Leukocyte trafficking and pain behavioral responses to a hydrogen sulfide donor in acute monoarthritis

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

“…Furthermore, in an in vivo murine model of acute arthritis induced by kaolin/ carrageenan [69], a bolus addition of 30-50 µM of Na 2 S inhibited leukocyte adhesion in postcapillary venules in acutely inflamed mouse knees. In contrast to the effects of H 2 S on the systemic vasculature, Na 2 S induced vessel constriction rather than vasodilatation.…”

“…NaSH (14 µmol/kg, intraperitoneal) significantly improved lung function (peak expiratory flow, peak inspiratory flow, intrapressure and maximum rising slope of intrapressure) and inhibited iNOS activation in the lung [64] Male C57B1/6 mice and male Wistar rats: Acute inflammation of the knee induced by kaolin-carrageenan S decreased synovial blood flow but had no effect on joint pain [69] Female C57BL/6 mice: Acute lung injury; B + S injury GYY4137 also decreased LPS-induced hypotension [32] In vitro cellular study using murine RAW264.7 macrophages significantly decreased reduced lung inflammation to a significantly greater extent than diclofenac alone; however, ACS15 was ineffective against pancreatic injury (i.e., acinar cell death, pancreatic neutrophil accumulation or plasma amylase) [129] Rats: OA-induced acute -independent oxidative burst [132] In vitro cellular study formyl-methionyl-leucylphenylalanine-and zymosan-activated serum stimulated polymorphonuclear cells …”

Halimeter ppb Levels as the Predictor of Erosive Gastroesophageal Reflux Disease

“…The fact that no significant difference observed in VSC levels according to severity of esophageal mucosal injury defined by LA classification and minimal lesion showed highest VSC concentration leaves possible insights of H2S role in pathogenesis of ERD like intervening of esophageal inflammation before the development of erosive lesions, sloughing of esophageal mucosa, and increased synthesis of VSCs in injured esophageal mucosa. [22][23][24] Currently, minimal change lesion is classified as NERD because of no definite presence of erosive or ulcerative changes in esophagogastric junction, [14][15][16] but there is high possibility that minimal change lesion could be one of early ERD supported with our objective finding that minimal change lesion showed highest levels of VSCs than either NERD or ERD. Hiatal hernia is closely associated with GERD and ERD was seen more frequently in patients with hiatal hernia than in patients without hiatal hernia.…”

“…As speculation of the underlying mechanism of halitosis related to GERD, injured esophageal mucosa could produce much more H2S than intact mucosa [21][22][23][24] and halitosis in GERD patients might reflect the presence of erosive changes in the affected esophagus, VSCs levels as discriminating point between NERD and ERD. The fact that no significant difference observed in VSC levels according to severity of esophageal mucosal injury defined by LA classification and minimal lesion showed highest VSC concentration leaves possible insights of H2S role in pathogenesis of ERD like intervening of esophageal inflammation before the development of erosive lesions, sloughing of esophageal mucosa, and increased synthesis of VSCs in injured esophageal mucosa.…”

Invariant natural killer T cells act as an extravascular cytotoxic barrier for joint-invading Lyme Borrelia

“…Murine joint intravital microscopy was performed as previously described (27). Briefly, the jugular vein of the anesthetized mice was cannulated to administer fluorochrome-labeled antibodies and additional anesthetic solution as required.…”