Protease/antiprotease network in allergy: The role of <i>Staphylococcus aureus</i> protease‐like proteins

Krysko, Olga; Teufelberger, Andrea Renate; Nevel, Sharon Van; Krysko, Dmitri V.; Bachert, Claus

doi:10.1111/all.13783

Cited by 42 publications

(35 citation statements)

References 112 publications

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“…Mutations in SERPINA3 leading to decreased α-1 anti-chymotrypsin serum levels were associated with the inflammatory lung diseases COPD and emphysema (43). Our study revealed a novel IL-33 regulation pathway of SERPINA3I inhibiting the IL-33 degrading mast cell chymase mMCP-4, which could be, with the equivalent human proteins, of general importance in allergic airway diseases (44). The human SERPINA3 is a known mast cell chymase inhibitor and could thus be relevant in IL-33 regulation (45).…”

Section: Discussionmentioning

confidence: 69%

Mouse Strain-Dependent Difference Toward the Staphylococcus aureus Allergen Serine Protease-Like Protein D Reveals a Novel Regulator of IL-33

et al. 2020

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Staphylococcus aureus (S. aureus) can secrete a broad range of virulence factors, among which staphylococcal serine protease-like proteins (Spls) have been identified as bacterial allergens. The S. aureus allergen serine protease-like protein D (SplD) induces allergic asthma in C57BL/6J mice through the IL-33/ST2 signaling axis. Analysis of C57BL/6J, C57BL/6N, CBA, DBA/2, and BALB/c mice treated with intratracheal applications of SplD allowed us to identify a frameshift mutation in the serine (or cysteine) peptidase inhibitor, clade A, and member 3I (Serpina3i) causing a truncated form of SERPINA3I in BALB/c, CBA, and DBA/2 mice. IL-33 is a key mediator of SplD-induced immunity and can be processed by proteases leading to its activation or degradation. Full-length SERPINA3I inhibits IL-33 degradation in vivo in the lungs of SplD-treated BALB/c mice and in vitro by direct inhibition of mMCP-4. Collectively, our results establish SERPINA3I as a regulator of IL-33 in the lungs following exposure to the bacterial allergen SplD, and that the asthma phenotypes of mouse strains may be strongly influenced by the observed frameshift mutation in Serpina3i. The analysis of this protease-serpin interaction network might help to identify predictive biomarkers for type-2 biased airway disease in individuals colonized by S. aureus.

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Section: Discussionmentioning

confidence: 69%

Mouse Strain-Dependent Difference Toward the Staphylococcus aureus Allergen Serine Protease-Like Protein D Reveals a Novel Regulator of IL-33

et al. 2020

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“…IL‐33, one of the epithelium‐derived cytokines, plays an important role in type 2 immunity and functions as a protease sensor 56 . When exposed to allergen proteases, full‐length IL‐33 is cleaved, thereby activating the production of type 2 cytokines from ILC2s 57,58 . Mice that lack ILC2s but have Th2 cells display reduced Th2 cytokine and IgE levels, suggesting the importance of ILC2s in bridging innate and adaptive Th2 responses 59 .…”

Section: Tight Junction In Asthmamentioning

confidence: 99%

Tight junctions in the development of asthma, chronic rhinosinusitis, atopic dermatitis, eosinophilic esophagitis, and inflammatory bowel diseases

