Staphylococcal enterotoxin B suppresses Alix and compromises intestinal epithelial barrier functions

Yan, Hao; Yi, Haitao; Xia, Lixin; Zhan, Zhenke; He, Wenting; Yang, Ping‐Chang; Liu, Zhigang

doi:10.1186/1423-0127-21-29

Cited by 10 publications

(9 citation statements)

References 19 publications

(22 reference statements)

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“…However, Yan et al did not report changes in TEER. 32 We ascribe this discrepancy to differences in epithelial cell methodology. We have previously observed differences in TEER and cytokine release between cell lines and primary nasal epithelial cells stimulated with the same triggers.…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus enterotoxin B disrupts nasal epithelial barrier integrity

Martens

Seys

Alpízar

et al. 2020

Clin Experimental Allergy

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Background: Staphylococcus aureus colonization and release of enterotoxin B (SEB) has been associated with severe chronic rhinosinusitis with nasal polyps (CRSwNP). The pathogenic mechanism of SEB on epithelial barriers, however, is largely unexplored. Objective: We investigated the effect of SEB on nasal epithelial barrier function. Methods: SEB was apically administered to air-liquid interface (ALI) cultures of primary polyp and nasal epithelial cells of CRSwNP patients and healthy controls, respectively. Epithelial cell integrity and tight junction expression were evaluated. The involvement of Toll-like receptor 2 (TLR2) activation was studied in vitro with TLR2 monoclonal antibodies and in vivo in tlr2 −/− knockout mice. Results: SEB applied to ALI cultures of polyp epithelial cells decreased epithelial cell integrity by diminishing occludin and zonula occludens (ZO)-1 protein expression. Antagonizing TLR2 prevented SEB-induced barrier disruption. SEB applied in the nose of control mice increased mucosal permeability and decreased mRNA expression of occludin and ZO-1, whereas mucosal integrity and tight junction expression remained unaltered in tlr2 −/− mice. Furthermore, in vitro SEB stimulation resulted in epithelial production of IL-6 and IL-8, which was prevented by TLR2 antagonization. Conclusion & Clinical relevance: SEB damages nasal polyp epithelial cell integrity by triggering TLR2 in CRSwNP. Our results suggest that SEB might represent a driving factor of disease exacerbation, rather than a causal factor for epithelial defects in CRSwNP. Interfering with TLR2 triggering might provide a way to avoid the pathophysiological consequences of S. aureus on inflammation in CRSwNP.

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Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus enterotoxin B disrupts nasal epithelial barrier integrity

Martens

Seys

Alpízar

et al. 2020

Clin Experimental Allergy

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“…Adding to the complexity of Alix' functions, a proteomic study designed to investigate mechanisms of disease progression in a bacterial-induced model of colitis identified Alix as one of the most downregulated proteins in the infected intestinal epithelium 19 . Similarly, exposure of human intestinal epithelial cells to staphylococcal enterotoxin B resulted in reduced expression of Alix, which the authors suggest as the cause of epithelial barrier dysfunction 20 . In this respect, it is noteworthy that several human diseases affecting intestinal, pulmonary and renal epithelia, including cancer, have been associated with disruption of the epithelial barrier 21 .…”

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confidence: 95%

Alix-mediated assembly of the actomyosin–tight junction polarity complex preserves epithelial polarity and epithelial barrier

et al. 2016

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Maintenance of epithelial cell polarity and epithelial barrier relies on the spatial organization of the actin cytoskeleton and proper positioning/assembly of intercellular junctions. However, how these processes are regulated is poorly understood. Here we reveal a key role for the multifunctional protein Alix in both processes. In a knockout mouse model of Alix, we identified overt structural changes in the epithelium of the choroid plexus and in the ependyma, such as asymmetrical cell shape and size, misplacement and abnormal beating of cilia, blebbing of the microvilli. These defects culminate in excessive cell extrusion, enlargement of the lateral ventricles and hydrocephalus. Mechanistically, we find that by interacting with F-actin, the Par complex and ZO-1, Alix ensures the formation and maintenance of the apically restricted actomyosin–tight junction complex. We propose that in this capacity Alix plays a role in the establishment of apical–basal polarity and in the maintenance of the epithelial barrier.

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“…Amongst the gut-colonizing pathogens, emerging literature reports have elucidated the detrimental implications of colonization by Staphylococcus aureus (Acton et al, 2009;Yan et al, 2014). S. aureus is known to be equipped with adhesins known as microbial surface component-recognizing adhesive matrix molecules for binding to ECM molecules such as collagen (Foster et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Bacteriocin-producing strains of Lactobacillus plantarum inhibit adhesion of Staphylococcus aureus to extracellular matrix: quantitative insight and implications in antibacterial therapy

Mukherjee

Ramesh

2015

Journal of Medical Microbiology

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In the present study, the adhesion of bacteriocin-producing probiotic strains of Lactobacillus plantarum onto extracellular matrix (ECM) proteins such as collagen and mucin and their potential to prevent pathogen invasion onto the ECM was ascertained. Fluorescence-based in vitro assays indicated that L. plantarum strains CRA21, CRA38 and CRA52 displayed considerable adhesion to ECM molecules, which was comparable to the probiotic Lactobacillus rhamnosus GG. Flow cytometry-based quantitative assessment of the adhesion potential suggested that L. plantarum CRA21 exhibited superior adhesion onto the ECM as compared with other lactic acid bacteria strains. Furthermore, fluorescence-based assays suggested that the highest inhibition of Staphylococcus aureus adhesion onto collagen and mucin by bacteriocin-producing L. plantarum strains was observed in the exclusion mode as compared with the competition and displacement modes. This observation was supported by the higher binding affinity (k d ) for the ECM exhibited by the L. plantarum strains as compared with S. aureus. Interestingly, a crude plantaricin A extract from food isolates of L. plantarum displayed potent antibacterial activity on ECM-adhered S. aureus cells. It is envisaged that the L. plantarum isolates displaying bacteriocinogenic and ECM-adhering traits can perhaps be explored to develop safe antibacterial therapeutic agents.

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Staphylococcal enterotoxin B suppresses Alix and compromises intestinal epithelial barrier functions

Cited by 10 publications

References 19 publications

Staphylococcus aureus enterotoxin B disrupts nasal epithelial barrier integrity

Staphylococcus aureus enterotoxin B disrupts nasal epithelial barrier integrity

Alix-mediated assembly of the actomyosin–tight junction polarity complex preserves epithelial polarity and epithelial barrier

Bacteriocin-producing strains of Lactobacillus plantarum inhibit adhesion of Staphylococcus aureus to extracellular matrix: quantitative insight and implications in antibacterial therapy

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