Roles of Periostin in Symptom Manifestation and Airway Remodeling in a Murine Model of Allergic Rhinitis

Hur, Dong Gu; Khalmuratova, Roza; Ahn, Seong Ki; Ha, Young Sool; Min, Yang Gi

doi:10.4168/aair.2012.4.4.222

Cited by 9 publications

(9 citation statements)

References 40 publications

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“…Interestingly, the contrary results regarding ADAM8 and mouse asthma models are somewhat similar to what was found in murine knockouts of periostin. 15,[48][49][50][51][52][53] Several studies on periostin-deficient mice, or with an antiperiostin mAb in wild-type mice, indicate that periostin promotes allergic inflammation, eosinophil recruitment, generation of type 2 cytokines and airway hyperresponsiveness, 15,48,[51][52][53] whereas other mouse studies indicate that periostin does not influence leucocyte recruitment but suppresses type 2 responses, airway remodelling and responsiveness. 15,49,50 There may be several possible explanations for the discrepancies in effects on airway remodelling and responsiveness in the mouse studies, but overall, those studies indicate that periostin is involved in and may promote and/or regulate airway inflammation and remodelling.…”

Section: Discussionmentioning

confidence: 99%

IL‐5‐stimulated eosinophils adherent to periostin undergo stereotypic morphological changes and ADAM8‐dependent migration

Johansson

Khanna

Bortnov

et al. 2017

Clin Experimental Allergy

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Summary Background IL-5 causes suspended eosinophils to polarize with filamentous (F)-actin and granules at one pole and the nucleus in a specialized uropod, the “nucleopod”, which is capped with P-selectin glycoprotein ligand-1 (PSGL-1). IL-5 enhances eosinophil adhesion and migration on periostin, an extracellular matrix protein upregulated in asthma by type 2 immunity mediators. Objective Determine how the polarized morphology evolves to foster migration of IL-5-stimulated eosinophils on a surface coated with periostin. Methods Blood eosinophils adhering to adsorbed periostin were imaged at different time points by fluorescent microscopy, and migration of eosinophils on periostin was assayed. Results After 10 min in the presence of IL-5, adherent eosinophils were polarized with PSGL-1 at the nucleopod tip and F-actin distributed diffusely at the opposite end. After 30–60 min, the nucleopod had dissipated such that PSGL-1 was localized in a crescent or ring away from the cell periphery, and F-actin was found in podosome-like structures. The periostin layer, detected with monoclonal antibody Stiny-1, shown here to recognize the FAS1 4 module, was cleared in wide areas around adherent eosinophils. Clearance was attenuated by metalloproteinase inhibitors or antibodies to disintegrin metalloproteinase 8 (ADAM8), a major eosinophil metalloproteinase, previously implicated in asthma pathogenesis. ADAM8 was not found in podosome-like structures, which are associated with proteolytic activity in other cell types. Instead, immunoblotting demonstrated proteoforms of ADAM8 that lack the cytoplasmic tail in the supernatant. Anti-ADAM8 inhibited migration of IL-5-stimulated eosinophils on periostin. Conclusions and Clinical Relevance Migrating IL-5-activated eosinophils on periostin exhibit loss of nucleopodal features and appearance of prominent podosomes along with clearance of the Stiny-1 periostin epitope. Migration and epitope clearance are both attenuated by inhibitors of ADAM8. We propose, therefore, that eosinophils remodel and migrate on periostin-rich extracellular matrix in the asthmatic airway in an ADAM8-dependent manner, making ADAM8 a possible therapeutic target.

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Section: Discussionmentioning

confidence: 99%

IL‐5‐stimulated eosinophils adherent to periostin undergo stereotypic morphological changes and ADAM8‐dependent migration

Johansson

Khanna

Bortnov

et al. 2017

Clin Experimental Allergy

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“…Our data are also consistent with previous work using the Postn null mouse showing that F2 B6;129 Postn knockout mice show reduced eosinophil recruitment to the lungs following A. fumigatus sensitization and challenge 9 . Periostin has also been shown to promote inflammation in other models of allergic disease including HDM-induced atopic dermatitis 22 , OVA-induced allergic rhinitis 23 and A. fumigatus- induced eosinophilic esophagitis 9 .…”

Section: Discussionmentioning

confidence: 99%

Periostin is required for maximal airways inflammation and hyperresponsiveness in mice

