5 research outputs found
Predictive value of complement activation fragments C3a and sC5b‐9 for development of severe disease in patients with acute pancreatitis
Mechanisms Mediating Porphyromonas gingivalis Gingipain RgpA-Induced Oral Mucosa Inflammation In Vivo
Suffusion of gingipain RgpA (GRgpA) elicited a significant concentration-dependent increase in the clearance of macromolecules from in situ hamster cheek pouch which was attenuated by NPC 17647, a selective bradykinin B(2) receptor antagonist. Leupeptin and a mixture of proteinase inhibitors also attenuated GRgpA-induced responses. These data indicate that GRgpA elicits plasma exudation from in situ oral mucosa in a catalytic site-dependent fashion by elaborating bradykinin
Advances in researches on the immune dysregulation and therapy of severe acute pancreatitis*
During the development and progression of severe acute pancreatitis (SAP), conspicuous immune dysregulation develops, which is mainly manifested as excessive immune response in the early stage and immunosuppression in the late stage. This process involves complex changes in a variety of immune molecules and cells, such as cytokines, complements, lymphocytes, and leukocytes. With the gradual deepening of studies on the development and progression of SAP, the role of immune dysregulation in the pathogenesis of SAP has attracted more and more attention. In this article, we review the advances in research on the immune dysregulation in SAP and the immunotherapy of this disease through exploring the formation of excessive immune response and immune suppression as well as their mutual transformation