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The lung’s main function of supporting gas exchange requires elaborate structures at microscopic scale, including hundreds of millions of alveoli and a finely branching airway and vascular network. The lung contacts 12,000 liters of outside air and 7,000 liters of circulating blood daily—hence the need for an exquisitely sensitive immune response to any environmental or bloodborne insult.
Closeup of microscopic alveolar structure.
In the context of injury or infection, the systemic immune system is rapidly deployed to the lung.  Among the immigrating immune cells are bloodborne monocytes, which arrive in large numbers by day 3 after acute insult and establish a long-term presence in the tissue as monocyte-derived macrophages.
UMAP of scRNAseq data for macrophages post lung injury.
scRNAseq for macrophages in the early fibrotic period after lung injury showing alveolar (C1), monocyte-derived (C3), and transitional (C2) lung macrophages. From Aran et al, Nature Immunology 2019.
In the context of injury or infection, the systemic immune system is rapidly deployed to the lung.  Among the immigrating immune cells are bloodborne monocytes, which arrive in large numbers by day 3 after acute insult and establish a long-term presence in the tissue as monocyte-derived macrophages.
CD68+ Macrophages with nuclear Mafb stain in an area of dense collagen revealed by second harmonic imaging.
Macrophages marked by CD68 (green) bearing the monocytic marker MAFB (red) in an area of dense fibrosis visualized by second harmonic imaging (blue). From Aran et al, Nature Immunology 2019.
The Bhattacharya Lab at the UCSF Parnassus Campus is focused on the functional role of monocyte-derived macrophages in the onset and persistence of fibrosis in the lung. We are addressing the following major questions, with a goal of discovering new targets for therapy for acute lung injury and fibrosis:
  • What molecules released by monocyte-derived macrophages and other immune cells signal to and activate pro-fibrotic programs in parenchymal cell types such as fibroblasts and epithelial cells?
  • What reciprocal signals derive from these parenchymal cells to modify the immune response?
  • How can this pathologic crosstalk be reversed to combat fibrosis and restore lung health?