Li Xinru, Zeng Qianrui, Liu Chang, Yi Xinchao, Luo Haodang, Tong Qin, Chen Hongliang, You Xiaoxing
Institute of Pathogenic Biology, Hengyang Medical College, Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, University of South China, Hengyang, People's Republic of China.
Department of Clinical Laboratory, The Affiliated Nanhua Hospital, Hengyang Medical College, University of South China, Hengyang, People's Republic of China.
J Inflamm Res. 2025 Feb 26;18:2909-2922. doi: 10.2147/JIR.S507526. eCollection 2025.
is a prevalent respiratory microbe that causes acute inflammation in the respiratory system. Surfactant proteins (SP), particularly SP-A and SP-D, are essential for the immunological protection against infection. Variant SP-A2 may lead to immune reactions, which could account for the variability in clinical manifestations among individuals. Mechanistically, these surfactant proteins may act as candidate receptors, facilitating both the adhesion of and internalization of community-acquired respiratory distress syndrome toxin. They also exhibit a high affinity for lipid ligands on the surface of membranes via their carbohydrate recognition domains, which aid in the direct clearing of the bacteria. In addition, SP-A and SP-D demonstrated synergistic effects in augmenting the intake and elimination of by alveolar macrophages. Furthermore, these surfactant proteins negatively regulate pulmonary inflammation by influencing lymphocyte and dendritic cell activities, reducing airway eosinophilic infiltration, and managing asthma-related inflammatory responses. A thorough understanding of the immunomodulatory roles of surfactant proteins in infection will shed light on how homeostasis is preserved during mycoplasma pneumonia and may guide the development of novel therapeutic strategies against this organism.
是一种常见的呼吸道微生物，可引起呼吸系统的急性炎症。表面活性蛋白（SP），尤其是SP-A和SP-D，对于抵抗感染的免疫保护至关重要。SP-A2变体可能导致免疫反应，这可能解释了个体临床表现的变异性。从机制上讲，这些表面活性蛋白可能作为候选受体，促进社区获得性呼吸窘迫综合征毒素的黏附和内化。它们还通过其碳水化合物识别域对膜表面的脂质配体表现出高亲和力，这有助于直接清除细菌。此外，SP-A和SP-D在增强肺泡巨噬细胞对[具体物质，原文未明确]的摄取和清除方面表现出协同作用。此外，这些表面活性蛋白通过影响淋巴细胞和树突状细胞的活性、减少气道嗜酸性粒细胞浸润以及控制哮喘相关的炎症反应来负向调节肺部炎症。深入了解表面活性蛋白在[具体感染，原文未明确]感染中的免疫调节作用将有助于揭示支原体肺炎期间如何维持内环境稳定，并可能指导针对这种病原体的新型治疗策略的开发。