Bentley

Chen

Hong

et al. 2014

Journal of Allergy and Clinical Immunology

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Background Periostin, a secreted extracellular matrix protein, has been localized to deposits of subepithelial fibrosis in asthma, and periostin levels have been linked to elevation of IL-13. Objective We hypothesized that periostin is required for airway inflammatory responses to a physiologic aeroallergen, house dust mite (HDM). Methods We studied F4-F6 B6;129-Postntm1Jmol/J wild-type (+/+) and null (−/−) mice as well as C57BL/6 mice treated with either IgM or OC-20 periostin neutralizing antibody. Mice were exposed to five doses of HDM intranasally over a 16 day period. Results HDM increased airways responsiveness in Postn wild-type but not null mice. In addition, HDM-treated C57BL/6 mice injected with OC-20 had a lower airways responsiveness than HDM-treated mice injected with IgM. Compared to Postn wild-type mice, Postn null mice showed decreases in HDM-induced inflammation and mucous metaplasia, as well as reduced IL-4, IL-25, CD68, Gob5 and periostin mRNA expression. OC-20 antibody gave similar results. HDM exposure increased periostin expression in the airway epithelium, subepithelium, smooth muscle and inflammatory cells. OC-20 blocked the HDM-induced IgE response, and T cells incubated with dendritic cells (DCs) from Postn null mice or treated with OC-20 showed deficient DNA synthesis and IL-13 responses compared to T cells incubated with wild-type DCs. Finally, adoptive transfer of bone marrow-derived DCs from periostin wild-type mice was sufficient to promote allergic responses in F6 periostin null littermates. Conclusions In mice, periostin is required for maximal airways hyperresponsiveness and inflammation following HDM sensitization and challenge. Periostin is required for maximal HDM-induced T cell responses.

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“…A number of studies have also demonstrated goblet cell hyperplasia, enlarged submucosal mucus glands, angiogenesis and lymphangiogenesis in the upper airways, including nasal mucosa of patients with AR [7,13,22]. Furthermore, immunohistochemical analysis revealed the intense deposition of collagen and proteoglycan in the superficial and submucosal layer of allergic nasal mucosa in human and murine AR model [13,23]. These histological changes are called tissue remodeling and may be notorious factors for the development of nasal symptoms, especially nasal obstruction in AR [13].…”

Section: Discussionmentioning

confidence: 99%

“…It is also reported that periostin promotes proliferation and migration of both fibroblasts and vascular endothelial cells into inflammatory sites, which are responsible for fibrosis, angiogenesis and Citation: Asano M, Mizuyoshi T, Ishikawa S, Asano K, Kobayashi H (2017) Suppressive Activity of Histamine H1 Receptor Antagonists, lymphangiogenesis [13]. The influence of periostin on the function of effector cells in allergic inflammatory responses was extensively examined by targeting eosinophils [6,23,26]. Periostin is reported to promote eosinophil migration and increase eosinophil adhesion to the extracellular matrix component fibronectin in vitro [6].…”

Section: Discussionmentioning

confidence: 99%

“…Periostin is reported to promote eosinophil migration and increase eosinophil adhesion to the extracellular matrix component fibronectin in vitro [6]. Intranasal instillation of allergens extracted from Aspergillus fumigatus [6] or ovalbumin [23,26] into periostin-knockout mice cannot induce eosinophil accumulation in airways as compared with wild type mice. Taken together, the results obtained from the present experiments strongly suggest that the suppressive effects of histamine H1 receptor antagonists on periostin production may account, at least in part, for the clinical efficacy of the agents in AR.…”

Section: Discussionmentioning

confidence: 99%

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Suppressive Activity of Histamine H1 Receptor Antagonists, Desloratadine and Levocetirizine, on the Production of Periostin from Nasal Epithelial Cells In vitro

Asano¹,

Mizuyoshi²,

Ishikawa³

et al. 2017

J Allergy Ther

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Background: Periostin, a 90-kDa endogenous extracellular matrix protein, is well known to be involved in the development and persistence of allergic rhinitis. Although histamine H1 receptor antagonists are recommended as first choice of agents in the treatment of allergic rhinitis, the influence of the agents on periostin production is not well understood. The present study was undertaken to examine the influence of histamine H1 receptor antagonists on periostin production from nasal epithelial cells after IL-4 stimulation in vitro. Methods: Human nasal epithelial cells (HNEpC) at a concentration of 1 × 10 5 cells/ml were stimulated with 10.0 ng/ml IL-4 in combination with either desloratadine (DLT), loratadine (LT), levocetirizine (LCT) or cetirizine (CT). After 48 h, culture supernatants were collected and assayed for periostin levels by ELISA. The influence of LCT on transcription factor, STAT6, activation and periostin mRNA expression were also examined by ELISA and real-time RT-PCR, respectively. Results: Treatment of cells with DLT, LT, LCT and CT suppressed the ability of HNEpC to produce periostin in response to IL-4 stimulation in dose-dependent manner. The minimum concentration that caused significant suppression is 0.01 µM for DLT, 0.05 µM for LT, 0.05 µM for LCT and 0.1 µM for CT. Treatment of HNEpC with LCT at more than 0.05 µM also suppressed STAT6 activation and periostin mRNA expression induced by IL-4 stimulation. Conclusion: The present results strongly suggest that histamine H1 receptor antagonists favorably modify the clinical conditions of allergic rhinitis through the suppression of periostin production from nasal epithelial cells after IL-4 stimulation.

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Roles of Periostin in Symptom Manifestation and Airway Remodeling in a Murine Model of Allergic Rhinitis

Cited by 9 publications

References 40 publications

IL‐5‐stimulated eosinophils adherent to periostin undergo stereotypic morphological changes and ADAM8‐dependent migration

IL‐5‐stimulated eosinophils adherent to periostin undergo stereotypic morphological changes and ADAM8‐dependent migration

Periostin is required for maximal airways inflammation and hyperresponsiveness in mice

Suppressive Activity of Histamine H1 Receptor Antagonists, Desloratadine and Levocetirizine, on the Production of Periostin from Nasal Epithelial Cells In vitro

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