COS7 cells expressing a series of polyL-GFP fusion proteins and GFP alone were serially observed for 120 h, and the numbers of Doxercalciferol transfected cells with and without visible aggregate formation were counted. When we assessed the time course of aggregate formation in COS7 cells transfected with pQBI25-L32 or vector alone, we found that, in contrast to cells transfected with vector alone, cells transfected with pQBI25-L32 show aggregates of fusion protein in their nuclei. This further supports a model where induction is initiated by interaction of the cell with the virus particle. Some alveoli contained single, scattered positive epithelial cells, mainly with the morphology of type II pneumocytes, others were entirely positive. Occasionally, positive desquamated alveolar epithelial cells/macrophages as well as positive syncytial cells were seen in alveolar lumina. On days 2, 3 and 7 p.i., staining was similar, but appeared gradually less extensive than on day 1 p.i. This was obvious in a lower number of alveoli exhibiting positive cells. However, entire alveoli with positive cells were found at each time point. These results indicate that a small number of cells in the respiratory tract constitutively express the htPPT-A transgene in uninfected mice. However, a large number of airway epithelial cells and macrophages are rapidly induced to express the htPPT-A gene after respiratory challenge with MHV-68. In mock-infected mice, SP expression was observed in occasional alveolar and bronchial epithelial cells. Some positive alveolar epithelial cells had the morphology of type II pneumocytes. Desquamated alveolar macrophages, if present, were intensely positive. On day 1 p.i., mice exhibited numerous individual and patches of tracheal and bronchial epithelial cells which stained positive for SP. In alveoli, positive epithelial cells were seen, some of which had the morphology of type II pneumocytes. Positive desquamated epithelial cells and macrophages were occasionally observed within alveolar lumina. Sensory C-type fibres are thought to provide the predominant source of tachykinins, including SP, in the lung and have a role in the pathophysiological response to challenge in the lungs which have been well documented. However, our manuscript provides strong evidence that as a response to infectious challenge, tachykinin production in the lung is initiated Quercitrin locally in nonneuronal cells.