Biological Properties and the Role of IL-25 in Disease Pathogenesis

Liu, Yuwan; Shao, Zewei; Shangguan, Guoqiang; Bie, Qingli; Zhang, Bin

doi:10.1155/2018/6519465

Cited by 35 publications

(49 citation statements)

References 70 publications

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“…Looking at the inflammatory pathway there are other interesting parameters which could influence the integrity of the epithelial barrier: Beside IL-33 there are other "alarmins" such as IL-25 and thymic stromal lymphopoietin (TSLP). IL-25 is another providing factor for Th2 driven inflammation and was shown to be increased in polyp tissue -as well as IL-33 and TSLP (23,24) .…”

Section: Discussionmentioning

confidence: 99%

The influence of corticosteroids and Azelastine on epithelial cell integrity in chronic rhinosinusitis with polyps

Vogel¹,

Kunz²,

Akdis³

et al. 2020

RHINOL

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Background:The pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) is still not completely understood. Regarding the pathogenesis an impaired barrier function of the sino-nasal epithelium has been shown in CRS. Intranasal corticosteroids are widely used for treatment and part of current guidelines. This study aims to analyse the influence of corticosteroids on the epithelial integrity in air-liquid-interface (ALI) epithelial cell cultures of patients with CRSwNP.Methodology: Polyp tissue from 11 patients with CRSwNP undergoing a sphenoethmoidectomy was collected. The epithelial cells were cultured in ALI. After differentiation of the cells, the permeability of the cell layer was defined by measuring the transepithelial resistance (TER). Commonly used corticosteroids, (Fluticasone & Mometasone) and Azelastine were added and their impact on the TER was documented and compared to the TER of ALI cultures without additives (controls). Results:After 48 hours, Fluticasone showed a significant increase of the TER. Mometasone and Azelastine had no significant impact on the TER. The paracellular passage of Dextran molecules in ALI cultures showed a negative correlation to the TER. Preoperative in vivo corticosteroid treatment had no effect on the baseline TER. Further analysis of the impact of preoperative corticosteroid treatment showed no effect on polyp size, sense of smell, histopathologic eosinophilic count and allergic sensitization. Conclusion:Fluticasone shows a direct effect in restoring sino-nasal epithelial barrier in-vitro, even in the absence of inflammatory cells.

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Section: Discussionmentioning

confidence: 99%

The influence of corticosteroids and Azelastine on epithelial cell integrity in chronic rhinosinusitis with polyps

Vogel¹,

Kunz²,

Akdis³

et al. 2020

RHINOL

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show abstract

“…IL-25, also called IL-17E, binds to the heterodimeric receptor composed of IL-17RA and IL17RB [ 10 ]. It is known to induce Th2 dominant response and cause allergic reaction [ 24 ]. Helminth-induced Th2 immune response can suppress inflammatory arthritis and bone loss via the IL-4/IL-13-induced STAT6 pathway [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…Such delayed-phase generation of IL-25 suppresses the production of pro-inflammatory cytokines, IL-6 and IL-17A, in RA synoviocytes [ 12 ]. IL-17RB is expressed in various cells, such as NKT, myeloid, Th9, mast, and dendritic cells, as well as basophils, eosinophils, and macrophages [ 24 ]. Osteoclast precursor cells, monocytes, have been previously shown to express IL-17RB and IL-17RA in a mouse model [ 26 ], as well as in human synoviocytes [ 12 ].…”

Section: Discussionmentioning

confidence: 99%

Interleukin (IL)-25 suppresses IL-22-induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway

