How bacterial pathogens of the gastrointestinal tract use the mucosal glyco-code to harness mucus and microbiota: New ways to study an ancient bag of tricks

Josenhans, Christine; Müthing, Johannes; Elling, Lothar; Bartfeld, Sina; Schmidt, Herbert

doi:10.1016/j.ijmm.2020.151392

Cited by 32 publications

(24 citation statements)

References 286 publications

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“…In the small intestine and colon, MUC2 is highly expressed and stimulates β‐defensin that has antimicrobial effects, while the colon also produces low levels of MUC5B 34,35 . Although the small intestine is covered by a single, loosely attached mucus layer, colonic mucus is much thicker due to the greater microbial density and is comprised of two layers: an outer (luminal) viscous mucous layer and an inner stratified layer of colonic mucus that adheres firmly to the underlying columnar epithelia (glycocalyx) 36 . Transmembrane mucins MUC3, MUC4, MUC12, MUC13 and MUC17 are constitutively expressed along the gastrointestinal tract (GIT) and occur in the glycocalyx.…”

Section: Gastrointestinal Tract Mucosamentioning

confidence: 99%

“…These changes contribute to chronic inflammation and the development and progression of disease layers: an outer (luminal) viscous mucous layer and an inner stratified layer of colonic mucus that adheres firmly to the underlying columnar epithelia (glycocalyx). 36 Transmembrane mucins MUC3, MUC4, MUC12, MUC13 and MUC17 are constitutively expressed along the gastrointestinal tract (GIT) and occur in the glycocalyx.…”

Section: G a S Trointe S Tinal Tr Ac T Mucosamentioning

confidence: 99%

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Impact of diet and the bacterial microbiome on the mucous barrier and immune disorders

Alemao

Budden

Gomez

et al. 2020

Allergy

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The prevalence of chronic immune and metabolic disorders is increasing rapidly. In particular, inflammatory bowel diseases, obesity, diabetes, asthma and chronic obstructive pulmonary disease have become major healthcare and economic burdens worldwide. Recent advances in microbiome research have led to significant discoveries of associative links between alterations in the microbiome and health, as well as these chronic supposedly noncommunicable, immune/metabolic disorders. Importantly, the interplay between diet, microbiome and the mucous barrier in these diseases has gained significant attention. Diet modulates the mucous barrier via alterations in gut microbiota, resulting in either disease onset/exacerbation due to a “poor” diet or protection against disease with a “healthy” diet. In addition, many mucosa‐associated disorders possess a specific gut microbiome fingerprint associated with the composition of the mucous barrier, which is further influenced by host‐microbiome and inter‐microbial interactions, dietary choices, microbe immigration and antimicrobials. Our review focuses on the interactions of diet (macronutrients and micronutrients), gut microbiota and mucous barriers (gastrointestinal and respiratory tract) and their importance in the onset and/or progression of major immune/metabolic disorders. We also highlight the key mechanisms that could be targeted therapeutically to prevent and/or treat these disorders.

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Section: Gastrointestinal Tract Mucosamentioning

confidence: 99%

Section: G a S Trointe S Tinal Tr Ac T Mucosamentioning

confidence: 99%

Impact of diet and the bacterial microbiome on the mucous barrier and immune disorders

Alemao

Budden

Gomez

et al. 2020

Allergy

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“…EHEC O157 outbreaks are mostly linked to the consumption of contaminated bovine-derived products, including animal contact in petting zoos with lower incidence, as sources of STEC infections [ 211 , 213 , 216 , 217 , 218 , 219 ]. After ingestion, EHEC selectively colonize the mucosa of the human large intestine with the “attaching and effacing” mechanism, genetically governed by a large pathogenicity island defined as the Locus of Enterocyte Effacement (LEE) [ 211 , 220 , 221 , 222 , 223 , 224 , 225 ]. Besides severe diarrhea and hemorrhagic colitis, EHEC raise life-threatening extraintestinal complications such HUS with frequent long-term and grave sequelae.…”

Section: Ehec-caused Diseases and Damage Of Human Target Cellsmentioning

confidence: 99%

Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome

Detzner

Pohlentz

Müthing

2020

Toxins

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The global emergence of clinical diseases caused by enterohemorrhagic Escherichia coli (EHEC) is an issue of great concern. EHEC release Shiga toxins (Stxs) as their key virulence factors, and investigations on the cell-damaging mechanisms toward target cells are inevitable for the development of novel mitigation strategies. Stx-mediated hemolytic uremic syndrome (HUS), characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal injury, is the most severe outcome of an EHEC infection. Hemolytic anemia during HUS is defined as the loss of erythrocytes by mechanical disruption when passing through narrowed microvessels. The formation of thrombi in the microvasculature is considered an indirect effect of Stx-mediated injury mainly of the renal microvascular endothelial cells, resulting in obstructions of vessels. In this review, we summarize and discuss recent data providing evidence that HUS-associated hemolytic anemia may arise not only from intravascular rupture of erythrocytes, but also from the extravascular impairment of erythropoiesis, the development of red blood cells in the bone marrow, via direct Stx-mediated damage of maturing erythrocytes, leading to “non-hemolytic” anemia.

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“…Mucinases and other proteases play a role in that process. Cleavage of O -acteyl residues from terminal O -glycans (e.g., Neu5,9Ac 2 ) by chromosomal and phage-encoded O -acetyl esterases results in deacetylated free sialic acids such as N -acetyl neuraminic acid, which can be metabolized by the bacteria [ 113 ]. The chemical structure of Neu5,9Ac 2 is shown.…”

Section: Figurementioning

confidence: 99%

Bacteriophages of Shiga Toxin-Producing Escherichia coli and Their Contribution to Pathogenicity

et al. 2021

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Shiga toxins (Stx) of Shiga toxin-producing Escherichia coli (STEC) are generally encoded in the genome of lambdoid bacteriophages, which spend the most time of their life cycle integrated as prophages in specific sites of the bacterial chromosome. Upon spontaneous induction or induction by chemical or physical stimuli, the stx genes are co-transcribed together with the late phase genes of the prophages. After being assembled in the cytoplasm, and after host cell lysis, mature bacteriophage particles are released into the environment, together with Stx. As members of the group of lambdoid phages, Stx phages share many genetic features with the archetypical temperate phage Lambda, but are heterogeneous in their DNA sequences due to frequent recombination events. In addition to Stx phages, the genome of pathogenic STEC bacteria may contain numerous prophages, which are either cryptic or functional. These prophages may carry foreign genes, some of them related to virulence, besides those necessary for the phage life cycle. Since the production of one or more Stx is considered the major pathogenicity factor of STEC, we aim to highlight the new insights on the contribution of Stx phages and other STEC phages to pathogenicity.

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How bacterial pathogens of the gastrointestinal tract use the mucosal glyco-code to harness mucus and microbiota: New ways to study an ancient bag of tricks

Cited by 32 publications

References 286 publications

Impact of diet and the bacterial microbiome on the mucous barrier and immune disorders

Impact of diet and the bacterial microbiome on the mucous barrier and immune disorders

Valid Presumption of Shiga Toxin-Mediated Damage of Developing Erythrocytes in EHEC-Associated Hemolytic Uremic Syndrome

Bacteriophages of Shiga Toxin-Producing Escherichia coli and Their Contribution to Pathogenicity

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