission of IBDs and the rationale for devising more effective therapeutic strategies for IBDs.

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Fecal Myeloperoxidase as a Biomarker for Inflammatory Bowel Disease

Cited by 80 publications

References 29 publications

Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis

Myeloid Cell Hypoxia-Inducible Factors Promote Resolution of Inflammation in Experimental Colitis

The Protective Effect of Spironolactone and Role of the Na /K -ATPase Pump on Intestinal Ischemia/Reperfusion Injury

Oral, but not rectal delivery of epigallocatechin-3-gallate alleviates colitis by regulating the gut microbiota, oxidative stress, inflammation, and barrier integrity

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