Impenetrable barriers or entry portals? The role of cell–cell adhesion during infection

Bonazzi, Matteo; Cossart, Pascale

doi:10.1083/jcb.201106011

Cited by 69 publications

(49 citation statements)

References 102 publications

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“…Indeed, a number of pathogens target cadherins in order to establish colonization of cells and tissues (Bonazzi and Cossart, 2011). Recognition of specific cadherins by bacteria often mediates either attachment of the microorganisms to the cell surface and/or internalization into the cell.…”

Section: Cadherins Targeted In Human Diseasementioning

confidence: 99%

Classical and desmosomal cadherins at a glance

Saito

Tucker

Kohlhorst

et al. 2012

Journal of Cell Science

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Section: Cadherins Targeted In Human Diseasementioning

confidence: 99%

Classical and desmosomal cadherins at a glance

Saito

Tucker

Kohlhorst

et al. 2012

Journal of Cell Science

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“…A number of intracellular pathogens interact with cell adhesion receptors for their uptake and subvert small GTPase signalling to enable invasion (Bonazzi and Cossart, 2011). Among them is Listeria monocytogenes, which binds directly to the extracellular domain of E-cadherin and triggers substantial modifications of actin filaments at junctions and in the cytoplasm to enable its engulfment and intracellular movements, respectively (Bonazzi and Cossart, 2011).…”

Section: Side Viewmentioning

confidence: 99%

Cycling around cell–cell adhesion with Rho GTPase regulators

McCormack

Welsh

Braga

2013

Journal of Cell Science

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SummaryThe formation and stability of epithelial adhesive systems, such as adherens junctions, desmosomes and tight junctions, rely on a number of cellular processes that ensure a dynamic interaction with the cortical cytoskeleton, and appropriate delivery and turnover of receptors at the surface. Unique signalling pathways must be coordinated to allow the coexistence of distinct adhesive systems at discrete subdomains along junctions and the specific properties they confer to epithelial cells. Rho, Rac and Cdc42 are members of the Rho small GTPase family, and are well-known regulators of cell-cell adhesion. The spatio-temporal control of small GTPase activation drives specific intracellular processes to enable the hierarchical assembly, morphology and maturation of cell-cell contacts. Here, we discuss the small GTPase regulators that control the precise amplitude and duration of the levels of active Rho at cell-cell contacts, and the mechanisms that tailor the output of Rho signalling to a particular cellular event. Interestingly, the functional interaction is reciprocal; Rho regulators drive the maturation of cell-cell contacts, whereas junctions can also modulate the localisation and activity of Rho regulators to operate in diverse processes in the epithelial differentiation programme.

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“…Epithelial cells form a tight barrier by means of expression of the junctional complex and mediate inflammatory responses by secreting eicosanoids, nucleotides, cytokines, and chemokines (1). Alterations in the integrity of the host epithelium during infection may cause life-threatening conditions.…”

mentioning

confidence: 99%

“…The homeostasis of the epithelium is severely challenged upon infection, a process that might affect the junctional complex (1). The junctional complex consists of anchoring junctions (desmosomes and adherens junctions), occluding junctions (tight junctions), and communicating junctions (gap junctions).…”

mentioning

confidence: 99%

Pseudomonas aeruginosa–Induced Apoptosis in Airway Epithelial Cells Is Mediated by Gap Junctional Communication in a JNK-Dependent Manner

Losa

Köhler

Bellec

et al. 2014

The Journal of Immunology

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Chronic infection and inflammation of the airways is a hallmark of cystic fibrosis (CF), a disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. The response of the CF airway epithelium to the opportunistic pathogen Pseudomonas aeruginosa is characterized by altered inflammation and apoptosis. In this study, we examined innate immune recognition and epithelial responses at the level of the gap junction protein connexin43 (Cx43) in polarized human airway epithelial cells upon infection by PAO1. We report that PAO1 activates cell surface receptors to elicit an intracellular signaling cascade leading to enhancement of gap junctional communication. Expression of Cx43 involved an opposite regulation exerted by JNK and p38 MAPKs. PAO1-induced apoptosis was increased in the presence of a JNK inhibitor, but latter effect was prevented by lentiviral expression of a Cx43-specific short hairpin RNA. Moreover, we found that JNK activity was upregulated by pharmacological inhibition of CFTR in Calu-3 cells, whereas correction of a CF airway cell line (CF15 cells) by adenoviral expression of CFTR reduced the activation of this MAPK. Interestingly, CFTR inhibition in Calu-3 cells was associated with decreased Cx43 expression and reduced apoptosis. These results indicate that Cx43 expression is a component of the response of airway epithelial cells to innate immune activation by regulating the survival/apoptosis balance. Defective CFTR could alter this equilibrium with deleterious consequences on the CF epithelial response to P. aeruginosa

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Impenetrable barriers or entry portals? The role of cell–cell adhesion during infection

Cited by 69 publications

References 102 publications

Classical and desmosomal cadherins at a glance

Classical and desmosomal cadherins at a glance

Cycling around cell–cell adhesion with Rho GTPase regulators

Pseudomonas aeruginosa–Induced Apoptosis in Airway Epithelial Cells Is Mediated by Gap Junctional Communication in a JNK-Dependent Manner

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