PMID- 1660899
OWN - NLM
STAT- MEDLINE
DCOM- 19920117
LR  - 20131121
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 149
IP  - 2
DP  - 1991 Nov
TI  - Surface contact modulation of inflammatory macrophage antibody dependent 
      cytotoxicity and prostanoid release.
PG  - 195-201
AB  - Adherence to extracellular matrix proteins modulates the functional and secretory 
      activities of mononuclear phagocytes, although the mechanisms regulating these 
      adherence-dependent changes are poorly understood. In this study, the ability of 
      rat inflammatory peritoneal macrophages (PM) to adhere to an endothelial 
      cell-derived extracellular matrix or a denatured collagen/fibronectin-coated 
      surface and perform antibody dependent cell cytotoxicity (ADCC) and secrete 
      reactive oxygen intermediates was compared with PM adherent to tissue culture 
      plastic. Prostaglandin E2 (PGE2) and thromboxane B2 (TxB2), two major 
      cyclooxygenase products released by inflammatory macrophages, were also measured 
      by PM adherent to the protein coated surfaces. Rat exudate PM were equally 
      adherent to tissue culture plastic or wells coated with either endothelial cell 
      derived matrix or denatured collagen (gelatin)/fibronectin. PM adherent to a 
      denatured collagen/fibronectin-coated wells demonstrated significantly less 
      cytolytic activity (15 +/- 2% lysis) when compared with either tissue culture 
      plastic adherent PM (43 +/- 7% lysis) or PM adherent to extracellular matrix (59 
      +/- 11% lysis). PM adherent to extracellular matrix released twofold more TxB2 
      than plastic adherent PM, while PM adherent to denatured collagen/fibronectin 
      released 40% more PGE2 than cells adherent to tissue culture plastic or 80% more 
      PGE2 than PM adherent to the extracellular matrix. PM adherent to denatured 
      collagen/fibronectin release less superoxide anion (27 +/- .9 nmoles/10(6) PM) 
      than PM adherent to either tissue culture plastic (43 +/- 1 nmoles/10(6) PM) or 
      the extracellular matrix (60 +/- 0.5 nmoles/10(6) PM). Furthermore, incubation of 
      plastic adherent PM with exogenous PGE2 reduced superoxide production in a 
      dose-dependent manner. These results demonstrate that the inhibition of ADCC and 
      secretion of reactive oxygen intermediates by PM adherent to a denatured 
      collagen/fibronectin surface correlated with an increased release of the 
      immunosuppressive prostanoid PGE2. Furthermore, the addition of exogenous PGE2 to 
      plastic adherent PM reproduced the depression in ADCC and superoxide anion 
      production observed by PM adherent to a denatured collagen/fibronectin surface. 
      These studies suggest that the increased production and release of PGE2 by 
      inflammatory macrophages adherent to a denatured collagen surface may act to 
      suppress cytotoxic mechanisms and thereby constitutes part of an autocrine 
      feedback mechanism regulating macrophage function during wound injury.
FAU - Gudewicz, P W
AU  - Gudewicz PW
AD  - Department of Physiology and Cell Biology, Albany Medical College, New York 
      12208.
FAU - Frewin, M B
AU  - Frewin MB
LA  - eng
GR  - AI-26072/AI/NIAID NIH HHS/United States
GR  - P01 GM-40761/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Fibronectins)
RN  - 11062-77-4 (Superoxides)
RN  - 54397-85-2 (Thromboxane B2)
RN  - 9007-34-5 (Collagen)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - *Antibody-Dependent Cell Cytotoxicity
MH  - Cattle
MH  - Cell Adhesion
MH  - Cell Line
MH  - Collagen
MH  - Dinoprostone/*metabolism/pharmacology
MH  - Extracellular Matrix/physiology
MH  - Fibronectins
MH  - Macrophages/*immunology/physiology
MH  - Male
MH  - Protein Denaturation
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Superoxides/metabolism
MH  - Thromboxane B2/*metabolism
EDAT- 1991/11/01 00:00
MHDA- 1991/11/01 00:01
CRDT- 1991/11/01 00:00
PHST- 1991/11/01 00:00 [pubmed]
PHST- 1991/11/01 00:01 [medline]
PHST- 1991/11/01 00:00 [entrez]
AID - 10.1002/jcp.1041490204 [doi]
PST - ppublish
SO  - J Cell Physiol. 1991 Nov;149(2):195-201. doi: 10.1002/jcp.1041490204.