Sugita

Kabashima

2020

Journal of Leukocyte Biology

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This review focuses on recent developments related to asthma, chronic rhinosinusitis, atopic dermatitis (AD), eosinophilic esophagitis, and inflammatory bowel diseases (IBD), with a particular focus on tight junctions (TJs) and their role in the pathogenetic mechanisms of these diseases. Lung, skin, and intestinal surfaces are lined by epithelial cells that interact with environmental factors and immune cells. Therefore, together with the cellular immune system, the epithelium performs a pivotal role as the first line physical barrier against external antigens. Paracellular space is almost exclusively sealed by TJs and is maintained by complex protein-protein interactions. Thus, TJ dysfunction increases paracellular permeability, resulting in enhanced flux across TJs. Epithelial TJ dysfunction also causes immune cell activation and contributes to the pathogenesis of chronic lung, skin, and intestinal inflammation. Characterization of TJ protein alteration is one of the key factors for enhancing our understanding of allergic diseases as well as IBDs. Furthermore, TJ-based epithelial disturbance can promote immune cell behaviors, such as those in dendritic cells, Th2 cells, Th17 cells, and innate lymphoid cells (ILCs), thereby offering new insights into TJ-based targets. The purpose of this review is to illustrate how TJ dysfunction can lead to the disruption of the immune homeostasis in barrier tissues and subsequent inflammation.This review also highlights the various TJ barrier dysfunctions across different organ sites, which would help to develop future drugs to target allergic diseases and IBD.

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“…Although IL-33 is considered to play significant roles in NPs, the precise mechanism of the effect of IL-33 on eosinophils in NPs remains unclear. Proteases, which are contained in antigens, bacteria, and fungi, can induce IL-33 from epithelial cells and thus promote the Th2 response [46,47]. CRSwNP is associated with a high rate of nasal colonization by Staphylococcus aureus (S. aureus), which is associated with a severe disease phenotype, and S. aureus superantigens have been implicated in the pathogenesis of the Th2 response in the nasal mucosa as they induce the release of several cytokines such as IL-33 [36,[48][49][50].…”

Section: Discussionmentioning

confidence: 99%

Enhanced 15-Lipoxygenase 1 Production is Related to Periostin Expression and Eosinophil Recruitment in Eosinophilic Chronic Rhinosinusitis

et al. 2020

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Background: The pathological features of chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) tissues include an eosinophilic infiltration pattern (eosinophilic CRS (ECRS)) or a less eosinophilic pattern (non-ECRS). Recently, it has been suggested that 15-lipoxygenase 1 (15-LOX-1) may have significant roles in allergic disease; however, the significance of 15-LOX-1 in CRS is not well understood. The objective of this study was to demonstrate the expression of 15-LOX-1 in CRS. Methods: The mRNA expression levels of 15-LOX-1 and periostin in nasal tissues were measured by quantitative real-time polymerase chain reaction. We also performed an immunofluorescence study of nasal tissues. Cells of the Eol-1 eosinophilic leukemic cell line were stimulated with interleukin-33 to test the induction of 15-LOX-1. Results: The expression level of 15-LOX-1 mRNA in nasal polyps (NPs) was significantly higher in ECRS patients than in non-ECRS patients. The immunofluorescence study revealed that both airway epithelial cells and eosinophils in NPs expressed 15-LOX-1. A significant correlation was seen between the number of eosinophils and the mRNA expression levels of 15-LOX-1 and periostin in nasal polyps. Moreover, interleukin-33 enhanced 15-LOX-1 expression in Eol-1 cells. Conclusions: 15-LOX-1 was shown to be a significant molecule that facilitates eosinophilic inflammation in ECRS.

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Protease/antiprotease network in allergy: The role of Staphylococcus aureus protease‐like proteins

Cited by 42 publications

References 112 publications

Mouse Strain-Dependent Difference Toward the Staphylococcus aureus Allergen Serine Protease-Like Protein D Reveals a Novel Regulator of IL-33

Mouse Strain-Dependent Difference Toward the Staphylococcus aureus Allergen Serine Protease-Like Protein D Reveals a Novel Regulator of IL-33

Tight junctions in the development of asthma, chronic rhinosinusitis, atopic dermatitis, eosinophilic esophagitis, and inflammatory bowel diseases

Enhanced 15-Lipoxygenase 1 Production is Related to Periostin Expression and Eosinophil Recruitment in Eosinophilic Chronic Rhinosinusitis

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