Does Helicobacter pylori affect gastric mucin expression? Relationship between gastric antral mucin expression and H. pylori colonization

Morgenstern, Sara; Koren, Rivka; Moss, Steven F.; Fraser, Gerald; Okon, E; Niv, Yaron

doi:10.1097/00042737-200101000-00004

Cited by 35 publications

(19 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…H. pylori uses its flagella for motility within the mucus layer in the acid-secreting stomach (296). In addition, H. pylori reduces mucin exocytosis (264), decreases gastric mucin synthesis by inhibiting UDP-galactosyltransferase (374), and causes an aberrant expression of the gastric mucins MUC1, MUC5AC, and MUC6 (52,276). It is interesting that mucins play also a role in Pseudomonas aeruginosa pathogenesis since an upregulated transcription of the MUC2 (216) and MUC5AC (90) mucin genes follows infection.…”

Section: Barrier Effect Against Pathogensmentioning

confidence: 99%

The Front Line of Enteric Host Defense against Unwelcome Intrusion of Harmful Microorganisms: Mucins, Antimicrobial Peptides, and Microbiota

2006

View full text Add to dashboard Cite

SUMMARY The intestinal tract is a complex ecosystem that combines resident microbiota and the cells of various phenotypes with complex metabolic activities that line the epithelial wall. The intestinal cells that make up the epithelium provide physical and chemical barriers that protect the host against the unwanted intrusion of microorganisms that hijack the cellular molecules and signaling pathways of the host and become pathogenic. Some of the organisms making up the intestinal microbiota also have microbicidal effects that contribute to the barrier against enteric pathogens. This review describes the two cell lineages present in the intestinal epithelium: the goblet cells and the Paneth cells, both of which play a pivotal role in the first line of enteric defense by producing mucus and antimicrobial peptides, respectively. We also analyze recent insights into the intestinal microbiota and the mechanisms by which some resident species act as a barrier to enteric pathogens. Moreover, this review examines whether the cells producing mucins or antimicrobial peptides and the resident microbiota act in partnership and whether they function individually and/or synergistically to provide the host with an effective front line of defense against harmful enteric pathogens.

show abstract

Section: Barrier Effect Against Pathogensmentioning

confidence: 99%

The Front Line of Enteric Host Defense against Unwelcome Intrusion of Harmful Microorganisms: Mucins, Antimicrobial Peptides, and Microbiota

2006

View full text Add to dashboard Cite

show abstract

“…It is interesting to note that several gastrointestinal pathogens have developed sophisticated strategies, including specific pathogenic factors, to escape this host defense mechanism. The prototype of these pathogens is Helicobacter pylori, which uses its flagella for growth and motility within the mucus layer (61), reduces gastric mucin synthesis (72) and mucin exocytosis (55), and causes the aberrant production of the gastric mucins MUC1, MUC5AC, and MUC6 (3,58). It has been demonstrated that one aEPEC strain expressing the intimin subtype omicron was more invasive than tEPEC in undifferentiated, nonintestinal HeLa and Hep-2 cells (30).…”

Section: Vol 78 2010 Atypical Epec Benefits From Mucin Elicitation 933mentioning

confidence: 99%

Two Atypical Enteropathogenic Escherichia coli Strains Induce the Production of Secreted and Membrane-Bound Mucins To Benefit Their Own Growth at the Apical Surface of Human Mucin-Secreting Intestinal HT29-MTX Cells

