Quantitative structural and biochemical analyses of tight junction dynamics following exposure of epithelial cells to house dust mite allergen Der p 1

Wan, Hong; Winton, Helen L; Soeller, Christian; Gruenert, Dieter C.; Thompson, Philip J.; Cannell, Mark B.; Stewart, Geoffrey A.; Garrod, David R.; Robinson, Clive

doi:10.1046/j.1365-2222.2000.00820.x

Cited by 166 publications

(144 citation statements)

References 36 publications

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“…These events have been poorly studied to date and they may be of great importance in the development of the allergic inflammation and our understanding of asthma pathology. It is currently believed that when HDM allergens interact with the bronchial epithelium, they induce direct damage through protease activity, disrupting the epithelial tight junctions and thereby increasing the bronchial epithelium permeability and facilitating trans-epithelial allergen delivery and interaction with antigen presenting cells [5][6][7]. We have demonstrated that HDM allergens can interact with the lung, particularly the airway epithelium, and induce asthma-like inflammation, i.e.…”

Section: Discussionmentioning

confidence: 89%

“…Der p 1 belongs to the papain-like cysteine protease family and exhibits cysteine protease activity [4]. This proteolytic activity has been suggested to be involved in the pathogenesis of allergies by: increasing the permeability of epithelial cells and allowing the passage of their own and other allergens across the epithelium [5][6][7]; cleaving and/or interacting with cell surface molecules and intrinsic protease inhibitors [8][9][10][11]; and modulating the function of a range of cells, such as basophils, mast cells, alveolar macrophages and airway epithelial cells [12][13][14][15]. The effect on the airway epithelium is especially interesting, as it is likely to be the first cell type to interact with the allergen.…”

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confidence: 99%

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House dust mite induces direct airway inflammation in vivo: implications for future disease therapy?

Alba

Raemdonck²,

Dekkak³

et al. 2009

European Respiratory Journal

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House dust mite (HDM) is the major source of allergen in house dust and is strongly associated with the development of asthma. HDM can evoke a direct, nonallergic inflammatory reaction in vitro. We aimed to determine whether this apparent nonallergic, inflammatory response can be observed in a more complex in vivo setting.Vehicle, Alum TM or HDM (Dermatophagoides pteronyssinus 5 mg, i.p. with Alum) sensitisedBrown-Norway rats were challenged intratracheally with vehicle (saline), HDM (Der p 10 mg) or heat-inactivated HDM on day 21. Lung function changes and the associated inflammatory response were evaluated. Tissue and bronchoalveolar lavage from Alum TM sensitised Der p challenged animals exhibited strong eosinophilia and neutrophilia associated with an early release of pro-inflammatory cytokines (interleukin-13 and 1b, eotaxin and thymus and activation-regulated chemokine). This response was not attenuated by removal of HDM-associated protease activity. Interestingly, the vehicle sensitised group (no Alum TM ) lacked this inflammatory response.HDM allergen evokes nonallergic airways inflammation with an inflammatory profile similar to that of the asthmatic airway. This response, independent of the protease activity of the HDM extract, appeared to be linked to prior administration of the adjuvant Alum TM and the subsequent increase in total immunoglobulin E. This finding could have important implications in the development of future asthma therapies.

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Section: Discussionmentioning

confidence: 89%

mentioning

confidence: 99%

House dust mite induces direct airway inflammation in vivo: implications for future disease therapy?

Alba

Raemdonck²,

Dekkak³

et al. 2009

European Respiratory Journal

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“…Alternatively, neutrophil recruitment to the airways could be mediated directly by HDM allergen. HDMs produce enzymes called proteases that cleave peptide bonds of tight junction in the epithelial cell layer (57)(58)(59), and this action occurs by the binding of proteases to protease activator receptors that are found on airway epithelial cells (60). The binding of proteases causes the production and secretion of IL-6 and -8 (61).…”

Section: Discussionmentioning

confidence: 99%

Fms-Like Tyrosine Kinase 3 Ligand Decreases T Helper Type 17 Cells and Suppressors of Cytokine Signaling Proteins in the Lung of House Dust Mite–Sensitized and –Challenged Mice

