Insulin-like growth factors enhance phagocytosis by human neutrophils in vitro

Gui Fang Jin, Yan Shi Guo, Chuck Ball, Clifford W. Houston

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Polymorphonuclear neutrophils (PMNs) were isolated from human blood, and PMN phagocytosis was assessed by measuring the chemiluminescence (CL) response in the presence of ZAP (opsonized zymosin particles containing luminol). The administration of 6.5 nM of insulin-like growth factor I (IGF-I), des(1-3)-IGF-I, IGF-II or insulin to PMNs for 20 min resulted in significant increases of the CL response for all test preparations. Des(1-3)-IGF-I, a truncated IGF-I with low affinity binding to IGF binding proteins (IGFBPs), was the most potent CL stimulator. The CL production evoked by 6.5 nM of des(1-3)-IGF-I was inhibited significantly by both 0.25 and 1.0 mM of EGTA (Ca2+ chelator), or 10 μM nifedipine (Ca2+ channel inhibitor), pertussis toxin (0.05 and 1.0 μg/ml) or cholera toxin (5 μg/ml). These results suggest that IGF-I and its homologues are potent stimulators of phagocytosis and that this action is modulated by IGFBP, and may require extracellular Ca2+ and/or IGF-I receptor G-protein coupling.

Original languageEnglish (US)
Pages (from-to)125-131
Number of pages7
JournalRegulatory Peptides
Volume49
Issue number2
DOIs
StatePublished - Dec 10 1993

Fingerprint

Somatomedins
Insulin-Like Growth Factor I
Phagocytosis
Neutrophils
Chemiluminescence
Luminescence
Insulin-Like Growth Factor Binding Proteins
Luminol
IGF Type 1 Receptor
Insulin-Like Growth Factor II
Cholera Toxin
Egtazic Acid
Pertussis Toxin
Nifedipine
Chelating Agents
GTP-Binding Proteins
In Vitro Techniques
Blood
Insulin

Keywords

  • Chemiluminescence
  • EGTA
  • G-protein
  • Insulin-like growth factor
  • Nifedipine
  • Phagocytosis

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology
  • Physiology
  • Neuroscience(all)

Cite this

Insulin-like growth factors enhance phagocytosis by human neutrophils in vitro. / Jin, Gui Fang; Guo, Yan Shi; Ball, Chuck; Houston, Clifford W.

In: Regulatory Peptides, Vol. 49, No. 2, 10.12.1993, p. 125-131.

Research output: Contribution to journalArticle

Jin, Gui Fang ; Guo, Yan Shi ; Ball, Chuck ; Houston, Clifford W. / Insulin-like growth factors enhance phagocytosis by human neutrophils in vitro. In: Regulatory Peptides. 1993 ; Vol. 49, No. 2. pp. 125-131.
@article{7443f86852a044cbbc4a356b418c9dfb,
title = "Insulin-like growth factors enhance phagocytosis by human neutrophils in vitro",
abstract = "Polymorphonuclear neutrophils (PMNs) were isolated from human blood, and PMN phagocytosis was assessed by measuring the chemiluminescence (CL) response in the presence of ZAP (opsonized zymosin particles containing luminol). The administration of 6.5 nM of insulin-like growth factor I (IGF-I), des(1-3)-IGF-I, IGF-II or insulin to PMNs for 20 min resulted in significant increases of the CL response for all test preparations. Des(1-3)-IGF-I, a truncated IGF-I with low affinity binding to IGF binding proteins (IGFBPs), was the most potent CL stimulator. The CL production evoked by 6.5 nM of des(1-3)-IGF-I was inhibited significantly by both 0.25 and 1.0 mM of EGTA (Ca2+ chelator), or 10 μM nifedipine (Ca2+ channel inhibitor), pertussis toxin (0.05 and 1.0 μg/ml) or cholera toxin (5 μg/ml). These results suggest that IGF-I and its homologues are potent stimulators of phagocytosis and that this action is modulated by IGFBP, and may require extracellular Ca2+ and/or IGF-I receptor G-protein coupling.",
keywords = "Chemiluminescence, EGTA, G-protein, Insulin-like growth factor, Nifedipine, Phagocytosis",
author = "Jin, {Gui Fang} and Guo, {Yan Shi} and Chuck Ball and Houston, {Clifford W.}",
year = "1993",
month = "12",
day = "10",
doi = "10.1016/0167-0115(93)90434-A",
language = "English (US)",
volume = "49",
pages = "125--131",
journal = "Regulatory Peptides",
issn = "0167-0115",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Insulin-like growth factors enhance phagocytosis by human neutrophils in vitro

AU - Jin, Gui Fang

AU - Guo, Yan Shi

AU - Ball, Chuck

AU - Houston, Clifford W.

PY - 1993/12/10

Y1 - 1993/12/10

N2 - Polymorphonuclear neutrophils (PMNs) were isolated from human blood, and PMN phagocytosis was assessed by measuring the chemiluminescence (CL) response in the presence of ZAP (opsonized zymosin particles containing luminol). The administration of 6.5 nM of insulin-like growth factor I (IGF-I), des(1-3)-IGF-I, IGF-II or insulin to PMNs for 20 min resulted in significant increases of the CL response for all test preparations. Des(1-3)-IGF-I, a truncated IGF-I with low affinity binding to IGF binding proteins (IGFBPs), was the most potent CL stimulator. The CL production evoked by 6.5 nM of des(1-3)-IGF-I was inhibited significantly by both 0.25 and 1.0 mM of EGTA (Ca2+ chelator), or 10 μM nifedipine (Ca2+ channel inhibitor), pertussis toxin (0.05 and 1.0 μg/ml) or cholera toxin (5 μg/ml). These results suggest that IGF-I and its homologues are potent stimulators of phagocytosis and that this action is modulated by IGFBP, and may require extracellular Ca2+ and/or IGF-I receptor G-protein coupling.

AB - Polymorphonuclear neutrophils (PMNs) were isolated from human blood, and PMN phagocytosis was assessed by measuring the chemiluminescence (CL) response in the presence of ZAP (opsonized zymosin particles containing luminol). The administration of 6.5 nM of insulin-like growth factor I (IGF-I), des(1-3)-IGF-I, IGF-II or insulin to PMNs for 20 min resulted in significant increases of the CL response for all test preparations. Des(1-3)-IGF-I, a truncated IGF-I with low affinity binding to IGF binding proteins (IGFBPs), was the most potent CL stimulator. The CL production evoked by 6.5 nM of des(1-3)-IGF-I was inhibited significantly by both 0.25 and 1.0 mM of EGTA (Ca2+ chelator), or 10 μM nifedipine (Ca2+ channel inhibitor), pertussis toxin (0.05 and 1.0 μg/ml) or cholera toxin (5 μg/ml). These results suggest that IGF-I and its homologues are potent stimulators of phagocytosis and that this action is modulated by IGFBP, and may require extracellular Ca2+ and/or IGF-I receptor G-protein coupling.

KW - Chemiluminescence

KW - EGTA

KW - G-protein

KW - Insulin-like growth factor

KW - Nifedipine

KW - Phagocytosis

UR - http://www.scopus.com/inward/record.url?scp=0027376042&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027376042&partnerID=8YFLogxK

U2 - 10.1016/0167-0115(93)90434-A

DO - 10.1016/0167-0115(93)90434-A

M3 - Article

VL - 49

SP - 125

EP - 131

JO - Regulatory Peptides

JF - Regulatory Peptides

SN - 0167-0115

IS - 2

ER -