Salidroside suppresses group 2 innate lymphoid cell-mediated allergic airway inflammation by targeting IL-33/ST2 axis

Cai, Hui; Wang, Jian; Mo, Yuqing; Ye, Ling; Zhu, Guiping; Song, Xixi; Zhu, Mengchan; Xue, Xiaomin; Yang, Chengyu; Jin, Meiling

doi:10.1016/j.intimp.2020.106243

Cited by 16 publications

(18 citation statements)

References 33 publications

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“…BALF was collected according to a method described previously [ 14 ]. Briefly, the trachea was cannulated through a 22-inch intravenous catheter and the lungs were lavaged with a total volume of 1 mL PBS for three successive aspirations to obtain BALF.…”

Section: Methodsmentioning

confidence: 99%

SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

Cai

et al. 2021

Respir Res

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Background Serine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. However, its role in the T-helper type 2 (Th2) response of allergic asthma is not known. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells. Methods Th2 cytokines and serum levels of house dust mite (HDM)-specific IgE in bronchoalveolar lavage fluid were examined by ELISA in an HDM-induced asthma model. The number and apoptosis of Th1 and Th2 cells in mouse lungs were measured by flow cytometry. Naïve CD4 T cells from patients with asthma were cultured under appropriate polarizing conditions to generate Th1 and Th2 cells. SERPINB10 expression in polarized Th1 and Th2 cells was quantified by real-time reverse transcription-quantitative polymerase chain reaction. SERPINB10 expression was knocked down in human CD4 T cells with lentivirus. Results Knockdown of SERPINB10 expression significantly diminished HDM-induced Th2 cytokine secretion and level of HDM-specific IgE. After HDM exposure, SERPINB10-knockdown mice had diminished numbers of Th2 cells, but similar numbers of Th1 cells, compared with those in negative-control mice. Th2 cells of SERPINB10-knockdown mice were more susceptible to apoptosis than that of control mice. Stimulating T-cell receptors (TCRs) with anti-CD3 antibody caused upregulation of SERPINB10 expression in polarized Th2 cells, but not polarized Th1 cells. Knockdown of SERPINB10 expression resulted in fewer numbers and greater apoptosis of polarized Th2 cells. Conclusion Our results suggest that SERPINB10 may contribute to allergic inflammation and the Th2 response of asthma by inhibiting the apoptosis of Th2 cells.

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Section: Methodsmentioning

confidence: 99%

SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

Cai

et al. 2021

Respir Res

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“…Finally, it delayed progression of renal fibrotic events (Elsherbiny et al, 2020). In addition, astragaloside IV (AS-IV; Bao et al, 2016), Cnidium Cnidii (Yang et al, 2020), and salidroside (Cai et al, 2020) have also been shown to reduce IL-33 to improve the disease condition. However, these studies were conducted in non-renal diseases, such as allergic inflammation.…”

Section: The Potential Value Of the Il-33/ St2 Pathway For Renal Fibrosismentioning

confidence: 99%

Interleukin-33/ Suppression of Tumorigenicity 2 in Renal Fibrosis: Emerging Roles in Prognosis and Treatment

Tan

Jing

2022

Front. Physiol.

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Chronic kidney disease (CKD) is a major public health problem that affects more than 10% of the population worldwide and has a high mortality rate. Therefore, it is necessary to identify novel treatment strategies for CKD. Incidentally, renal fibrosis plays a central role in the progression of CKD to end-stage renal disease (ESRD). The activation of inflammatory pathways leads to the development of renal fibrosis. In fact, interleukin-33 (IL-33), a newly discovered member of the interleukin 1 (IL-1) cytokine family, is a crucial regulator of the inflammatory process. It exerts pro-inflammatory and pro-fibrotic effects via the suppression of tumorigenicity 2 (ST2) receptor, which, in turn, activates other inflammatory pathways. Although the role of this pathway in cardiac, pulmonary, and hepatic fibrotic diseases has been extensively studied, its precise role in renal fibrosis has not yet been completely elucidated. Recent studies have shown that a sustained activation of IL-33/ST2 pathway promotes the development of renal fibrosis. However, with prolonged research in this field, it is expected that the IL-33/ST2 pathway will be used as a diagnostic and prognostic tool for renal diseases. In addition, the IL-33/ST2 pathway seems to be a new target for the future treatment of CKD. Here, we review the mechanisms and potential applications of the IL-33/ST2 pathway in renal fibrosis; such that it can help clinicians and researchers to explore effective treatment options and develop novel medicines for CKD patients.

