PMID- 1832880
OWN - NLM
STAT- MEDLINE
DCOM- 19911113
LR  - 20181130
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 5
IP  - 3
DP  - 1991 Sep
TI  - Immobilized IgG immune complex induces secretion of tumor necrosis factor-alpha 
      by porcine alveolar macrophages.
PG  - 249-55
AB  - Tumor necrosis factor-alpha (TNF-alpha) is an important inflammatory mediator 
      produced by activated monocytes and macrophages. We have previously shown that 
      porcine alveolar macrophages (PAM) mediate bystander cytotoxicity through 
      hydrogen peroxide production following activation with immobilized IgG immune 
      complex (IIC) (J. Immunol. 1983; 131:1438-1442). In this report, we have 
      investigated whether IIC induces TNF-alpha secretion by PAM. Isolated PAM from 
      Minnesota miniature swine were cultured for 18 h with and without recombinant 
      human interferon-gamma (rhIFN-gamma). Cultured PAM were then incubated with IIC 
      or IgG immune complex in suspension (SIC). The supernatants generated were 
      assessed for cytotoxic activity using a TNF-alpha-sensitive WEHI-164 cell line. 
      Anti-recombinant human TNF-alpha (rhTNF-alpha) monoclonal antibody neutralized 
      the observed cytotoxicity of IIC-activated PAM supernatant completely, indicating 
      that this cytotoxicity is mediated by TNF-alpha. IIC induced TNF-alpha secretion 
      by PAM after 3 h of incubation, reaching a plateau from 6 to 12 h and decreasing 
      thereafter. TNF-alpha release was enhanced by pretreatment of PAM with 
      rhIFN-gamma. SIC did not induce significant levels of TNF-alpha secretion by PAM; 
      however, SIC with cytochalasin B-pretreated PAM induced equivalent levels of 
      TNF-alpha secretion as IIC-activated PAM. We conclude that IIC or SIC with 
      cytochalasin B pretreatment, both of which prevent internalization of IgG immune 
      complex-bound Fc receptor (FcR), provide a signal for PAM to generate TNF-alpha 
      through FcR modulation. This suggests that in vivo, deposited (immobilized) IgG 
      immune complexes-bound FcR may be a stimulus for activation of PAM to generate 
      TNF-alpha rather than circulating (mobilized) immune complexes, which may 
      contribute to the pathogenesis of diffuse interstitial fibrosis of the lung, 
      especially in idiopathic pulmonary fibrosis.
FAU - Kim, J W
AU  - Kim JW
AD  - Department of Microbiology and Immunology, University of Health Sciences/The 
      Chicago Medical School, Illinois 60064.
FAU - Wierda, W G
AU  - Wierda WG
FAU - Kim, Y B
AU  - Kim YB
LA  - eng
GR  - HL-36012/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (Antigens, Differentiation)
RN  - 0 (Receptors, Fc)
RN  - 0 (Receptors, IgG)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 3CHI920QS7 (Cytochalasin B)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antigen-Antibody Complex/chemistry/*immunology
MH  - Antigens, Differentiation/*physiology
MH  - Cytochalasin B/pharmacology
MH  - Cytotoxicity, Immunologic
MH  - Endocytosis/drug effects
MH  - Female
MH  - Immunity, Cellular
MH  - Interferon-gamma/pharmacology
MH  - Macrophage Activation
MH  - Macrophages, Alveolar/*immunology
MH  - Male
MH  - Receptors, Fc/*physiology
MH  - Receptors, IgG
MH  - Recombinant Proteins
MH  - Solubility
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 1991/09/01 00:00
MHDA- 1991/09/01 00:01
CRDT- 1991/09/01 00:00
PHST- 1991/09/01 00:00 [pubmed]
PHST- 1991/09/01 00:01 [medline]
PHST- 1991/09/01 00:00 [entrez]
AID - 10.1165/ajrcmb/5.3.249 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 1991 Sep;5(3):249-55. doi: 10.1165/ajrcmb/5.3.249.