Pericytes are key regulators of the microvasculature through their close interactions with the endothelium. However, pericytes play additional roles in tissue homeostasis and repair, in part by transitioning into myofibroblasts. Accumulation of myofibroblasts is a hallmark of fibrotic diseases such as idiopathic pulmonary fibrosis (IPF). To understand the contribution and role of pericytes in human lung fibrosis, we isolated these cells from non-IPF control and IPF lung tissues based on expression of platelet-derived growth factor receptor-β (PDGFR-β), a common marker of pericytes. When cultured in a specialized growth medium, PDGFR-β+ cells retain the morphology and marker profile typical of pericytes. We found that IPF pericytes migrated more rapidly and invaded a basement membrane matrix more readily than control pericytes. Exposure of cells to transforming growth factor-β, a major fibrosis-inducing cytokine, increased expression of α-smooth muscle actin and extracellular matrix genes in both control and IPF pericytes. Given that pericytes are uniquely positioned in vivo to respond to danger signals of both systemic and tissue origin, we stimulated human lung pericytes with agonists having pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Both control and IPF lung pericytes increased expression of proinflammatory chemokines in response to specific PAMPs and DAMPs released from necrotic cells. Our results suggest that control and IPF lung pericytes are poised to react to tissue damage, as well as microbial and fibrotic stimuli. However, IPF pericytes are primed for migration and matrix invasion, features that may contribute to the function of these cells in lung fibrosis.

An 83-year-old man with a history of chronic kidney disease (stage V) as a result of hypertensive nephrosclerosis and coronary artery disease was admitted to the hospital with dyspnea and bilateral lower extremity edema. Owing to oliguria and progressive renal dysfunction, hemodialysis was initiated the following day via a previously-placed left arm arteriovenous fistula. As a result of delirium and bradycardia, he required prolonged hospitalization. Three weeks into his course, he became hypothermic and obtunded.Physical examination revealed a thin elderly man with the following vital signs: temperature, 33.8 C; pulse, 55 beats/min; respirations, 20 breaths/min; and blood pressure, 118/80 mm Hg. Cardiovascular examination was significant for bradycardia. Lung examination revealed decreased bibasilar air movement without adventitious sounds. His abdomen was scaphoid and not tender. Extremities showed bilateral 3þ edema to the level of the knees. Laboratory data showed a WBC count of 4.0 Â 10 3 /mm 3 (previously 7.1), potassium of 2.9 mEq/L, and BUN/creatinine of 82/3.65 mg/dL. Owing to the leukopenia, hypothermia, and change in mental status, a sepsis work-up was initiated. A prior chest radiograph (not shown) revealed pleural effusions (right greater than left), bilateral lower lobe infiltrates, and mild pulmonary edema. Bedside abdominal ultrasound (AUS) was performed. The following ultrasound (US) videos were taken with a high-frequency probe over the anterior surface of the liver with the patient at 20 upright (Videos 1, 2).

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