Department of Health Security, National Institute for Health and Welfare, Kuopio, Finland.
ISGlobal, Barcelona Institute for Global Health - Campus MAR, Barcelona, Spain.
Indoor Air. 2018 May;28(3):450-458. doi: 10.1111/ina.12454. Epub 2018 Mar 24.
Cross-sectional studies have shown that exposure to indoor moisture damage and mold may be associated with subclinical inflammation. Our aim was to determine whether early age exposure to moisture damage or mold is prospectively associated with subclinical systemic inflammation or with immune responsiveness in later childhood. Home inspections were performed in children's homes in the first year of life. At age 6 years, subclinical systemic inflammation was measured by serum C-reactive protein (CRP) and blood leukocytes and immune responsiveness by ex vivo production of interleukin 1-beta (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α) in whole blood cultures without stimulation or after 24 hours stimulation with phorbol 12-myristate 13-acetate and ionomycin (PI), lipopolysaccharide (LPS), or peptidoglycan (PPG) in 251-270 children. Moisture damage in child's main living areas in infancy was not significantly associated with elevated levels of CRP or leukocytes at 6 years. In contrast, there was some suggestion for an effect on immune responsiveness, as moisture damage with visible mold was positively associated with LPS-stimulated production of TNF-α and minor moisture damage was inversely associated with PI-stimulated IL-1β. While early life exposure to mold damage may have some influence on later immune responsiveness, it does not seem to increase subclinical systemic inflammation in later life.
横断面研究表明,室内潮湿损坏和霉菌暴露可能与亚临床炎症有关。我们的目的是确定儿童生命的第一年暴露于潮湿损坏或霉菌是否与亚临床系统性炎症或后期儿童的免疫反应性相关。在儿童的家中进行了家庭检查。在 6 岁时,通过血清 C 反应蛋白(CRP)和血液白细胞来测量亚临床系统性炎症,并通过全血培养中白细胞介素 1-β(IL-1β)、IL-6 和肿瘤坏死因子α(TNF-α)的体外产生来测量免疫反应性,在没有刺激或用佛波醇 12-肉豆蔻酸 13-乙酸盐和离子霉素(PI)、脂多糖(LPS)或肽聚糖(PPG)刺激 24 小时后,在 251-270 名儿童中进行。婴儿期儿童主要生活区域的潮湿损坏与 6 岁时 CRP 或白细胞升高水平没有显著相关性。相比之下,对于免疫反应性,存在一些影响的迹象,因为有可见霉菌的潮湿损坏与 LPS 刺激的 TNF-α产生呈正相关,而轻微的潮湿损坏与 PI 刺激的 IL-1β呈负相关。虽然早期生活中暴露于霉菌损坏可能对后期的免疫反应性有一定影响,但它似乎不会增加后期生活中的亚临床系统性炎症。