Abstract

Adiponectin is an adipokine associated with the healthy obese phenotype. Adiponectin increases insulin sensitivity and has cardio and vascular protection actions. Studies related to adiponectin, a modulator of the innate and acquired immunity response, have suggested a role of this molecule in asthma. Studies based on various asthma animal models and on the key cells involved in the allergic response have provided important insights about this relation. Some of them indicated protection and others reversed the balance towards negative effects. Many of them described the cellular pathways activated by adiponectin, which are potentially beneficial for asthma prevention or for reduction in the risk of exacerbations. However, conclusive proofs about their efficiency still need to be provided. In this article, we will, briefly, present the general actions of adiponectin and the epidemiological studies supporting the relation with asthma. The main focus of the current review is on the mechanisms of adiponectin and the impact on the pathobiology of asthma. From this perspective, we will provide arguments for and against the positive influence of this molecule in asthma, also indicating the controversies and sketching out the potential directions of research to complete the picture.

Highlights

  • IntroductionAsthma is a clinical diagnosis that covers a variety of phenotypes and endotypes

  • Asthma is a clinical diagnosis that covers a variety of phenotypes and endotypes.In the continuous effort towards personalized medicine, remarkable progress has been made to characterize the specific pathobiological marker or mechanism which best defines specific endotypes.The association between obesity and some difficult to treat forms of asthma raised the possibility of low-grade inflammation, impaired metabolism and dysfunctional adipose tissue secretion as pathogenic mechanisms

  • Depend on the polarization of the cell; in M1 macrophages, ADPN triggers the expression of proinflammatory cytokines (IL-6, TNFα, IL-12), whereas in M2 macrophages it induces the expression of IL-10 [35,36] and IL-1 receptor antagonist [37]

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Summary

Introduction

Asthma is a clinical diagnosis that covers a variety of phenotypes and endotypes. The association between obesity and some difficult to treat forms of asthma raised the possibility of low-grade inflammation, impaired metabolism and dysfunctional adipose tissue secretion as pathogenic mechanisms. Adipocytes have a large secretion panel including molecules with dual function in metabolism and in the modulation of inflammation. An excess of adipose tissue has deleterious effects as hyperinsulinemia, which increases airway hyperreactivity, shifts T lymphocytes to the Th2-type response and promotes mast cell degranulation and airway remodeling [1]. Among the numerous molecules secreted by adipocytes, adiponectin (ADPN) is associated with the healthy obese phenotype. ADPN increases sensitivity to insulin, has cardio and vascular protection actions and modulates immune responses. We will evaluate this possibility by examining pro and con arguments

General Considerations
Main Roles of ADPN
Mechanism of Action
Circulating ADPN
Epidemiological Studies
Main Results
Main Results de Lima
Dysfunctional Airway Epithelium
Hyperresponsiveness of the Airway Smooth Muscle
Enhanced Mucus Hypersecretion
Inflammation and Immune Response
43 M2 markers
Airway Remodeling
Vascular Modifications
Reduction in Respiratory Muscle Strength
Obesity-Related Asthma
Conclusions
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