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Abstract
Respiratory syncytial virus (RSV) is a major cause of respiratory viral infections in infants and children. Alveolar macrophages (AMs) play a crucial role in combatting airborne pathogens, strongly express CD169, and are localized in the lung alveoli. Therefore, we used CD169-diphtheria toxin receptor (DTR) transgenic mice to explore the roles of CD169+ cells in immune responses to mucosal RSV infection. The administration of diphtheria toxin to CD169-DTR mice induced specific AM depletion and reduced the recruitment of Ly6Chi monocytes. Notably, CD169+ cell depletion reduced levels of innate cytokines, such as interferon-β, IL-6, and TNF-α, in bronchoalveolar lavage fluid during RSV infection without affecting the production of proinflammatory chemokines. Moreover, the depletion of CD169+ cells increased the recruitment of inflammatory cells to the lung during the early stage of RSV infection, although not during the later stages of RSV infection. Furthermore, the depletion of CD169+ cells reduced the recruitment of effector CD8+ T cells to the lungs after RSV mucosal infection. Our findings suggest that modulating the number of CD169+ cells to enhance immune responses to RSV infection may be useful as a new therapeutic strategy.
Highlights
Respiratory syncytial virus (RSV) is a major respiratory pathogen and the leading cause of bronchiolitis and infant hospital admissions throughout the developed world [1,2,3]
CD169 is a known marker of alveolar macrophages (AMs) [24], and a previous study showed that diphtheria toxin (DT) administration to CD169-diphtheria toxin receptor (DTR) mice results in significant AM depletion and induces slight neutrophil recrui tment to the lungs but does not contribute to disease in infection experiments [25]
Our results suggest that the DT treatment results in an at least 95% depletion of AMs and partially affects the recruitment of monocytes to the lungs of CD169-DTR mice
Summary
Respiratory syncytial virus (RSV) is a major respiratory pathogen and the leading cause of bronchiolitis and infant hospital admissions throughout the developed world [1,2,3]. RSV is a primary cause of opportunistic respiratory infections in elderly and immunocompromised patients [4]. When infecting the lung mucosa, RSV directly or indirectly targets various cell types, including primary epithelial cells, alveolar macrophages (AMs), and dendritic cells (DCs) [7, 8]. Alveolar macrophages localize in the alveoli where they play crucial roles in the maintenance of lung homeostasis and the clearance of airway dust, constituting a front line of defense against airborne pathogens such as RSV [9, 10].
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