Epidemiological evidence establishes obesity as an independent risk factor for increased susceptibility and severity to viral respiratory pneumonias associated with H1N1 influenza and SARS-CoV-2 pandemics. Given the global obesity prevalence, a better understanding of the mechanisms behind obese susceptibility to infection is imperative. Altered immune cell metabolism and function are often perceived as a key causative factor of dysregulated inflammation. However, the contribution of adipocytes, the dominantly altered cell type in obesity with broad inflammatory properties, to infectious disease pathogenesis remains largely ignored. Thus, skewing of adipocyte-intrinsic cellular metabolism may lead to the development of pathogenic inflammatory adipocytes, which shape the overall immune responses by contributing to either premature immunosenescence, delayed hyperinflammation, or cytokine storm in infections. In this review, we discuss the underappreciated contribution of adipocyte cellular metabolism and adipocyte-produced mediators on immune system modulation and how such interplay may modify disease susceptibility and pathogenesis of influenza and SARS-CoV-2 infections in obese individuals.

流行病学证据表明，肥胖是增加与 H1N1 流感和 SARS-CoV-2 大流行相关的病毒性呼吸道肺炎的易感性和严重性的独立危险因素。鉴于全球肥胖流行，必须更好地了解肥胖对感染易感性背后的机制。改变的免疫细胞代谢和功能通常被认为是炎症失调的关键致病因素。然而，脂肪细胞（肥胖症中主要改变的细胞类型，具有广泛的炎症特性）对传染病发病机制的贡献在很大程度上仍被忽视。因此，脂肪细胞内在细胞代谢的偏差可能导致致病性炎症脂肪细胞的发展，其通过促进过早免疫衰老来塑造整体免疫反应，延迟的过度炎症，或感染中的细胞因子风暴。在这篇综述中，我们讨论了脂肪细胞细胞代谢和脂肪细胞产生的介质对免疫系统调节的未被充分认识的贡献，以及这种相互作用如何改变肥胖个体的流感和 SARS-CoV-2 感染的疾病易感性和发病机制。