Oliver B G G, Lim S, Wark P, Laza-Stanca V, King N, Black J L, Burgess J K, Roth M, Johnston S L
Discipline of Pharmacology, The University of Sydney, Sydney, NSW 2006, Australia.
Thorax. 2008 Jun;63(6):519-25. doi: 10.1136/thx.2007.081752. Epub 2008 Feb 1.
Rhinovirus infection is responsible for considerable morbidity and mortality as the major cause of exacerbations of asthma, and is also known to induce exacerbations of cystic fibrosis and chronic obstructive pulmonary disease. Exacerbations of these diseases are also frequently associated with bacterial and atypical bacterial infection. Alveolar macrophages are the major immune cells in the airways and are important in defence against bacterial infections.
The authors investigated whether rhinovirus modifies cytokine release, the pattern recognition receptor expression and phagocytosis by human alveolar macrophages in response to bacterial products.
Viable rhinovirus was detected in macrophages up to 3 days after exposure and viral RNA expression persisted for 10 days. Infectious but not UV inactivated rhinovirus increased tumour necrosis factor alpha (TNFalpha) and interleukin (IL)8 release by macrophages. In contrast, infectious rhinovirus impaired lipopolysaccharide and lipoteichoic acid induced TNFalpha and IL8 secretion by macrophages. Rhinovirus induced impairment of macrophage antibacterial immune responses did not involve IL10, prostaglandin E(2) or downregulation of Toll-like receptor 2. Furthermore, the macrophage phagocytic response to labelled bacterial particles, but not to latex beads, was impaired.
The authors have identified impairment of cytokine responses to bacterial lipopolysaccharide and lipoteichoic acid by alveolar macrophages in response to infectious rhinovirus. Virus induced impairment of antibacterial host defence has important implications in the pathogenesis of exacerbations of respiratory diseases.
鼻病毒感染作为哮喘加重的主要原因，会导致相当高的发病率和死亡率，并且还已知会引发囊性纤维化和慢性阻塞性肺疾病的加重。这些疾病的加重也经常与细菌和非典型细菌感染相关。肺泡巨噬细胞是气道中的主要免疫细胞，在抵御细菌感染中起重要作用。
作者研究了鼻病毒是否会改变人肺泡巨噬细胞对细菌产物的细胞因子释放、模式识别受体表达和吞噬作用。
在暴露后长达3天的巨噬细胞中检测到活的鼻病毒，病毒RNA表达持续10天。有感染性但未被紫外线灭活的鼻病毒增加了巨噬细胞释放肿瘤坏死因子α（TNFα）和白细胞介素（IL）8。相比之下，有感染性的鼻病毒损害了巨噬细胞对脂多糖和脂磷壁酸诱导的TNFα和IL8分泌。鼻病毒诱导的巨噬细胞抗菌免疫反应受损不涉及IL10、前列腺素E（2）或Toll样受体2的下调。此外，巨噬细胞对标记细菌颗粒而非乳胶珠的吞噬反应受损。
作者发现肺泡巨噬细胞对感染性鼻病毒的反应中，对细菌脂多糖和脂磷壁酸的细胞因子反应受损。病毒诱导的抗菌宿主防御受损对呼吸道疾病加重的发病机制具有重要意义。
