Multiple
infectious diseases lead to impaired lung function. Revealing the cellular mechanisms involved in this impairment is crucial for the understanding of how the lungs shift from a physiologic to a pathologic state in each specific condition. In this context, we explored the pathogenesis of
Paracoccidioidomycosis, which affects pulmonary functioning. The presence of cells expressing
Nestin-GFP has been reported in different tissues, and their roles as tissue-specific progenitors have been stablished in particular organs. Here, we explored how
Nestin-GFP+ cells are affected after lung
infection by Paracoccidioides brasiliensis, a model of lung granulomatous
inflammation with fibrotic outcome. We used
Nestin-GFP transgenic mice, parabiosis surgery, confocal microscopy and flow cytometry to investigate the participation of
Nestin-GFP+ cells in Paracoccidioides brasiliensis pathogenesis. We revealed that these cells increase in the lungs post-
Paracoccidioides brasiliensis infection, accumulating around
granulomas. This increase was due mainly to
Nestin-GPF+ cells derived from the blood circulation, not associated to blood vessels, that co-express markers suggestive of hematopoietic cells (Sca-1, CD45 and CXCR4). Therefore, our findings suggest that circulating
Nestin-GFP+ cells participate in the Paracoccidioides brasiliensis pathogenesis in the lungs.