Leptin and resistin in overweight patients with and without asthma

Muc, Magdalena; Todo-Bom, Ana; Mota-Pinto, Anabela; Vale-Pereira, Sofia; Loureiro, Carlos

doi:10.1016/j.aller.2013.03.004

Cited by 22 publications

(19 citation statements)

References 20 publications

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“…18,23 Importantly, BALB/c mice are prone to develop allergic-like Th2 immune responses, 24 being more adequate for asthma models. In addition, clinical studies have demonstrated that obesity worsens asthma symptoms in women; 10,12,25 therefore the present study was developed in a female model. We have shown that mice fed an HFD not only gained more weight than mice fed a standard diet ( Fig.…”

Section: Hfd Efficiently Induces Obesitymentioning

confidence: 99%

Obesity affects peripheral lymphoid organs immune response in murine asthma model

et al. 2019

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Summary Asthma and obesity present rising incidence, and their concomitance is a reason for concern, as obese individuals are usually resistant to conventional asthma treatments and have more exacerbation episodes. Obesity affects several features in the lungs during asthma onset, shifting the T helper type 2 (Th2)/eosinophilic response towards a Th17/neutrophilic profile. Moreover, those individuals can present reduced atopy and delayed cytokine production. However, the impact of obesity on follicular helper T (Tfh) cells and B cells that could potentially result in antibody production disturbances are still unclear. Therefore, we aimed to assess the peripheral response to ovalbumin (OVA) in a concomitant model of obesity and asthma. Pulmonary allergy was induced, in both lean and obese female BALB/c mice, through OVA sensitizations and challenges. Mediastinal lymph nodes (MLNs) and spleen were processed for immunophenotyping. Lung was used for standard allergy analysis. Obese‐allergic mice produced less anti‐OVA IgE and more IgG2a than lean‐allergic mice. Dendritic cells (CD11c+ MHCIIhigh) expressed less CD86 and more PDL1 in obese‐allergic mice compared with lean‐allergic mice, in the MLNs. Meanwhile, B cells (CD19+ CD40+) were more frequent and the amount of PDL1/PD1+ cells was diminished by obesity, with the opposite effects in the spleen. Tfh cells (CD3+ CD4+ CXCR5+ PD1+) expressing FoxP3 were more frequent in obese mice, associated with the predominance of Th (CD3+ CD4+) cells expressing interleukin‐4/GATA3 in the MLNs and interleukin‐17A/RORγT in the spleen. Those modifications to the main components of the germinal centers could be resulting in the increased IgG2a production, which – associated with the Th17/neutrophilic profile – contributes to asthma worsening and represents an important target for future treatment strategies.

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Section: Hfd Efficiently Induces Obesitymentioning

confidence: 99%

Obesity affects peripheral lymphoid organs immune response in murine asthma model

et al. 2019

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“…Adipokines regulate energy homeostasis through hunger and satiety control (96,97) . Some adipokines such as leptin or resistin are produced in excess in obesity (98) , while others, such as adiponectin and ghrelin are reduced. This imbalance promotes pro-inflammatory responses and leads to inflammation (99)(100)(101) .…”

Section: Possible Linksmentioning

confidence: 99%

“…Surely, some part of the link can be explained by overestimation due to fat mass on the thoracic chest mimicking asthma symptoms (65) ; part of the weight increase may also be due to medication or decreased activity caused by exercise-induced wheezing attacks, resulting in reverse causation (61) . There is no doubt that the endocrine role of adipose tissue (adipokines) is a strong physiological link and very plausibly could be a mechanism in causing a chain of disruption leading to inflammation and narrowing of airways (98,(105)(106)(107) . Despite existing evidence indicating that adipokines may be a plausible link between obesity and asthma, clinical studies bring inconclusive results.…”

Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

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“…Although the levels of both adipokines were higher in patients with overweight and asthma as compared to healthy overweight subjects, these differences were not significant. Patients with and without asthma and overweight (BMI ≥ 25) and with an increased waist circumference showed a higher level of leptin [17].…”

Section: Reviewmentioning

confidence: 99%

The role of adipokines in the pathogenesis and course of selected respiratory diseases

Chwalba¹,

Machura²,

Ziora³

et al. 2019

Endokrynologia Polska

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Adipose tissue is also a secretory organ producing active substances called adipokines. Some of them (apelin, resistin, adiponectin, leptin, chemerin, or visfatin) may play a role in the pathogenesis and course of respiratory diseases, e.g. COPD, asthma, pulmonary hypertension, or lung cancer. There are limited and conflicting data on the role of adipokines in asthma. It has been confirmed, however, that visfatin and leptin can be markers of inflammation in COPD. Elevated concentrations of leptin and resistin play a pro-inflammatory role in the development of cancer cachexia. The role of adipokines has also been demonstrated in pulmonary hypertension, and the apelinadiponectin axis disruption may exacerbate pulmonary hypertension.

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Leptin and resistin in overweight patients with and without asthma

Cited by 22 publications

References 20 publications

Obesity affects peripheral lymphoid organs immune response in murine asthma model

Obesity affects peripheral lymphoid organs immune response in murine asthma model

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

The role of adipokines in the pathogenesis and course of selected respiratory diseases

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