The shared response between helminth infection and allergic asthma involves increased expression of cell cycle-related genes. In these models there is apparently a more rapid turnover or proliferation of cells than in other models. This can be explained by an increased lung epithelial renewal or proliferation, or alternatively by an increase in proliferation for immune cells involved. Although the latter possibility is feasible, the former matches known clinical pathology for asthma models. Asthma is associated with hyperplasia of the mucin-secreting goblet cells and in the studies used this is also described for asthma as well as helminth infection. This is in agreement with the finding that these genes are not found to be induced in in vitro models using isolated immune cells. As pulmonary inflammation often involves leukocyte infiltration, it raises the question whether the common responses occur primarily in sessile lung cells or can be attributed to infiltrating immune cells. Although the common upregulated cluster contains some markers associated with monocytes and macrophages or lymphocytes, these do not show a parallel expression pattern, as would be expected if the gene expression responses are caused by cellular influx. In addition, the common cluster does not include several other markers associated with these types of immune cells, nor those associated with granulocyte lineages, even though several of these are present in the initial 4551 gene set used. For these markers that are not part of the common cluster, the expression changes to the controls are much weaker than those in the common cluster and the responses are also much less consistent across the various models. Finally, two of the studies include time points where gene expression responses are at their maximum before a detectable cellular influx is found by pathological analysis, namely the response one day after RSV infection and the early response after PM exposure. Therefore, it can be concluded that the common infection response can be predominantly attributed to gene expression changes in sessile pulmonary cells rather than to leukocyte influx. Besides a common up-regulated cluster, we also identified a cluster Torin 1 characterized by a common down-regulation in response to inflammation. This cluster contained a large number of genes involved in growth and development, both of which are important processes for continuous renewal of lung epithelium. As can be seen from Fig. 1, the extent of the down-regulation in this cluster is moderate compared to the LDN-193189 effects in the common up-regulated subsets. This suggests that the effects found are not a direct targeted response, but rather a secondary effect that reflects tissue damage or that the induction of an inflammatory response goes at the expense of normally active processes in lung tissue.