Rodríguez-Herrera Andrea Jazel, Setembre Batah Sabrina, Faci do Marco Maria Júlia, González-Zambrano Carlos Mario, Dias-Melicio Luciane Alarcão, Fabro Alexandre Todorovic
Department of Pathology and Forensic Medicine, Ribeirão Preto Medical School (FMRP), University of São Paulo (USP), Ribeirão Preto 14049-900, SP, Brazil.
Laboratory of Immunopathology and Infectious Agents (LIAI), Experimental Research Unity (UNIPEX), Sector 5, Botucatu Medical School, São Paulo State University (UNESP), Botucatu 18618-687, SP, Brazil.
Infect Dis Rep. 2025 Jul 12;17(4):84. doi: 10.3390/idr17040084.
BACKGROUND/OBJECTIVE: Pulmonary fungal infections are a significant diagnostic challenge, primarily affecting immunocompromised individuals, such as those with HIV, cancer, or organ transplants, and they often lead to substantial morbidity and mortality if untreated. These infections trigger acute inflammatory and immune responses, which may progress to chronic inflammation. This process involves myofibroblast recruitment, the deposition of extracellular matrix, and vascular remodeling, ultimately contributing to pulmonary hypertension. Despite its clinical relevance, pulmonary hypertension secondary to fungal infections remains under-recognized in practice and poorly studied in research.
RESULTS/CONCLUSION: This narrative mini-review explores three key mechanisms underlying vascular remodeling in this context: (1) endothelial injury caused by fungal emboli or autoimmune reactions, (2) direct vascular remodeling during chronic infection driven by inflammation and fibrosis, and (3) distant vascular remodeling post-infection, as seen in granulomatous diseases like paracoccidioidomycosis. Further research and clinical screening for pulmonary hypertension in fungal infections are crucial to improving patient outcomes.
背景/目的：肺部真菌感染是一项重大的诊断挑战，主要影响免疫功能低下的个体，如艾滋病毒感染者、癌症患者或器官移植受者，如果不进行治疗，往往会导致严重的发病率和死亡率。这些感染引发急性炎症和免疫反应，可能会发展为慢性炎症。这个过程涉及肌成纤维细胞的募集、细胞外基质的沉积和血管重塑，最终导致肺动脉高压。尽管其具有临床相关性，但真菌感染继发的肺动脉高压在实际中仍未得到充分认识，在研究中也很少被研究。
结果/结论：本篇叙述性小型综述探讨了在这种情况下血管重塑的三个关键机制：（1）真菌栓子或自身免疫反应引起的内皮损伤，（2）由炎症和纤维化驱动的慢性感染期间的直接血管重塑，以及（3）感染后远处血管重塑，如在副球孢子菌病等肉芽肿性疾病中所见。对真菌感染中的肺动脉高压进行进一步研究和临床筛查对于改善患者预后至关重要。
