However, Yoshimoto et alĪdministration of IL-27 could inhibit OVA-induced airway Inflammation and improve pathological changes when administered inĪ therapeutic mode following OVA challenge ( 22, 23).
Pathological changes, whereas IL-27 does not reduce airway OVA-induced mouse model have shown that preventative intranasalĪdministration of IL-27 reduced airway inflammation and improved Novel, promising preventative agent for alleviating asthmaĭevelopment and exacerbation. Jirmo et alĬritical for the control of allergic asthma. Phenotypes, suggesting that IL-27 plays a pivotal role in the Mice challenged with ovalbumin (OVA) exhibited increased asthmatic IL-27 may be stimulated as aĬounter-regulatory cytokine to suppress Th2 inflammation ( 17- 19). With increasing severity of asthma ( 17- 19). Several studies have found that high levels of IL-27Ĭombined with activation of the type-2 signature are associated Important role in the pathogenesis of asthma. Role in airway inflammation and AHR, which are the hallmarks ofĪsthma ( 15, 16). (Th2) production and T-helper 17 (Th17) differentiation ( 13, 14). ( 11, 12) and directly suppresses T-helper 2 Pleiotropic effects on T-helper cell responses ( 9, 10).įor example, it induces T-helper 1 (Th1) cell differentiation
Produced by activated antigen-presenting cells and exhibits Of the subunit p28 (IL-27p28) and Epstein Barr virus-induced gene 3 Interleukin 27 (IL-27) is a novel cytokine composed Therefore, it is necessary to identify early effective primary Although corticosteroids andīronchodilators can control disease symptoms ( 5, 6),Īsthma is not readily preventable or curable ( 7, 8). Shares similar clinical manifestations and typical features ofĪirway inflammation, airway hyperresponsiveness (AHR) and airway Heterogeneous disease that comprises different phenotypes and That the number will reach 400 million by 2025 ( 2). Taken together, these findings demonstrated that intranasal administration of IL‑27 ameliorated Th2‑related allergic lung inflammation and remodeling in mouse models of asthma by repairing both the STAT1 and STAT3 pathways.Īsthma is one of the most common chronic diseasesĪnd more than 300 million individuals worldwide currently suffer Moreover, the phosphorylation levels of STAT1 and STAT3 were increased. Following administration of IL‑27, the mRNA expression levels of STAT1 and T‑bet were upregulated, while those of GATA3 were downregulated. Furthermore, IL‑27 prevented airway remodeling in a chronic model of asthma. The results indicated that intranasal administration of IL‑27 ameliorated airway inflammation and hyperresponsiveness in an acute model of asthma. Airway remodeling was assessed by conventional pathological techniques. Their corresponding mRNA expression levels were determined by quantitative PCR.
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In addition, the expression levels of signal transducer and activator of transcription (STAT) 1, STAT3, GATA‑binding protein‑3 (GATA3) and T‑bet (T‑box transcription factor) were analyzed in T cells by western blot analysis. Total and differential cell counts were determined from Wright‑Giemsa‑stained cytospins, whereas the cytokine levels were detected using ELISA. In the present study, mice were induced and challenged with ovalbumin and received subsequent intranasal administration of IL‑27. Although interleukin 27 (IL‑27) has been reported as an initiator and suppressor of T‑helper 1 (Th1) and T‑helper 2 (Th2) responses, respectively, its effects on the development of asthma remain unclear. Type 2 cytokine‑associated immunity may be involved in the pathogenesis of allergic asthma.
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