Inflammatory response to inhalation of COVID-19 in the pulmonary vasculature. Healthy lung: Depicted is a healthy lung (left) and a bronchiole (center) within the lung emphasizing the vasculature and alveolar sacs. A schematic of a histological cross section through an alveolar-capillary unit showing alveolar air sacs (white) lined by alveolar type 1 cells (purple) and separated from capillaries by a basement membrane (blue). The alveolar sac is studded with alveolar type 2 cells (yellow) and alveolar macrophages (green). The inset highlights the air-blood interface that is separated by the alveolar type 1 cell, basement membrane, and the capillary, from top to bottom. COVID lung: The left panel depicts inflammatory signaling through cytokine receptors (IL-1βR, TNFR, and IL-6R) and receptors of innate immunity (TLRs and NOD2) following SARS-CoV-2 infection. The right panel demonstrates sequelae of SARS-CoV-2 infection at the level of the alveolus. Deposition of debris and inflammatory products results in the formation of a hyaline membrane that lines the alveolar sac and impairs exchange (dark pink). Expression of leukocyte receptors results in monocytic infiltrates (purple) and neutrophil extravasation (light pink). Proliferation of alveolar type 2 cells is observed (yellow). Loss of barrier function results in capillary leak (tan). Loss of vascular integrity results in alveolar hemorrhage (red). Microvascular occlusion (red brown) and extravascular fibrin formation (brown) occur. Endothelial swelling and sluffing ensues. TLRs, toll-like receptors; TNFR, tumor necrosis factor receptor.