Supplemental L-arginine HCI augments bacterial phagocytosis in human polymorphonuclear leukocytes

Abstract

That L-arginine (L-Arg) augments the host response to acute bacterial sepsis suggests that this amino acid intervenes early in the immune response, perhaps via the nitric oxide synthetase (NOS) pathway. The effect of L-Arg supplementation on in vitro phagocytosis of fluorescein-labeled, heat-killed Staphylococcus aureus by peripheral blood neutrophils (PMNs) from 12 normal human volunteers was studied. Separated PMNs were incubated for 2 h with labeled bacteria, with and without supplemental L-Arg, D-arginine, glycine, and/or the NOS inhibitors L-canavanine, aminoguanidine, or L-NG-nitroarginine methyl ester. PMNs were fixed and extracellular fluorescence quenched with crystal violet. By flow cytometry and confocal microscopy, L-Arg supplementation was shown to result in a highly significant increase in PMN bacterial phagocytosis, the maximal effect being seen with L-Arg 380 microM and falling off with higher concentrations. This augmentation was completely abrogated by NOS inhibitors in molar excess, but inhibitors alone did not suppress phagocytosis below that of unsupplemented controls. Neither D-arginine nor glycine affected phagocytosis; the L-Arg effect was stereospecific and not related to utilization of L-Arg as an energy source. L-Arg supplementation significantly enhances bacterial phagocytosis in human neutrophils, perhaps by effects on cytoskeletal phenomena, and this appears to be mediated through NOS activity. Phagocytosis by nonspecific immune cells which intervene early in the response to sepsis is critically important, and beneficial effects of L-Arg on the clinical course of sepsis may be due at least in part to augmentation of phagocyte function.

Arginine and glutamine supplementation to culture media improves the performance of various channel catfish immune cells

“…It Table 4 Proliferation capacity upon non-specific stimulation of peripheral blood lymphocytes incubated with supplemented levels of ARG and/or GLN. has been proven that ARG might modulate phagocytosis by MØ [7,41,42], where NO seems to play a crucial role affecting the MØ cytoskeleton [42,43]. Both, supplemental ARG and E. ictaluri has been proven to induce NO synthesis in channel catfish MØ [18,44].…”

Glutathione availability modulates alveolar macrophage function in the chronic ethanol-fed rat

“…After 2 h of culture, macrophages were washed and fluorescein-labeled inactivated Staphylococcus aureus (Molecular Probes, Eugene, OR) were added in a 1:100 ratio (macrophage to bacteria) (22). After a 2-h culture period, cells were washed and phagocytosis of S. aureus was determined via quantitative digital analysis of fluorescence (QImaging, Burnaby, BC, Canada) and data analysis using Image-Pro Plus for Windows (Jandel Scientific).…”

Nitric oxide mediated Staphylococcus aureus pathogenesis and protective role of nanoconjugated vancomycin

“…To pro-inflammatory cytokines and mediators, TNF-毩 and NO play important roles in inflammatory process, so do anti-inflammatory factors such as Then the change on them might be used for explaining the anti-inflammatory effects of many drugs. NO is from arginine after the activation of iNOS and it is an important effect molecule involved in immune regulation and defense [35] .…”