Min

Won²,

Bo-Mi³

et al. 2020

Arthritis Res Ther

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Background The present study aimed to evaluate the suppressive role of interleukin (IL)-25 in IL-22-induced osteoclastogenesis and receptor activator of nuclear factor κB ligand (RANKL) expression in rheumatoid arthritis (RA). Methods Serum from patients with RA and osteoarthritis (OA), and healthy controls, and synovial fluid from patients with RA and OA were collected, and the levels of IL-22 and IL-25 were measured. RA and OA synovial tissues were stained against IL-25. Fibroblast-like synoviocytes (FLSs) of patients with RA were cultured with IL-22, in the presence or absence of IL-25, and RANKL expression was measured by real-time PCR and enzyme-linked immunosorbent assay (ELISA). Human peripheral blood monocytes were cultured under IL-22/RANKL + M-CSF, with or without IL-25, and tartrate-resistant acid phosphatase (TRAP)-positive cells and osteoclast-related markers were investigated to determine osteoclastogenesis. Results Serum and synovial IL-25 levels in RA were upregulated compared to those in OA and healthy control, and elevated expression of IL-25 in RA synovial tissue was re-confirmed. IL-25 and IL-22 levels showed significant correlation in serum and synovial fluid. Pre-treatment of FLS with IL-25 reduced IL-22-induced RANKL expression at the RNA level. The suppressive effects of IL-25 were confirmed to occur through the STAT3 and p38 MAPK/IκBα pathways. IL-25 reduced osteoclast differentiation and suppressed the expression of osteoclast-related markers. Conclusion In the current study, we demonstrated the regulatory effect of IL-25 on IL-22-induced osteoclastogenesis. Therapeutic approach involving augmentation of IL-25 regulatory response may serve as a novel treatment option for RA, especially by suppressing osteoclastogenesis.

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“…It is known to induce Th2 dominant response and cause allergic reaction [24]. Helminth-induced Th2 immune response can suppress in ammatory arthritis and bone loss via the IL-4/IL-13-induced STAT6 pathway [25].…”

Section: Suppression Of Il-22-mediated Rankl Expression In Fls After mentioning

confidence: 99%

“…Such delayed-phase generation of IL-25 suppresses the production of pro-in ammatory cytokines, IL-6 and IL-17A, in RA synoviocytes [12]. IL-17RB is expressed in various cells, such as NKT, myeloid, Th9, mast, and dendritic cells, as well as basophils, eosinophils, and macrophages [24]. Osteoclast precursor cells, monocytes, have been previously shown to express IL-17RB and IL-17RA in a mouse model [26], as well as in human synoviocytes [12].…”

Section: Suppression Of Il-22-mediated Rankl Expression In Fls After mentioning

confidence: 99%

Interleukin (IL)-25 suppresses IL-22 induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway

Min

Won

Kim

et al. 2020

Preprint

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Background The present study aimed to evaluate the suppressive role of interleukin (IL)-25 in IL-22-induced osteoclastogenesis and receptor activator of nuclear factor κB ligand (RANKL) expression in rheumatoid arthritis (RA). Methods Serum from patients with RA and osteoarthritis (OA), and healthy controls, as well as synovial fluid from patients with RA and OA were collected, and the levels of IL-22 and IL-25 were measured. RA and OA synovial tissues were stained against IL-25. Fibroblast-like synoviocytes (FLSs) of patients with RA were cultured with IL-22, in the presence or absence of IL-25, and RANKL expression was measured by real-time PCR and enzyme-linked immunosorbent assay (ELISA). Human peripheral blood monocytes were cultured under IL-22/RANKL + M-CSF, with or without IL-25, and tartrate-resistant acid phosphatase (TRAP)-positive cells and osteoclast-related markers were investigated to determine osteoclastogenesis. Results Serum and synovial IL-25 levels in RA were up-regulated compared to those in OA and healthy control, and elevated expression of IL-25 in RA synovial tissue was re-confirmed. IL-25 and IL-22 levels showed significant correlation in serum and synovial fluid. Pre-treatment of FLS with IL-25 reduced IL-22-induced RANKL expression at the RNA level. The suppressive effects of IL-25 were confirmed to occur through the STAT3 and p38 MAPK/IκBα pathways. IL-25 reduced osteoclast differentiation and suppressed the expression of osteoclast-related markers. Conclusion In the current study, we demonstrated the regulatory effect of IL-25 on IL-22-induced osteoclastogenesis. Therapeutic approach involving augmentation of IL-25 regulatory response may serve as a novel treatment option for RA, especially by suppressing osteoclastogenesis.

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Biological Properties and the Role of IL-25 in Disease Pathogenesis

Cited by 35 publications

References 70 publications

The influence of corticosteroids and Azelastine on epithelial cell integrity in chronic rhinosinusitis with polyps

The influence of corticosteroids and Azelastine on epithelial cell integrity in chronic rhinosinusitis with polyps

Interleukin (IL)-25 suppresses IL-22-induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway

Interleukin (IL)-25 suppresses IL-22 induced osteoclastogenesis in rheumatoid arthritis via STAT3 and p38 MAPK/IκBα pathway

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