Recent insights into pulmonary repair following virus-induced inflammation of the respiratory tract.

摘要: A hallmark of infection by respiratory viruses is productive and the subsequent destruction airway epithelium. These can also target other stromal cell types as well in certain instances, CD45+ hematopoietic cells either resident lungs or part inflammatory response to infection. The mechanisms which virus produces injury these include direct with cytopathic effects a consequence replication. Host mediated damage culprit pulmonary both innate adaptive immune produce soluble cell-associated pro-inflammatory mediators. Recently, it has become increasingly clear that addition control excess inflammation elimination, resolution requires an active repair process, necessary regain normal function restore homeostasis. must re-establish epithelial barrier regenerate microarchitecture lung. Emerging areas research have highlighted importance cells, particularly newly described lymphoid alternatively activated macrophages stem process. may impede alter will be important for identifying therapeutic targets aimed at limiting host expediting recovery.