Repeated inhalation of sevoflurane inhibits airway inflammation in an <scp>OVA</scp>‐induced mouse model of allergic airway inflammation

Shen, Qiying; Fang, Lei; Wu, Hui-Mei; He, Fang; Ding, Peishan; Liu, Rong‐Yu

doi:10.1111/resp.12439

Cited by 11 publications

(8 citation statements)

References 39 publications

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“…Other pathways have also been investigated and reported on in Respirology this year; sevoflurane, a volatile agent routinely used in anaesthesia, possesses anti‐inflammatory effects in animal models of acute lung injury. Shen et al found that repeated inhalation of sevoflurane inhibited allergic airway inflammation by reducing inflammatory cell infiltrates, modulating the imbalance of high‐mobility group box (HMGB) 1, tumour necrosis factor‐α and IL‐10 responses and mitigating allergen‐specific IgE responses and globlet cell hyperplasia in mice. HMGB1 is a non‐histone DNA‐binding nuclear protein acting as an endogenous ‘danger signal’, which triggers innate immune reactions .…”

Section: Asthmamentioning

confidence: 99%

Year in review 2015: Asthma and chronic obstructive pulmonary disease

et al. 2016

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Asthma continues to cause substantial morbidity and mortality, affecting some 300 million people worldwide, with a large proportion of those poorly controlled.1-3 In the last year, Respirology published a broad-based range of papers focusing on this important disease, ranging from questionnaire studies to molecular biology in mouse models. 4,5 This range of papers emphasizes the breadth of asthma research underway and the role of Respirology in disseminating these advances.

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Section: Asthmamentioning

confidence: 99%

Year in review 2015: Asthma and chronic obstructive pulmonary disease

et al. 2016

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“…Previous studies have demonstrated that sevoflurane attenuated oleic acid-induced pulmonary oedema, decreased tumour nuclear factor- α , and ameliorated the alveolar damage score in dogs; sevoflurane was also shown to benefit patients with acute lung injury [ 26 , 27 ]. The results of previous studies in our laboratory show that the OVA-mediated increases in inflammatory cells around bronchi, goblet cell hyperplasia, and total numbers and differential counts of inflammatory cells in BALF were significantly inhibited by sevoflurane [ 13 ]. In accordance with the results of our colleagues, this study confirms the anti-inflammatory effects of sevoflurane, which is similar to MCC950.…”

Section: Discussionmentioning

confidence: 99%

“…Sevoflurane, a commonly used volatile anaesthetic, has been used as a last-resort treatment for life-threatening asthma in children [ 9 ]. Apart from bronchodilation [ 10 – 12 ], our coworkers have confirmed that sevoflurane suppressed allergic airway inflammation by inhibiting inflammatory infiltrates and mucus production, as well as keeping balance of cytokine responses [ 13 ]. However, whether sevoflurane inhibits the Th2 response and NLRP3 inflammasome activation in allergic airway inflammation remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane Inhibits the Th2 Response and NLRP3 Expression in Murine Allergic Airway Inflammation

Wang

Zha

Shen

et al. 2018

Journal of Immunology Research

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Background Our colleagues have demonstrated an impressive therapeutic role of sevoflurane in a murine allergic airway inflammation model, but the mechanisms underlying this effect remain undefined. In this study, we tried to investigate the effect of sevoflurane on the resolution of allergic airway inflammation and to assess whether NLRP3 or the NLRP3 inflammasome is involved in this process. Methods Female (C57BL/6) mice were sensitized and challenged with ovalbumin (OVA). Then, some of the mice received MCC950 (10 mg/kg; i.p.) or 3% sevoflurane. Total and differential inflammatory cell numbers, proinflammatory cytokines in bronchoalveolar lavage fluid (BALF), the peribronchial inflammation density, and mucus production were evaluated. In addition, we analysed the protein levels of NLRP3, the apoptosis-associated speck-like protein containing the caspase activation and recruitment domain (ASC), pro-caspase-1, and caspase-1 in the lung tissue. Results We found that OVA-induced inflammatory cell recruitment to peribronchial regions, goblet cell hyperplasia, the serum levels of IgE, inflammatory cells, and the Th2 cytokine secretion in BALF was potently suppressed by sevoflurane with an efficacy comparable with that suppressed by MCC950 treatment. Furthermore, sevoflurane, similar to MCC950, clearly inhibited the OVA-induced activity of NLRP3 in the lungs. In addition, we found that OVA challenge failed to increase the expression of ASC, pro-caspase-1, and caspase-1 in the lungs and the levels of IL-18 and IL-1β in BALF. Conclusion Taken together, our data showed that sevoflurane ameliorated allergic airway inflammation by inhibiting Th2 responses and NLRP3 expression. The NLRP3 independent of inflammasomes participated in the pathogenesis of allergic asthma in this model.

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“…Clinical and experimental research has demonstrated that inhalation of SVF may reduce inflammation in patients with ALI (28)(29)(30). SVF is a widely used anesthetic agent, and the protective effect of SVF under conditions of hypoxia or endotoxemia has been extensively studied (31).…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane attenuates ventilator‑induced lung injury by regulating c‑PLA2 expression

Yang

Wang

et al. 2018

Mol Med Report

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The aim of the present study was to investigate the potential role of club cell secretory protein (CCSP), an endogenous modulator, in reducing pulmonary inflammation induced by sevoflurane following one‑lung ventilation (OLV). Healthy Japanese white rabbits were randomly assigned to six groups: Sham‑operated group (group S); respiratory management of OLV group (group O); OLV + sevoflurane treated group (group OF), club cells exfoliated + sham‑operated group (group NA), club cells exfoliated + OLV group (group NAO); and club cells exfoliated + OLV + sevoflurane treated group (group NAOF). At the end of the experimental observation, all animals in the different groups were sacrificed and lung injury was evaluated according to the lung wet/dry weight ratio and histological scoring system. Lung homogenates were harvested to detect the mRNA and protein expression of cytosolic phospholipase A2 (c‑PLA2) and CCSP. The content of arachidonic acid was measured using an ELISA. Following OLV treatment, c‑PLA2 expression was increased, CCSP expression was decreased and lung injury scores were significantly increased. Sevoflurane inhalation in the OLV‑treated group induced an upregulation of CCSP and a downregulation of c‑PLA2 expression. In the group NAO, in which the club cells were simultaneously exfoliated, OLV caused more severe lung damage and induced higher expression of c‑PLA2 compared with that in group O. However, sevoflurane inhalation reduced the extent of lung injury and the expression of c‑PLA2, even when the endogenous modulator of lung inflammation, CCSP, was exfoliated (group NAOF). These results indicated that OLV promoted lung inflammation through the CCSP and c‑PLA2 pathway. However, the results from the club cells exfoliated group indicated that the CCSP may not be involved in the protective effect exerted by sevoflurane inhalation.

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Repeated inhalation of sevoflurane inhibits airway inflammation in an OVA‐induced mouse model of allergic airway inflammation

Cited by 11 publications

References 39 publications

Year in review 2015: Asthma and chronic obstructive pulmonary disease

Year in review 2015: Asthma and chronic obstructive pulmonary disease

Sevoflurane Inhibits the Th2 Response and NLRP3 Expression in Murine Allergic Airway Inflammation

Sevoflurane attenuates ventilator‑induced lung injury by regulating c‑PLA2 expression

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