Abstract
Obesity becomes pandemic, predisposing these individuals to great risk for lung injury. In this review, we focused on the anti-inflammatories and addressed the following aspects: adipocytokines and obesity, inflammation and other mechanisms, adipocytokines and lung injury in obesity bridged by inflammation, and potential therapeutic targets. To sum up, the majority of evidence supported that adiponectin, omentin, and secreted frizzled-related protein 5 (SFRP5) were reduced significantly in obesity, which is associated with increased inflammation, indicated by increase of TNFα and IL-6, through activation of toll-like receptor (TLR4) and nuclear factor light chain κB (NF-κB) signaling pathways. Administration of these adipocytokines promotes weight loss and reduces inflammation. Zinc-α2-glycoprotein (ZAG), vaspin, IL-10, interleukin-1 receptor antagonist (IL-1RA), transforming growth factor β (TGF-β1), and growth differentiation factor 15 (GDF15) are also regarded as anti-inflammatories. There were controversial reports. Furthermore, there is a huge lack of studies for obesity related lung injury. The effects of adiponectin on lung transplantation, asthma, chronic obstructive pulmonary diseases (COPD), and pneumonia were anti-inflammatory and protective in lung injury. Administration of IL-10 agonist reduces mortality of acute lung injury in rabbits with acute necrotizing pancreatitis, possibly through inhibiting proinflammation and strengthening host immunity. Very limited information is available for other adipocytokines.
Highlights
One-third of the adult Americans are obese and 2/3 are overweight [1, 2]
This may be associated with activation and polarization of macrophages, stimulation of AMPK and COX2, and its effect on endothelium [71, 72]
Interleukin-1 receptor antagonist (IL-1RA) was secreted naturally to encounter the effect of IL-1 and neutralize the proinflammatory effect of IL-1β, by competitively binding to IL-1 receptor I (IL-1RI). As it secrets at the time of IL-1 secretion, which is generally increased at the states of inflammation such as obesity, T2DM, and lung injury, it is understandable that interleukin-1 receptor antagonist (IL-1RA) is elevated in obese and diabetic subjects in Whitehall II cohorts [151] and a few other clinical trials
Summary
One-third of the adult Americans are obese and 2/3 are overweight [1, 2]. Obesity increases histrionically and is becoming pandemic worldwide in the past decades, predisposing these populations to great risk for gastric esophageal reflux disease (GERD) and subsequent aspiration pneumonia, asthma, obstructive sleep apnea syndrome (OSAS), and related comorbidities and mortality in lung injury, such as acute lung injury (ALI) and ARDS (acute/adult respiratory distress syndrome), even after being adjusted for other risk factors [3,4,5,6]. Recent data supported that obesity is a major risk factor for lung injury, and the adipose tissue derived adipokines and cytokines seem to play a very important role during this process [66,67,68,69,70] This may be associated with activation and polarization of macrophages, stimulation of AMPK and COX2, and its effect on endothelium [71, 72]. Some studies [132, 133] revealed higher ZAG level in serum and white adipose tissue of obese/overweight individuals, as well as patients with chronic kidney disease, suggesting a possibility of “ZAG resistance,” like leptin resistance It appeared that ZAG exerts its function as a lipid mobilizer in cancer cachexia more significantly. Related clinical trials are highly recommended to further define this, its bioactivity, safety, efficacy, and therapeutic indications
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