Cytokines and Obstructive Sleep Apnea in Childhood: Study of a Group of Children

first_pagesettingsOrder Article Reprints Open AccessArticle Cytokines and Obstructive Sleep Apnea in Childhood: Study of a Group of Children by Luana Maria Nosetti 1ORCID,Claudio Tirelli 2,*ORCID,Franca Marino 1,3ORCID,Michela Gaiazzi 1,Lucia Sacchi 4ORCID,Mara De Amici 5,Fiorella Barocci 6ORCID,Ramona Maio 1,Marco Cosentino 3ORCID andLuigi Nespoli 7,* 1 Department of Clinical and Experimental Medicine, University of Insubria, 21100 Varese, Italy 2 Pulmonology Unit, ASST Santi Paolo e Carlo, Department of Health Sciences, University of Milan, 20122 Milan, Italy 3 Center of Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy 4 Department of Electrical, Computer and Biomedical Engineering, University of Pavia, 27100 Pavia, Italy 5 Immuno-Allergology Laboratory of the Clinical Chemistry Unit, Pediatric Clinic Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy 6 Formerly Medicine Unit Laboratory, ASST Rhodense Garbagnate Milanese, 20024 Rho, Italy 7 Clinic of Pediatrics, University of Insubria, 21100 Varese, Italy * Authors to whom correspondence should be addressed. Biologics 2024, 4(1), 44-54; https://doi.org/10.3390/biologics4010004 Submission received: 24 October 2023 / Revised: 22 January 2024 / Accepted: 24 January 2024 / Published: 1 February 2024 (This article belongs to the Section Cytokines and Allied Mediators) Downloadkeyboard_arrow_down Browse Figure Versions Notes Abstract Introduction: Obstructive Sleep Apnea (OSA) in children is characterized by repeated episodes of partial or complete obstruction of the upper airways that impair normal ventilation and cause hypoxia and sleep disruption. These episodes activate innate and adaptive immunity resulting in the production of proinflammatory cytokines: IL-1β, IL-6, TNF-α, and reactive oxygen species. The hypothalamic–pituitary–adrenal (HPT) axis is also activated with alteration of the circadian rhythm of cortisol synthesis. OSA in children, and even more in adults, induces a systemic inflammatory condition that contributes to the genesis of clinical complications: poor growth, learning disabilities, cardiovascular changes, insulin resistance, and metabolic syndrome. Methods: A total of 42 non-obese children (age 1–15 years) were enrolled among those sent to our sleep center to perform full polysomnography (PSG). After PSG, 6 children did not show OSA (controls), 20 had mild OSA (m OSA), and 16 had medium-severe OSA (MS OSA). In vitro IL-1β, TNF-α, and serum cortisol levels were measured at 2 and 8 am in the analyzed groups. Results: Cortisol levels did not differ between controls and OSA children. At 2 am, there were no differences between controls and OSA in TNF-α production, whereas at 8 am, TNF-α was reduced in MS-OSA. IL-1β production showed no differences between OSA and controls. Conclusions: In our population, only TNF-α production is suppressed in MS-OSA: this might indicate a role of OSA severity in inducing inflammation. In adults, the phenomenon is more pronounced due to the habitual greater severity/duration of OSA, presence of comorbidities (cardiovascular and metabolic), and different immune system function.