et al. 2010

View full text Add to dashboard Cite

In rabbit ligated ileal loops, two atypical enteropathogenic Escherichia coli (aEPEC) strains, 3991-1 and 0421-1, intimately associated with the cell membrane, forming the characteristic EPEC attachment and effacement lesion of the brush border, induced a mucous hypersecretion, whereas typical EPEC (tEPEC) strain E2348/69 did not. Using cultured human mucin-secreting intestinal HT29-MTX cells, we demonstrate that apically aEPEC infection is followed by increased production of secreted MUC2 and MUC5AC mucins and membrane-bound MUC3 and MUC4 mucins. The transcription of the MUC5AC and MUC4 genes was transiently upregulated after aEPEC infection. We provide evidence that the apically adhering aEPEC cells exploit the mucins' increased production since they grew in the presence of membrane-bound mucins, whereas tEPEC did not. The data described herein report a putative new virulence phenomenon in aEPEC.The intestinal mucus offers numerous ecological advantages to bacteria present in the lumen and intestinal epithelium, providing a source of energy by producing the saccharides used for sustained growth by both the indigenous enteric microbiota and pathogens (26). Moreover by producing mucus, goblet cells contribute to the physical and chemical barriers that protect the host against the unwanted intrusion of enterovirulent microorganisms (48). Currently, 17 human mucin-type glycoproteins have been assigned to the MUC gene family, MUC1 and -2, MUC3A, MUC3B, MUC4, MUC5B, MUC5AC,, with the approval of the Human Genome Organization Gene Nomenclature Committee (HUGO/GNC; http://www.hugo-international.org/hugo/) (8, 9, 57). A cluster of four mucin genes (MUC2, MUC5B, MUC5AC, and MUC6) code for secreted mucins. Eight genes (MUC1, MUC3A, MUC3B, MUC4, MUC12, MUC13, MUC16, and MUC17) that code for membrane-associated mucins have been characterized. In mucin-secreting intestinal cells, the secreted mucins are packaged and stored into large intracellular vesicles (17, 39).Pathogenic Escherichia coli causes intestinal and extraintestinal diseases (35). There are six well-defined categories of intestinal pathogenic E. coli, each characterized by specific virulence factors that affect a wide range of cellular processes via signaling events. Enteropathogenic E. coli (EPEC), the first pathotype of E. coli to be described, produces characteristic cellular lesions known as "attaching and effacing" (A/E) lesions in the intestinal mucosa after the bacteria have intimately attached to the enterocyte brush border membrane and caused cytoskeletal changes that lead to effacement of the microvilli. The EPEC group is subdivided into typical (tEPEC) and atypical (aEPEC) forms. The aEPEC group consists of a large number of O serogroups (29, 74). These strains have been shown to carry the locus of the enterocyte effacement (LEE) pathogenicity island (PAI), but to lack the EAF (EPEC adherence factor) plasmid that encodes the bundle-forming pilus (BFP) and the Shiga toxin genes (35). LEE encodes the components of a type 3 secretion system (T3SS), an ...

show abstract

“…When the synthesis of these factors is diminished, gastric mucosa becomes more susceptible to injury [31,32]. H pylori infection may reduce the superficial mucin layer overlying gastric mucosa and thereby impair mucosal defenses [33][34][35].…”

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

Pathogenesis and therapy of gastric and duodenal ulcer disease

Shiotani

Graham

2002

Medical Clinics of North America

View full text Add to dashboard Cite

Does Helicobacter pylori affect gastric mucin expression? Relationship between gastric antral mucin expression and H. pylori colonization

Abstract: The change in MUC 5 synthesis may reflect H. pylori colonization.

Cited by 35 publications

References 13 publications

The Front Line of Enteric Host Defense against Unwelcome Intrusion of Harmful Microorganisms: Mucins, Antimicrobial Peptides, and Microbiota

The Front Line of Enteric Host Defense against Unwelcome Intrusion of Harmful Microorganisms: Mucins, Antimicrobial Peptides, and Microbiota

Two Atypical Enteropathogenic Escherichia coli Strains Induce the Production of Secreted and Membrane-Bound Mucins To Benefit Their Own Growth at the Apical Surface of Human Mucin-Secreting Intestinal HT29-MTX Cells

Pathogenesis and therapy of gastric and duodenal ulcer disease

Contact Info

Product

Resources

About