Relation between vitamin D deficiency and Pseudomonas aeruginosa colonization in patients with bronchiectasis

医学 铜绿假单胞菌 支气管扩张 殖民地化 微生物学 免疫学 内科学 细菌 遗传学 生物
作者
Yaoshen Wen,Ruoxuan Dai,Heng Yang,Jielu Lin,Rujia Tao,Ling Yang,Jin‐Fu Xu,Hai‐Wen Lu
出处
期刊:BMC Pulmonary Medicine [Springer Nature]
卷期号:25 (1)
标识
DOI:10.1186/s12890-025-03548-6
摘要

The relationship between vitamin D deficiency and Pseudomonas aeruginosa (P. aeruginosa) colonization in bronchiectasis patients is not well understood. This study was conducted at Shanghai Pulmonary Hospital from June 2014 to May 2018. Serum 25-hydroxyvitamin D levels were measured in patients with bronchiectasis, and clinical data including sputum culture results were collected. To investigate the relationship between vitamin D levels and P. aeruginosa colonization, we conducted correlation analysis and logistic regression. Additionally, in vitro experiments with bone marrow-derived macrophages (BMDMs) infected with P. aeruginosa strain PAO1 were performed to further explore the influence of vitamin D on the bacterial infection and inflammatory response. Among the 195 patients with bronchiectasis, 83.1% (162/195) were vitamin D deficient. A significant negative correlation was observed between serum vitamin D levels and the BSI (Bronchiectasis Severity Index) score. Patients with vitamin D deficiency showed higher rates of P. aeruginosa colonization compared to those with adequate vitamin D levels. Female gender and vitamin D deficiency were identified as risk factors for P. aeruginosa colonization in patients with bronchiectasis. Additionally, serum interleukin (IL)-1β levels were significantly elevated in the vitamin D-deficiency group. In vitro experiments, 1,25-dihydroxyvitamin D [1,25D] was shown to inhibit PAO1 phagocytosis in BMDMs and to suppress IL-1β secretion. Vitamin D deficiency was strongly associated with an increased risk of P. aeruginosa colonization in patients with bronchiectasis. Furthermore, vitamin D demonstrated protective effects by reducing P. aeruginosa survival in cells and modulating the inflammatory dysregulation induced by the bacterium.
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