McGee

Stallworth

Agrawal

et al. 2010

Am J Respir Cell Mol Biol

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We previously reported that Fms-like tyrosine kinase 3 ligand (Flt3-L) reversed airway hyperresponsiveness (AHR) and airway inflammation, and increased the number of regulatory CD11c high CD8a high CD11b low dendritic cells and CD4 1 CD25 1 ICOS 1 Foxp3 1 IL-10 1 T-regulatory cells in the lung of allergen-sensitized and -challenged mice. In this study, we evaluated the effect of Flt3-L on Th17 cells and expression of suppressors of cytokine signaling (SOCS) proteins in the lungs of house dust mite (HDM)-sensitized and -challenged mice. BALB/c mice were sensitized and challenged with HDM, and AHR to methacholine was established. Mice were treated with Flt3-L (5 mg, intraperitoneal) daily for 10 days. Levels of IL-4, -5, -6, -8, and -13, and transforming growth factor (TGF)-b in the bronchoalveolar lavage fluid (BALF) were examined by ELISA. Flt3-L treatment reversed existing AHR to methacholine and substantially decreased eosinophils, neutrophils, IL-5, -6, -8, and IL-13, and TGF-b levels in the BALF. HDM-sensitized and -challenged mice showed a significant increase in lung CD4 1 IL-17 1 IL-23R 1 CD25 2 T cells with high expression of retinoic acid-related orphan receptor (ROR)-gt transcripts. However, administration of Flt3-L substantially decreased the number of lung CD4 1 IL-17 1 IL-23R 1 CD25 2 T cells, with significantly decreased expression of ROR-gt mRNA in these cells. HDM sensitization caused a significant increase in the expression of SOCS-1, -3, and -5 in the lung. Flt3-L treatment abolished the increase in SOCS-1 and SOCS-3 proteins, whereas SOCS-5 expression was significantly reduced. These data suggest that the therapeutic effect of Flt3-L in reversing the hallmarks of allergic asthma in a mouse model is mediated by decreasing IL-6 and TGF-b levels in the BALF, which, in turn, decrease CD4 1 IL-17 1 IL-23R 1 ROR-gt 1 CD25 2 T cells and the expression of SOCS-1 and SOCS-3 in the lung of HDM-sensitized and -challenged mice.

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“…In other respects, some of the data previously reported for the action of Der p 1 via PAR 2 (14) appear somewhat contradictory. In one study by those investigators (12), it was shown that Der p 1 and Der p 9 induce the release of GM-CSF, IL-6, and IL-8 in bronchial epithelial cells. However, it was suggested in that study that these two mite allergens act presumably via different receptors (potentially PARs), since the calcium response generated in the BEAS-2B target cells by Der p 1 treatment (Fig.…”

Section: Discussionmentioning

confidence: 99%

The House Dust Mite Allergen Der p 1, Unlike Der p 3, Stimulates the Expression of Interleukin-8 in Human Airway Epithelial Cells via a Proteinase-activated Receptor-2-independent Mechanism

Adam

Hansen

Astudillo

et al. 2006

Journal of Biological Chemistry

151

124

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Quantitative structural and biochemical analyses of tight junction dynamics following exposure of epithelial cells to house dust mite allergen Der p 1

Abstract: Der p 1 could contribute to sensitization and allergic responses by degrading the function of the airway epithelial barrier.

Cited by 166 publications

References 36 publications

House dust mite induces direct airway inflammation in vivo: implications for future disease therapy?

House dust mite induces direct airway inflammation in vivo: implications for future disease therapy?

Fms-Like Tyrosine Kinase 3 Ligand Decreases T Helper Type 17 Cells and Suppressors of Cytokine Signaling Proteins in the Lung of House Dust Mite–Sensitized and –Challenged Mice

The House Dust Mite Allergen Der p 1, Unlike Der p 3, Stimulates the Expression of Interleukin-8 in Human Airway Epithelial Cells via a Proteinase-activated Receptor-2-independent Mechanism

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