ABSTRACT
Conglutinin is a high molecular-weight lectin originally detected in bovine serum. It belongs to the family of collectins that bind sugar residues in a Ca(2+)-dependent manner and are effector molecules in innate immunity. Conglutinin appears to play an important role in immune defense mechanisms, showing antiviral and antibacterial activities when tested in vivo and in vitro. The present study evaluated the effect of conglutinin on the respiratory bursts in bovine peripheral phagocytes. Using nitroblue tetrazolium and hydrogen peroxide assays, we showed that sugar ligand-bound conglutinin stimulated the production of superoxide and H2O2 in granulocytes whereas the non-sugar-bound form of conglutinin inhibited these processes. These results indicate that both forms of conglutinin are able to interact with surface leukocyte receptors but have opposite effects on phagocytic activity. Our findings suggest that conglutinin bound to sugar residues on microbial surfaces can induce oxygen burst in phagocytes, and thereby mediates the elimination of pathogens and prevents the spread of infection.
Subject(s)
Animals , Female , Cattle/immunology , Collectins/pharmacology , Enzyme-Linked Immunosorbent Assay/veterinary , Granulocytes/drug effects , Hydrogen Peroxide/immunology , Immunity, Innate/drug effects , Phagocytosis/immunology , Reactive Oxygen Species/immunology , Respiratory Burst/drug effects , Serum Globulins/pharmacology , Statistics, Nonparametric , Superoxides/immunologyABSTRACT
The leukotoxins [9(10)-and 12(13)-EpOME] are produced by activated inflammatory leukocytes such as neutrophils. High EpOME levels are observed in disorders such as acute respiratory distress syndrome and in patients with extensive burns.Although the physiological significance of the EpOMEs remains poorly understood,in some systems, the EpOMEs act as a protoxin,with their corresponding epoxide hydrolase metabolites,9,10-and 12,13-DiHOME, specifically exerting toxicity.Both the EpOMEs and the DiHOMEs were also recently shown to have neutrophil chemotactic activity.We evaluated whether the neutrophil respiratory burst,a surge of oxidant production thought to play an important role in limiting certain bacterial and fungal infections,is modulated by members of the EpOME metabolic pathway.We present evidence that the DiHOMEs suppress the neutrophil respiratory burst by a mechanism distinct from that of respiratory burst inhibitors such as cyclosporin H or lipoxin A4,which inhibit multiple aspects of neutrophil activation.