Neutrophil serine proteases: potential key regulators of cell signalling during inflammation

Correlation of IL-8 and C - reactive protein Serum Levels with the Severity of Inflammatory Acne Vulgaris: a Comparative Study

“…Subsequently; potential key regulators of cell signaling released as cathepsin G, serine proteases, proteinase and leucocyte elastase at sites of inflammation. This followed by activating different IL-8 receptors [27]. This point was supported in the present study by the presence of a highly significant moderate positive correlation (r = 0.36, p = 0.003) between the severity of acne and IL-8 level was found.…”

Increased Neutrophil Elastase and Proteinase 3 and Augmented NETosis Are Closely Associated With β-Cell Autoimmunity in Patients With Type 1 Diabetes

“…In addition to its classical roles for host defense against infection, neutrophil serine proteases are an important regulator of inflammation and innate immunity (17,19,37,38). NE and PR3 are both involved in maturation and release of proinflammatory cytokines, such as tumor necrosis factor-a, interleukin-1b, and interleukin-18, and also induces expression and activation of Toll-like receptors (39)(40)(41)(42), all of which are important mediators of insulitis and b-cell destruction (43,44).…”

“…Neutrophil activation and degranulation can result in the release of neutrophil serine proteases into the extracellular medium and circulation, where they not only help to eliminate the invaded pathogens but also serve as the humoral regulators of the immune responses during acute and chronic inflammation, modulating cellular signaling network by processing chemokines, and activating specific cell-surface receptors (17)(18)(19). Abnormal activities of neutrophil serine proteases have been implicated in the pathogenesis of several inflammatory and autoimmune diseases, including chronic obstructive pulmonary disease, cystic fibrosis, Wegener granulomatosis, Papillon-Lefèvre syndrome, and small-vessel vasculitis (20).…”

Emerging roles of serine proteinases in tissue turnover in arthritis

“…NE and CTG inactivate (or "disarm") PAR-1 and PAR-2, while NE also inactivates PAR-3 (see ref. 171 and the references therein) such that serine proteinases may be key proteolytic regulators of PAR-mediated signaling in the context of joint inflammation as well as neutrophil infiltration. The therapeutic potential of PARs in arthritis has recently been reviewed (159).…”