“…However, in states of ongoing inflammation and fibrosis, such as sarcoidosis, chronic bronchitis, and idiopathic pulmonary fibrosis, there is ongoing tissue destruction and remodeling leading to persistence of HA degradation products (4,33,41). Although the precise physiologic concentration of LMW HA is unknown, during inflammation, there is increased overall HA as reflected in the serum (patients with rheumatoid arthritis, 150 ng/ml; patients with liver failure, 390 ng/ml; healthy control subjects, 36 ng/ml) and BAL (patients with sarcoidosis, 430 mg/ml) (33)(34)(35). Similarly, during inflammation and tissue destruction, adenosine is released into the extracellular space and can act as a negative regulator of both inflammation and immune-mediated tissue destruction (9,11).…”