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“…Flow cytometry of lung ILC2s was performed as in our previous study ( 19 ). Lung tissues were prepared as single-cell suspensions.…”

Section: Methodsmentioning

confidence: 99%

“…After treatment with red blood cell (RBC) lysis solution and incubation with CD16/32 monoclonal antibody (MultiSciences, China) for 10 min to block Fc receptors, cells were stained with a mixture of APC-eFluor 780-conjugated anti-CD45 (30-F11, eBioscience), PerCP-cy5.5-conjugated anti-lineage markers (CD3e, CD11b, CD45R/B220, Ly-76, Ly-6G, and Ly-6C) (BD Pharmingen), fluorescein isothiocyanate (FITC)-conjugated anti-Thy1.2 (53-2.1, eBioscience), and APC-conjugated anti-ST2 (DIH9, BioLegend) for 30 min. ILC2s were identified as CD45 + Lin − Thy1.2 + ST2 + as previously described (19)(20)(21). CD4 + T cells were stained with a mixture of Percp-cy5.5-conjugated anti-CD3e (BioLegend), BV510-conjugated anti-CD4 (BD Bioscience), and APC-cy7-conjugated anti-CD45 (BioLegend) for 30 min on ice.…”

Section: Flow Cytometry Of Lung Ilc2s and Cd4 + T Cellsmentioning

confidence: 99%

Small Proline-Rich Protein 3 Regulates IL-33/ILC2 Axis to Promote Allergic Airway Inflammation

Zhu

Cai

et al. 2022

Front. Immunol.

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Small proline-rich proteins (SPRRs), components of cornified cell envelope precursors, have recently been found to participate in airway diseases. However, their role in allergic airway inflammatory conditions remains unknown. Here, we explored the expression of SPRR3 in house dust mite (HDM)-sensitized/challenged mice and attempted to elucidate the regulatory role of SPRR3 in allergic airway inflammation. SPRR3 was identified via bioinformatics analysis of Gene Expression Omnibus (GEO) databases and further confirmed to be upregulated in the lungs of asthmatic mice. Knockdown of SPRR3 via the intratracheal route significantly inhibited eosinophils in bronchoalveolar lavage fluid (BALF) and suppressed the expressions of type 2 cytokines (IL-4, IL-5, and IL-13) in BALF and lung tissues. Further, SPRR3 knockdown reduced the expression of IL-33 and further attenuated the activation of the PI3K/AKT/NF-κB signaling pathway in the recruitment of group 2 innate lymphoid cells (ILC2s) to inhibit allergic airway inflammation. In vitro, SPRR3 siRNA could alleviate HDM-induced inflammatory responses in BEAS-2B cells. This study reveals the regulatory role of SPRR3 in allergic airway inflammation, identifying this protein as a potential novel therapeutic target for asthma.

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Salidroside suppresses group 2 innate lymphoid cell-mediated allergic airway inflammation by targeting IL-33/ST2 axis

Cited by 16 publications

References 33 publications

SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

Interleukin-33/ Suppression of Tumorigenicity 2 in Renal Fibrosis: Emerging Roles in Prognosis and Treatment

Small Proline-Rich Protein 3 Regulates IL-33/ILC2 Axis to Promote Allergic Airway Inflammation

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