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Inhibitory effect of glycyrrhizin on the production of CCL2 by various sources of immunosuppressive neutrophils (PMN‐II)
Author(s) -
Jones Vickie C,
Shigematsu Kenji,
Kobayashi Makiko,
Sanford Arthur P,
Herndon David N,
Suzuki Fujio
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.672.35
Subject(s) - glycyrrhizin , chemistry , chemokine , stimulation , interleukin 8 , ficoll , pharmacology , immunology , ccl2 , phagocytosis , in vitro , medicine , peripheral blood mononuclear cell , immune system , cytokine , biochemistry
Three subtypes of PMN (PMN‐N, PMN‐I and PMN‐II) have been demonstrated. Among them, PMN‐II have been characterized as cells that participate in the increased susceptibility of burned hosts to bacterial translocation‐associated infectious complications. Since host‐mediated antibacterial effects of glycyrrhizin (GL) were demonstrated in these infections, in this study, the inhibitory effects of GL on the CCL2 production by various sources of PMN‐II were examined. CCL2 has been determined as an effector chemokine on the PMN‐II immunosuppressive activity. PMN‐II were prepared from peripheral blood of burn patients by Ficoll‐Hypaque and dextran sedimentations. Also, PMN‐II were induced from band PMN (isolated peripheral blood PMN from healthy volunteers 3 hrs after having exercised for 1 hr) by stimulation with SAC (0.0075%), GM‐CSF (0.1 ng/ml), VEGF (0.1 ng/ml) or terbutaline (β2‐AR agonist, 10 −6 M). All of these PMN preparations were identified as PMN‐II by their abilities to produce CCL2 and IL‐10. In the results, the production of CCL2 by PMN‐II isolated from peripheral blood of severely burned patients was inhibited by 10 μg/ml of GL (Minophagen Pharmaceutical Co., Ltd., Tokyo, Japan). Also, the production of CCL2 by PMN‐II preparations, prepared in vitro from band PMN of exercised volunteers after stimulation with SAC, GM‐CSF, VEGF or terbutaline, was inhibited by GL (10 μg/ml). These results suggest that PMN‐II‐associated deficiency of the host antimicrobial resistance may be effectively intervened by GL. This study was supported by SHC NA #8840.