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At least 91 records · Page 5Linked to original sources
PubMed1983

Dimethyl sulfoxide inhibits phagocyte influx into infected pleural spaces and phagocyte locomotion in vitro.

Influx of polymorphonuclear leukocytes (PMNs) and monocytes (MNs) into pleural spaces was decreased in dimethyl sulfoxide (DMSO)-treated rabbits infected intrapleurally with Staphylococcus aureus. In addition, pleural fluids contained S. aureus longer and marked pleural thickening with fibrosis occurred in DMSO-treated rabbits. DMSO also inhibited stimulated locomotion of PMN and MN in vitro, suggesting that the aforementioned responses in vivo may have occurred because of DMSO-mediated inhibition of the locomotion of PMN and MN.

Animals↗
PubMed1967

Role of the phagocyte in host-parasite interactions. XII. Hydrogen peroxide-myeloperoxidase bactericidal system in the phagocyte.

An antimicrobial system in polymorphonuclear neutrophils (PMN) consisting of myeloperoxidase and hydrogen peroxide has been proposed. This system appears to be activated during phagocytosis as a result of the stimulated metabolic activities. A lysed-granules (LG) fraction was prepared from guinea pig exudative PMN. LG alone possessed bactericidal activity which was related to the pH of the reaction; the lower the pH, the more marked the activity. When low concentrations of both H(2)O(2) and LG were combined under conditions where neither factor alone exhibited significant killing power, there was a striking increase in bactericidal activity. This enhanced activity was much greater than an additive effect. The LG-peroxide antibacterial system was most active over a pH range of 4.0 to 6.0. The activity of the LG-peroxide system was essentially abolished by peroxidase inhibitors, NaN(3), KCN, and aminotriazole. The antibacterial activity of this system was nonspecific in nature, being equally effective against gram-negative and gram-positive organisms.

Animals↗
PubMed1982

Combined serum bactericidal and phagocytic activities of defibrinated human blood against Serratia marcescens. Use of phenylbutazone to selectively block phagocytic killing activity and of Group A (phage tail) bacteriocins to kill extraphagocytic bacteria.

Fresh, defibrinated human blood (65 vol%) from normal adults reduced cell inocula of Serratia marcescens, comprising 'delayed serum-sensitive', 'pseudo-serum-resistant', and 'non-serum-sensitive' human serum susceptibility categories, by up to approximately 3 log10 units, provided cell inocula did not significantly exceed 10(5) colony-forming units/ml at 0 time. Phenylbutazone (2 mg/ml) antagonized neither serum bactericidal activity nor the biological activity of group A (phage tail) bacteriocins bA+ 16 and bA+ 18. These bacteriocins were suitable for killing extraphagocytic S. marcescens cells, since they were not internalized by peripheral blood leukocytes. Phenylbutazone at 2 mg/ml failed to interfere with ingestion of S. marcescens by leukocytes; however, this drug inhibited intraphagocytic killing of ingested S. marcescens bacteria. Pilot experiments, utilizing this latter system, disclosed that rifampin effectively killed intraphagolysosomal bacteria.

Adult↗