Epithelial Intermediate Filaments: Guardians against Microbial Infection?

Geisler, Florian; Leube, Rudolf E.

doi:10.3390/cells5030029

Cited by 40 publications

(33 citation statements)

References 162 publications

(205 reference statements)

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“…, 2011). Taken together, these findings indicate it is likely that the highly conserved distribution pattern is advantageous to intestinal cells and suggests that it strengthens the mucosal barrier function (Geisler and Leube, 2016). …”

Section: Introductionmentioning

confidence: 78%

A novel function for the MAP kinase SMA-5 in intestinal tube stability

Geisler

Gerhardus

Carberry

et al. 2016

MBoC

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Section: Introductionmentioning

confidence: 78%

A novel function for the MAP kinase SMA-5 in intestinal tube stability

Geisler

Gerhardus

Carberry

et al. 2016

MBoC

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“…Comparatively little is known about IF network dynamics and microbial infections (Geisler and Leube 2016). A fascinating situation, however, is encountered during infection with enteropathogenic Escherichia coli.…”

Section: Stress Induces Alterations In If Motilitymentioning

confidence: 99%

Intracellular Motility of Intermediate Filaments

Leube

Moch

Windoffer

2017

Cold Spring Harb Perspect Biol

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SUMMARYThe establishment and continuous cell type-specific adaptation of cytoplasmic intermediate filament (IF) networks are linked to various types of IF motility. Motor protein-driven active transport, linkage to other cellular structures, diffusion of small soluble subunits, and intrinsic network elasticity all contribute to the motile behavior of IFs. These processes are subject to regulation by multiple signaling pathways. IF motility is thereby connected to and involved in many basic cellular processes guarding the maintenance of cell and tissue integrity. Disturbances of IF motility are linked to diseases that are characterized by cytoplasmic aggregates containing IF proteins together with other cellular components.

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“…β-catenin plays a key role in cell-cell adhesion and stabilizing cell-cell contacts, whilst the β-catenin/E-cadherin complex regulates the integrity of the AJs (Tian et al, 2011;Nelson et al, 2004;Van den Bossche et al, 2012). EIF, which is together with actin one of the major cytoskeletal components of epithelial cells, mediates barrier functions in epithelial cells and protects together with other cytoskeletal proteins against microbial invasions (Geisler and Leube, 2016).…”

Section: Introductionmentioning

confidence: 99%

Breakdown of the Paracellular Tight and Adherens Junctions in the Gut and Blood Brain Barrier and Damage to the Vascular Barrier in Patients with Deficit Schizophrenia<strong></strong>

Maes¹,

Sirivichayakul²,

Kanchanatawan³

et al. 2019

Preprint

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Deficit schizophrenia is characterized by leaky tight and adherens junctions and bacterial translocation. Here we examine whether (deficit) schizophrenia is accompanied by leaky paracellular, transcellular and vascular barriers in the gut and blood brain barriers. We measured IgA responses to occludin, claudin-5, E-cadherin and β-catenin (paracellular pathway, PARA), talin, actin, vinculin and epithelial intermediate filament (transcellular pathway, TRANS) and plasmalemma vesicle-associated protein (PLVAP, vascular pathway) in 78 schizophrenia patients and 40 controls. IgA responses to claudin-5, E-cadherin and β-catenin, the sum of the four PARA proteins and the ratio PARA/TRANS were significantly higher in deficit schizophrenia than in non-deficit schizophrenia and controls. A large part of the variance in PHEMN (psychosis, hostility, excitation, mannerism and negative) symptoms, psychomotor retardation, formal thought disorders, verbal fluency, word list memory, word list recall and executive functions was explained by the PARA/TRANS ratio coupled with plasma IgA responses to Gram-negative bacteria, IgM to malondialdehyde, CCL-11 (eotaxin), IgA levels of the ratio of noxious to more protective tryptophan catabolites (NOX/PRO TRYCATs) and a plasma immune activation index. Moreover, IgA levels to Gram-negative bacteria were significantly associated with IgA to E-cadherin, β-catenin and PLVAP, while IgA levels to claudin-5 were significantly predicted by IgA to E-cadherin, NOX/PRO TRYCAT ratio, Gram-negative bacteria and CCL11. The phenomenology of the deficit syndrome is to a large extent explained by the cumulative effects of lowered natural IgM, breakdown of the paracellular and vascular pathways, increased bacterial translocation, peripheral immune-inflammatory responses and indices of BBB breakdown.

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Epithelial Intermediate Filaments: Guardians against Microbial Infection?

Cited by 40 publications

References 162 publications

A novel function for the MAP kinase SMA-5 in intestinal tube stability

A novel function for the MAP kinase SMA-5 in intestinal tube stability

Intracellular Motility of Intermediate Filaments

Breakdown of the Paracellular Tight and Adherens Junctions in the Gut and Blood Brain Barrier and Damage to the Vascular Barrier in Patients with Deficit Schizophrenia<strong></strong>

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