Dataset Information

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients.

ABSTRACT:

Introduction

The involvement of mucin, lectin, and apoptosis in colitis is still unclear. This study aimed to investigate changes in MUC2 expression, inflammation, and changes in lectin expression in colitis patients.

Methods

A total of 17 patients were divided into two groups including 11 hemorrhoid patients as a control group and 6 colitis patients. MUC2 mutation analysis was carried out using immunofluorescent and FISH techniques. Assessment of caspase-3, Ki-67, NF-kB, and lectin expressions was also carried out by immunofluorescent technique then analyzed by confocal laser scanning microscope.

Results

The MUC2, caspase-3, and lectin expressions were significantly lower in the colitis group than in the control group (p?ConclusionsIt was concluded that in colitis there was a change in MUC2 expression due to changes in lectins accompanied by apoptotic defects.conclusion.

SUBMITTER: Wibowo AA

PROVIDER: S-EPMC6556545 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Publications

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients.

Wibowo Agung A AA Pardjianto Bambang B Sumitro Sutiman B SB Kania Nia N Handono Kusworini K

Biochemistry and biophysics reports 20190605

<h4>Introduction</h4>The involvement of mucin, lectin, and apoptosis in colitis is still unclear. This study aimed to investigate changes in MUC2 expression, inflammation, and changes in lectin expression in colitis patients.<h4>Methods</h4>A total of 17 patients were divided into two groups including 11 hemorrhoid patients as a control group and 6 colitis patients. MUC2 mutation analysis was carried out using immunofluorescent and FISH techniques. Assessment of caspase-3, Ki-67, NF-kB, and lect ...[more]

PMID: 31198858

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Project description:BackgroundInflammatory bowel disease (IBD), including Crohn disease (CD) and ulcerative colitis (UC), is a multifactorial disorder characterized by chronic inflammation and altered gut barrier function. Dysbiosis, a condition defined by dysregulation of the gut microbiome, has been reported in patients with IBD and in experimental models of colitis. Although several factors have been implicated in directly affecting gut microbial composition, the genetic determinants impacting intestinal dysbiosis in IBD remain relatively unknown.MethodsWe compared the microbiome of normal, uninflamed wild-type (WT) mice with that of a murine model of UC (ie, Winnie strain). Winnie mice possess a missense mutation in Muc2 that manifests in altered mucus production as early as 4 weeks of age, with ensuing colonic inflammation. To better address the potential role of mutant Muc2 in promoting dysbiosis in Winnie mice, we evaluated homozygous mutant mice (Winnie-/-) with their WT littermates that, after weaning from common mothers, were caged separately according to genotype. Histologic and inflammatory status were assessed over time, along with changes in their respective microbiome compositions.ResultsDysbiosis in Winnie mice was already established at 4 weeks of age, before histologic evidence of gut inflammatory changes, in which microbial communities diverged from that derived from their mothers. Furthermore, dysbiosis persisted until 12 weeks of age, with peak differences in microbiome composition observed between Winnie and WT mice at 8 weeks of age. The relative abundance of Bacteroidetes was greater in Winnie compared with WT mice. Verrucomicrobia was detected at the highest relative levels in 4-week-old Winnie mice; in particular, Akkermansia muciniphila was among the most abundant species found at 4 weeks of age.ConclusionsOur results demonstrate that mutant genetic determinants involved in the complex regulation of intestinal homeostasis, such as that observed in Winnie mice, are able to promote early gut dysbiosis that is independent from maternal microbial transfer, including breastfeeding. Our data provide evidence for intestinal dysbiosis attributed to a Muc2-driven mucus defect that leads to colonic inflammation and may represent an important target for the design of future interventional studies.

Dataset Information

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients.

Introduction

Methods

Results

Publications

Decreased expression of MUC2 due to a decrease in the expression of lectins and apoptotic defects in colitis patients.

Similar Datasets

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