Purpose: The relationship between asthma and obesity is well established, although the pathophysiological mechanisms linking both diseases remain unknown. Adiponectin is a hormone secreted by adipose cells, plays a role in the modulation of inflammation and may be the key linking these two types of inflammation.
Methods: We conducted a cross-sectional study with asthma with different body mass indices (BMI); the patients were classified as eutrophic, overweight, or obese. We assessed disease control using the GINA consensus, and the levels of adiponectin, C-reactive protein (CRP) and interleukin 33 (IL-33) in each of the patients.
Results: We evaluated 75 of the 96 patients eligible for the study, including 25 in each BMI group. The CRP levels were significantly higher in the obese patients compared with both the eutrophic (p = 0.01) and the overweight (p = 0.03) patients. The mean adiponectin level was 21.82 ± 9.93 mg/L for the eutrophic asthmatics, which is a level that was significantly higher than in the overweight (15.31 ± 6.27 mg/L, p = 0.0140) and the obese (16.69 ± 11.45 mg/L, p = 0.0287) patients. The patients with higher adiponectin levels exhibited smaller FEV1 (p = 0.02) and lower FVC (p = 0.003). The IL-33 levels were not different between the groups.
Conclusions: Adiponectin does not protect against the development of inflammation in the setting of asthma and may in fact exacerbate the disease via its anti-TH1 inflammatory effects, allowing for increased TH2 differentiation and a more severe allergic response.
Keywords: Adiponectin; Asthma; Interleukin 33; Obesity; TH2 inflammation.