Autoantibody of interleukin-17A induced by recombinant Mycobacterium smegmatis attenuates airway inflammation in mice with neutrophilic asthma

Chen Ling; Xu Wanting; Mao SongZhu RuochenZhang Jianhua

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Autoantibody of interleukin-17A induced by recombinant Mycobacterium smegmatis attenuates airway inflammation in mice with neutrophilic asthma

机译：Autoantibody of interleukin-17A induced by recombinant Mycobacterium smegmatis attenuates airway inflammation in mice with neutrophilic asthma

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Objective Previous studies have shown Interleukin (IL)-17A as an important contributor to the development of severe asthma, which is mainly characterized by neutrophilic inflammation and less response to corticosteroids. Consequently, the IL-17A-neutrophil axis could be a potential therapeutic target. Previously, we constructed a recombinant Mycobacterium smegmatis (rMS) expressing fusion protein Ag85A-IL-17A, and confirmed it could induce production of IL-17A autoantibody in vivo. This study uses a murine model of neutrophilic asthma to further investigate the effects of rMS on airway inflammation. Methods DO11.10 mice were divided into four groups: phosphate buffered saline (PBS), asthma, rMS and MS. This murine model of neutrophilic asthma was established with ovalbumin (OVA) challenge, whereby PBS, rMS and MS were administered intranasally. Anti-inflammatory effects on inflammatory cell infiltration and expression of inflammatory mediators in bronchoalveolar lavage fluid (BALF) were evaluated, along with histopathological changes in lung tissues. Results A sustained high-titer IL-17A autoantibody was detected in sera of the rMS group. Compared to the asthma group, the number of neutrophils, IL-17A, CXCL-1 levels and MPO activity in the rMS group were all significantly reduced (p < 0.01). Histological analysis showed rMS remarkably suppressed inflammatory infiltration around bronchia. The inflammation score and the mucus score in the rMS group were both significantly lower than those in the asthma group (p < 0.001). Conclusion rMS ameliorated airway inflammation in mice with neutrophilic asthma caused by inducing IL-17A autoantibody and regulating the IL-17A-neutrophil axis, thus offering a possible novel treatment for neutrophilic asthma.

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《The journal of asthma》 |2022年第10期|2117-2126|共10页
作者
Chen Ling; Xu Wanting; Mao SongZhu RuochenZhang Jianhua;
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作者单位

Shanghai Jiao Tong University,Shanghai Jiao Tong Univ Affiliated Peoples Hosp 6;

Shanghai Jiao Tong University,Shanghai Jiao Tong Univ;

Sch Med,Shanghai Jiao Tong Univ;

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正文语种英语
中图分类呼吸系及胸部疾病;
关键词
Asthma; autoantibody; IL-17A; neutrophil; Mycobacterium smegmatis; airway inflammation; RECEPTOR; IL-17; MECHANISMS; EXPRESSION; CELLS; BETA; HYPERRESPONSIVENESS; RESPONSES; IMMUNITY; LUNG;

Autoantibody of interleukin-17A induced by recombinant Mycobacterium smegmatis attenuates airway inflammation in mice with neutrophilic asthma

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