Role of Leptin in the Association Between Body Adiposity and Persistent Asthma: A Longitudinal Study

Li, Zhen; Leynaert, Bénédicte; Dumas, Orianne; Gil, Oscar Diaz; Garcia‐Aymerich, Judith; Colomer, Montserrat Fitó; Moual, Nicole Le; Pison, Christophe; Romieu, Isabelle; Siroux, Valérie; Camargo, Carlos A.; Varraso, Raphäelle; Nadif, Rachel

doi:10.1002/oby.22466

Cited by 14 publications

(9 citation statements)

References 22 publications

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“…One study found an association between serum leptin levels and asthma control assessed by the Asthma Control Questionnaire (ACQ) [169]. The second recent longitudinal study reported an indirect effect mediated by leptin in the association between adiposity and persistent asthma [170]. Collectively, these results support that leptin may be a mediator that contributes to explain the association between obesity and both asthma persistence and control (Figure 1).…”

Section: Adipokinesmentioning

confidence: 80%

Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation

Bantulà

Roca‐Ferrer

Arismendi

et al. 2021

JCM

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Asthma and obesity are two epidemics affecting the developed world. The relationship between obesity and both asthma and severe asthma appears to be weight-dependent, causal, partly genetic, and probably bidirectional. There are two distinct phenotypes: 1. Allergic asthma in children with obesity, which worsens a pre-existing asthma, and 2. An often non allergic, late-onset asthma developing as a consequence of obesity. In obesity, infiltration of adipose tissue by macrophages M1, together with an increased expression of multiple mediators that amplify and propagate inflammation, is considered as the culprit of obesity-related inflammation. Adipose tissue is an important source of adipokines, such as pro-inflammatory leptin, produced in excess in obesity, and adiponectin with anti-inflammatory effects with reduced synthesis. The inflammatory process also involves the synthesis of pro-inflammatory cytokines such as IL-1β, IL-6, TNFα, and TGFβ, which also contribute to asthma pathogenesis. In contrast, asthma pro-inflammatory cytokines such as IL-4, IL-5, IL-13, and IL-33 contribute to maintain the lean state. The resulting regulatory effects of the immunomodulatory pathways underlying both diseases have been hypothesized to be one of the mechanisms by which obesity increases asthma risk and severity. Reduction of weight by diet, exercise, or bariatric surgery reduces inflammatory activity and improves asthma and lung function.

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Section: Adipokinesmentioning

confidence: 80%

Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation

Bantulà

Roca‐Ferrer

Arismendi

et al. 2021

JCM

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“…Increased leptin and IL-6 levels in asthma patients have recently been identified in several studies, strengthening the link of these pro-inflammatory cytokines with airway inflammation in asthma [ 63 – 65 ].…”

Section: Adipose Tissue and Inflammationmentioning

confidence: 99%

Obesity, Inflammation, and Severe Asthma: an Update

Sharma

Cowan

2021

Curr Allergy Asthma Rep

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Purpose of Review Obesity-associated difficult asthma continues to be a substantial problem and, despite a move to address treatable traits affecting asthma morbidity and mortality, it remains poorly understood with limited phenotype-specific treatments. The complex association between asthma, obesity, and inflammation is highlighted and recent advances in treatment options explored. Recent Findings Obesity negatively impacts asthma outcomes and has a causal link in the pathogenesis of adult-onset asthma. Imbalance in the adipose organ found in obesity favours a pro-inflammatory state both systemically and in airways. Obesity may impact currently available asthma biomarkers, and obesity-associated asthma specific biomarkers are needed. Whilst surgical weight loss interventions are associated with improvements in asthma control and quality of life, evidence for pragmatic conservative options are sparse. Innovative approaches tackling obesity-mediated airway inflammation may provide novel therapies. Summary The immunopathological mechanisms underlying obesity-associated asthma require further research that may lead to novel therapeutic options for this disease. However, weight loss appears to be effective in improving asthma in this cohort and focus is also needed on non-surgical treatments applicable in the real-world setting.

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“…Using a newly developed analytic method, a longitudinal study from France demonstrated that leptin is an important factor mediating the association between high body mass index (BMI) and persistent asthma over time (16). Through collecting bronchoalveolar lavage (BAL) by bronchoscopy from lean and obese asthmatics and controls, Holguin et al (17) demonstrated that increases of the BMI were positively associated with the concentration of leptin in BAL fluid (BALF).…”

Section: Introductionmentioning

confidence: 99%

Regulatory effect of mitoQ on the mtROS‑NLRP3 inflammasome pathway in leptin‑pretreated BEAS‑2 cells

Lei

Zhu

et al. 2021

Exp Ther Med

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Obese asthma is a phenotype of asthma whose occurrence is gradually increasing in both adults and children. The majority of studies have demonstrated that obesity is a major risk factor for asthma and the effect of obesity on the lungs is considerable. NOD-, LRR-and pyrin domain-containing protein 3 (NLRP3) inflammasome has been previously demonstrated to serve a role in obese asthma mediated by mitochondrial reactive oxygen species (mtROS). The aim of the present in vitro study was to investigate the effect of leptin on airway epithelial cells and the protective effect of the mitochondrial-targeted antioxidant mitoquinone (mitoQ). Human normal bronchial epithelial cell lines BEAS-2 cells were used and divided into 6 groups: Control group (negative control), DMSO group (solvent control), lipopolysaccharide (LPS) group (positive control), LPS + mitoQ group, Leptin group and Leptin + mitoQ group. CCK8 assay was used to establish the optimal concentration and incubation time of the drugs. mitoTracker probe and mitoSOX reagent were used to detect the integrity of mitochondrial membranes and the content of mtROS. mRNA expression levels were detected by reverse transcription-quantitative PCR analysis. It was revealed that the mitochondrial membrane was disrupted in the Leptin group, which recovered after treatment with mitoQ. As a result, the production of mitochondrial reactive oxygen species (mtROS) in the Leptin group was significantly increased (P<0.01), but following treatment with mitoQ, this overproduction of mtROS was significantly decreased to normal levels (P<0.01). Furthermore, the expression levels of NOD-, LRR-and pyrin domain-containing protein 3 NLRP3 and caspase-1 mRNA in the leptin-pretreated BEAS-2 cells were significantly increased compared with those in the control group (P<0.01), while they were decreased following mitoQ treatment (P<0.01). Taken together, these data suggested that leptin may promote airway inflammation partially through upregulating the mtROS-NLRP3 inflammasome signaling pathway in airway epithelial cells and mitoQ may be a potential treatment for obese asthma.

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Role of Leptin in the Association Between Body Adiposity and Persistent Asthma: A Longitudinal Study

Cited by 14 publications

References 22 publications

Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation

Asthma and Obesity: Two Diseases on the Rise and Bridged by Inflammation

Obesity, Inflammation, and Severe Asthma: an Update

Regulatory effect of mitoQ on the mtROS‑NLRP3 inflammasome pathway in leptin‑pretreated BEAS‑2 cells

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