Apical-basal polarity in the gut

Thottacherry, Joseph Jose; Chen, Jia; Johnston, Daniel St

doi:10.1016/j.semcdb.2022.12.007

Cited by 3 publications

(1 citation statement)

References 83 publications

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“…However, since the underlying data rely on cell line experiments, it remains poorly understood how the features and context of primary IECs affect the invasion process. Tumor-derived cell lines are fast-growing, exhibit a high degree of dynamics, and when grown flat on glass or plastic surfaces lack both the confluent polarized cell arrangement, and the densely microvilliated and heavily glycosylated apical surface structures characteristic of enterocytes and colonocytes (24,25). Notably, in recent comparative work, stark differences were indeed observed between how S.Tm invades cultured cell lines versus absorptive IECs in vivo in mice (10).…”

Section: Introductionmentioning

confidence: 99%

Maturation of Human Intestinal Epithelial Cell Layers Fortifies the Apical Surface againstSalmonellaAttack

van Rijn,

Lopes,

Ceylan

et al. 2024

Preprint

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The active invasion of intestinal epithelial cells (IECs) represents a key event in the infection cycle of many gut pathogens. Studies of howSalmonella entericaTyphimurium (S.Tm) bacteria enter transformed cell lines have shaped the paradigm for swift type-three-secretion-system-1 (TTSS-1)-driven IEC invasion, fueled by expansive membrane ruffles. However, comparative studies suggest that non-transformed IECs in the intact gut context comprise a much more challenging target for the attack. The molecular and cellular features that explain these discrepancies remain undefined. By live-cell imaging in human enteroid-and colonoid-derived IEC layers, we demonstrate that the maturation state of gut epithelia dramatically impacts permissiveness toS.Tm invasion. IEC layers kept under immature progenitor-cell-promoting conditions are permissive to the bacterial invasion, whereas maturation towards an enterocyte/colonocyte fate reduces the frequency ofS.Tm-induced epithelial entry structures, and lowers the invasion efficiency by up to tenfold. This phenotypic shift during IEC maturation couples to an altered expression of actin regulatory proteins implicated in the invasion process, and an increased dependence on theS.Tm TTSS-1 effector SipA for successful entry. In addition, IEC maturation involves upregulation of cell surface mucins, e.g. MUC13, and shifts in glycocalyx composition, as revealed by multiple lectin stainings. Enzymatic treatment of the apical surface with the StcE mucinase converts maturing IEC layers back to theS.Tm-invasion-permissive state of their immature counterparts. Taken together, these results showcase how the maturation state of human IECs dictates the susceptibility to invasion by a prototype enterobacterium.

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Section: Introductionmentioning

confidence: 99%

Maturation of Human Intestinal Epithelial Cell Layers Fortifies the Apical Surface againstSalmonellaAttack

van Rijn,

Lopes,

Ceylan

et al. 2024

Preprint

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Endocytosis in cancer and cancer therapy

et al. 2023

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Why put yourself on a pedestal? The pathogenic role of the A/E pedestal

Miner,

Rauch

2024

Infect Immun

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Certain Escherichia coli ( E. coli ) strains are attaching and effacing (A/E) lesion pathogens that primarily infect intestinal epithelial cells. They cause actin restructuring and polymerization within the host cell to create an actin-rich protrusion below the site of adherence, termed the pedestal. Although there is clarity on the pathways initiating pedestal formation, the underlying purpose(s) of the pedestal remains ambiguous. The conservation of pedestal-forming activity across multiple pathogens and redundancy in formation pathways indicate a pathogenic advantage. However, few decisive conclusions have been drawn, given that the results vary between model systems. Some research argues that the pedestal increases the colonization capability of the bacterium. These studies utilize A/E pathogens specifically deficient in pedestal formation to evaluate adhesion and intestinal colonization following infection. There have been many proposed mechanisms for the colonization benefit conferred by the pedestal. One suggested benefit is that the pedestal allows for direct cytosolic anchoring through incorporation of the established host cortical actin, causing a stable link between the pathogen and cell structure. The pedestal may confer enhanced motility, as enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) are better able to migrate on the surface of host cells and infect neighboring cells in the presence of the pedestal. Additionally, some research suggests that the pedestal improves effector delivery. This review will investigate the purpose of pedestal formation using evidence from recent literature and will critically evaluate the methodology and model systems. Most importantly, we will contextualize the proposed functions to reconcile potential synergistic effects.

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Apical-basal polarity in the gut

Cited by 3 publications

References 83 publications

Maturation of Human Intestinal Epithelial Cell Layers Fortifies the Apical Surface againstSalmonellaAttack

Maturation of Human Intestinal Epithelial Cell Layers Fortifies the Apical Surface againstSalmonellaAttack

Endocytosis in cancer and cancer therapy

Why put yourself on a pedestal? The pathogenic role of the A/E pedestal

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