Table 1. List of the effect of adipokines in adipose tissue and airway cells.
Adipokine | Effect in adipose tissue | Effect in airway cells | References |
---|---|---|---|
Leptin | Increases lipolysis Promotes adipogenesis Causes the release of pro-inflammatory cytokines including IL-6 and TNFα |
Causes bronchodilation Increases production of chemokines and cytokines - Eotaxin, MCP-1, IL-8, IL-6 and CXCL10 |
[42,43] |
Adiponectin | Increases glucose uptake in fat cells Enhances adipogenesis and lipid storage |
Increases release of anti-inflammatory cytokine IL-10 Decreases release of pro-inflammatory IL-6 and TNFα |
[44] |
IL-6 | Increases leptin secretion and lipolysis Suppresses satiety signals, therefore increasing hunger |
Promotes ciliogenesis | [45,46] |
Resistin | Inhibits adiponectin secretion and induces lipolysis Activates innate immune response Regulates expression of PAI-1 |
Up-regulates mucin production | [39,47–49] |
TNFα | Causes mitochondrial dysfunction Alters adipokine production Induces lipolysis Impairs insulin signalling |
Induces apoptosis in cells infected by Legionella pneumophila | [50–54] |
Angiotensin | Activates Ca2+ signalling pathways Promotes adipocyte browning |
Angiotensin I converted into angiotensin II in lungs | [55,56] |
Visfatin | Involved in brown adipocyte thermogenesis and can decrease UCP-1 expression at high concentrations | Increases mucin production via activation of NF-κB pathway | [57,58] |
MCP-1 | Causes insulin resistance and recruits macrophages | Up-regulates mucin production through CCR2 receptor | [59,60] |
TGF-β1 | Regulates adipocyte browning | Induces PAI-1 expression in airway epithelial cells | [61,62] |
PAI-1 | Causes inflammation | Causes AHR, inflammation and remodelling | [63,64] |
IL-8 | Causes insulin resistance via inhibition of Akt phosphorylation | Increases Ca2+ release from airway smooth muscles cells, leads to constriction of airways | [65,66] |
IL-10 | Prevents adipocyte differentiation and lipid accumulation | Reduces airway inflammation and hyperresponsiveness | [67,68] |
IL-17α | Induced expression of TNFα, IL-6, IL-1β, leptin, and glucose transporter 4 | Causes bronchoconstriction and AHR | [69,70] |
IL-1β | Inhibits insulin signalling and glucose transport Increases lipolysis Increases inflammation |
Involved in airway cell migration | [71,72] |
Effect of adipokines on adipose tissue and airway cells which may lead to widespread systemic effects in disease. In adipose tissue, this may include increased inflammation, altered lipid and glucose homoeostasis and regulation of adipocyte browning. In airway cells, adipokines can control the inflammatory response, AHR, bronchoconstriction, bronchodilation and mucin production. In both cell types, these effects can lead to an exacerbation or relief from inflammatory diseases.
Abbreviations: CCR2, C–C chemokine receptor 2; CXCL10, C–X–C motif chemokine ligand 10; MCP-1, monocyte chemoattractant protein 1; NF-κB, nuclear factor κ-light-chain-enhancer of activated B cell; PAI-1, plasminogen activator inhibitor 1; TGF-β1, transforming growth factor β 1; UCP-1, uncoupling protein 1.