Bantulà, MarinaTubita, ValeriaRoca Ferrer, JordiMullol i Miret, JoaquimValero, AntonioBobolea, IrinaPascal i Capdevila, MarionaHollanda Ramírez, Ana M. deVidal, JosepPicado Vallés, CésarArismendi, Ebymar2023-06-212023-06-212022-06-292077-0383https://hdl.handle.net/2445/199582Obesity and asthma are associated with systemic inflammation maintained by mediators released by adipose tissue and lung. This study investigated the inflammatory serum mediator profile in obese subjects (O) (n = 35), non-obese asthma (NOA) patients (n = 14), obese asthmatics (OA) (n = 21) and healthy controls (HC) (n = 33). The effect of weight loss after bariatric surgery (BS) was examined in 10 OA and 31 O subjects. We analyzed serum markers including leptin, adiponectin, TGF-?1, TNFR2, MCP-1, ezrin, YKL-40, ST2, IL-5, IL-9, and IL-18. Compared with HC subjects, the O group showed increased levels of leptin, TGF-?1, TNFR2, MCP-1, ezrin, YKL-40, and ST2; the OA group presented increased levels of MCP-1, ezrin, YKL-40, and IL-18, and the NOA group had increased levels of ezrin, YKL-40, IL-5, and IL-18. The higher adiponectin/leptin ratio in NOA with respect to OA subjects was the only significant difference between the two groups. IL-9 was the only cytokine with significantly higher levels in OA with respect to O subjects. TNFR2, ezrin, MCP-1, and IL-18 concentrations significantly decreased in O subjects after BS. O, OA, and NOA showed distinct patterns of systemic inflammation. Leptin and adiponectin are regulated in asthma by obesity-dependent and-independent mechanisms. Combination of asthma and obesity does not result in significant additive effects on circulating cytokine levels. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.19 p.application/pdfengcc by (c) Bantulà, Marina et al, 2022http://creativecommons.org/licenses/by/3.0/es/AsmaObesitatAsthmaObesityinfo:eu-repo/semantics/article2023-06-20info:eu-repo/semantics/openAccess933062035807067