Adipokine adiponectin is a potential protector to human bronchial epithelial cell for regulating proliferation, wound repair and apoptosis: Comparison with leptin and resistin

Zhu, Xiao Lin; Qin, Xiao; Xiang, Yang; Tan, Yu; Qu, Xiang Pin; Liu, Hui Jun

doi:10.1016/j.peptides.2012.11.017

Cited by 21 publications

(19 citation statements)

References 30 publications

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“…Adiponectin is another important adipokine secreted by the adipocytes, levels of which have been reported to be lower in obese patients and to have an anti-inflammatory role, as previously mentioned. It has been reported that human bronchial epithelial cells are also capable of expressing adiponectin; in these cells, adiponectin probably acts as an endogenous repair promoter, antioxidant, and anti-apoptotic agent against ozone [ 33 ]. In the asthma context, it appears that adiponectin does not protect against the development of inflammation, and may in fact exacerbate the disease via its anti-Th1 inflammatory effects, allowing for increased Th2 differentiation and a more severe allergic response [ 34 ].…”

Section: Resultsmentioning

confidence: 99%

“…In the asthma context, it appears that adiponectin does not protect against the development of inflammation, and may in fact exacerbate the disease via its anti-Th1 inflammatory effects, allowing for increased Th2 differentiation and a more severe allergic response [ 34 ]. Although an association between adiponectin and pulmonary function has been described, there is conflicting data regarding the relationship between adiponectin levels and the presence of asthma, indicating that serum levels may not accurately reflect levels of adiponectin in the lungs [ 33 ]. The visceral adipose tissue of asthmatic-obese patients had significantly lower adiponectin at the time of bariatric surgery, while 12 months after the surgery the levels tended to be higher in subcutaneous adipose tissue [ 22 ].…”

Section: Resultsmentioning

confidence: 99%

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Obesity and Asthma: A Missing Link

Gomez-Llorente

Romero

Chueca

et al. 2017

IJMS

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Obesity and asthma are two chronic conditions that affect millions of people. Genetic and lifestyle factors such as diet, physical activity, and early exposure to micro-organisms are important factors that may contribute to the escalating prevalence of both conditions. The prevalence of asthma is higher in obese individuals. Recently, two major phenotypes of asthma with obesity have been described: one phenotype of early-onset asthma that is aggravated by obesity, and a second phenotype of later-onset asthma that predominantly affects women. Systemic inflammation and mechanical effect, both due to the expansion of the adipose tissue, have been proposed as the main reasons for the association between obesity and asthma. However, the mechanisms involved are not yet fully understood. Moreover, it has also been suggested that insulin resistance syndrome can have a role in the association between these conditions. The intestinal microbiota is an important factor in the development of the immune system, and can be considered a link between obesity and asthma. In the obese state, higher lipopolysaccharide (LPS) serum levels as a consequence of a microbiota dysbiosis have been found. In addition, changes in microbiota composition result in a modification of carbohydrate fermentation capacity, therefore modifying short chain fatty acid (SCFA) levels. The main objective of this review is to summarize the principal findings that link obesity and asthma.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Obesity and Asthma: A Missing Link

Gomez-Llorente

Romero

Chueca

et al. 2017

IJMS

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show abstract

“…Although the more common T H 2 activation-dependent asthma phenotype leads to airway eosinophilia, asthma can also involve airway neutrophilic inflammation, which in turn is clinically important, as most severe forms of asthma involve elevated neutrophil levels and sputum neutrophils negatively correlate with lung function [48,49,21]. Furthermore, adiponectin may also work as a protective anti-apoptotic agent against bronchial epithelium injury caused by ozone exposure [50].…”

Section: Adiponectin and Its Protective Role In Asthmamentioning

confidence: 99%

Obesity and asthma: beyond TH2 inflammation

2015

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“…Adiponectin can also induce effects in a receptor-independent fashion. Multiple cell types in the lung express adiponectin binding proteins, including the bronchial epithelium [ 31 , 32 ], airway smooth muscle [ 33 ], and pulmonary vasculature [ 34 , 35 ]. Expression of AdipoR2 and T-cadherin mRNA by bronchial epithelial cells is greater among obese patients with asthma than obese controls [ 36 ].…”

Section: Adiponectinmentioning

confidence: 99%

“…Because several S1P receptors with diverse effects exist, it is conceivable that the seemingly contradictory pro- and anti-inflammatory effects of adiponectin result from stimulus and cell-type specific differences in the expression of S1P receptors. It has not been determined whether adiponectin couples to ceramidase activity in the lungs, but adiponectin does inhibit apoptosis in bronchial epithelial cells [ 32 ], and loss of such antiapoptotic effects may explain why adiponectin deficient mice develop emphysema-like changes as they age [ 40 ]. Moreover, adiponectin induced effects in bronchial epithelial cells include augmented wound healing and proliferation as well as IL-8 release [ 31 , 32 ].…”

Section: Adiponectinmentioning

confidence: 99%

Adiponectin, Leptin, and Resistin in Asthma: Basic Mechanisms through Population Studies

2013

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Adipokines, factors produced by adipose tissue, may be proinflammatory (such as leptin and resistin) or anti-inflammatory (such as adiponectin). Effects of these adipokines on the lungs have the potential to evoke or exacerbate asthma. This review summarizes basic mechanistic data through population-based and clinical studies addressing the potential role of adipokines in asthma. Augmenting circulating concentrations of adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. Murine data is supported by human data that suggest that low serum adiponectin is associated with greater risk for asthma among women and peripubertal girls. Further, higher serum total adiponectin may be associated with lower clinical asthma severity among children and women with asthma. In contrast, exogenous administration of leptin results in augmented allergic airway hyperresponsiveness in mice. Alveolar macrophages obtained from obese asthmatics are uniquely sensitive to leptin in terms of their potential to augment inflammation. Consistent with this basic mechanistic data, epidemiologic studies demonstrate that higher serum leptin is associated with greater asthma prevalence and/or severity and that these associations may be stronger among women, postpubertal girls, and prepubertal boys. The role of adipokines in asthma is still evolving, and it is not currently known whether modulation of adipokines may be helpful in asthma prevention or treatment.

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Adipokine adiponectin is a potential protector to human bronchial epithelial cell for regulating proliferation, wound repair and apoptosis: Comparison with leptin and resistin

Cited by 21 publications

References 30 publications

Obesity and Asthma: A Missing Link

Obesity and Asthma: A Missing Link

Obesity and asthma: beyond TH2 inflammation

Adiponectin, Leptin, and Resistin in Asthma: Basic Mechanisms through Population Studies

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