Protein S protects against allergic bronchial asthma by modulating Th1/Th2 balance.

Abstract:

BACKGROUND:Bronchial asthma is a chronic disease characterized by inflammation, obstruction, and hyperresponsiveness of the airways. There is currently no curative therapy for asthma. Type 2 helper T cell response plays a critical role in the pathogenesis of the disease. Protein S is a glycoprotein endowed with anticoagulant, anti-inflammatory, and anti-apoptotic properties. Whether protein S can suppress bronchial asthma and be useful for its therapy is unknown. METHODS:To address this question here we compared the development of allergen-associated bronchial asthma between wild type and protein S-overexpressing transgenic mice. Mice were sensitized and challenged with ovalbumin. We also evaluated the circulating levels of total and active protein S in patients with bronchial asthma and healthy controls. RESULTS:The circulating level of total protein S and of its active form was significantly decreased in patients with bronchial asthma compared to controls. Allergic protein S transgenic mice showed a significant reduction of airway hyperresponsiveness, lung tissue inflammatory cell infiltration, lung levels of Th2 cytokines and IgE compared to their wild-type counterparts. Administration of exogenous human protein S also decreased airway hyperresponsiveness and Th2-mediated lung inflammation in allergic wild-type mice compared with their untreated mouse counterparts. Human protein S significantly shifted the Th1/Th2 balance to Th1 and promoted the secretion of Th1 cytokines (IL-12, tumor necrosis factor-α) from dendritic cells. CONCLUSIONS:These observations suggest the strong protective activity of protein S against the development of allergic bronchial asthma implicating its potential usefulness for the disease treatment.

journal_name

Allergy

journal_title

Allergy

authors

Asayama K,Kobayashi T,D'Alessandro-Gabazza CN,Toda M,Yasuma T,Fujimoto H,Okano T,Saiki H,Takeshita A,Fujiwara K,Fridman D'Alessandro V,Nishihama K,Totoki T,Inoue R,Takei Y,Gabazza EC

doi

10.1111/all.14261

subject

Has Abstract

pub_date

2020-09-01 00:00:00

pages

2267-2278

issue

9

eissn

0105-4538

issn

1398-9995

journal_volume

75

pub_type

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