PMID- 7474654
OWN - NLM
STAT- MEDLINE
DCOM- 19951213
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 48
IP  - 3
DP  - 1995 Sep
TI  - Tumor necrosis factor-alpha augments the pro-inflammatory interaction between PMN 
      and GBM via a CD18 dependent mechanism.
PG  - 698-704
AB  - Acute glomerulonephritis is frequently associated with intraglomerular neutrophil 
      (PMN) accumulation and the intensity of the inflammatory reaction is correlated 
      with elevated concentrations of pro-inflammatory cytokines such as tumor necrosis 
      factor-alpha (TNF alpha). PMN are thought to damage glomeruli due to a 
      combination of reactive oxygen species and proteolytic enzymes. Using an in vitro 
      model of anti-GBM nephritis the effects of TNF alpha on GBM damage by PMN were 
      evaluated. The interaction of GBM and PMN resulted in a low grade respiratory 
      burst that was significantly augmented by the addition of TNF alpha. Luminol 
      dependent chemiluminescence (LCL) was increased from 2.4 x 10(6) to 48.1 x 10(6) 
      (P < 0.05). The GBM induced LCL could be > 85% inhibited by blocking with 
      monoclonal antibodies (mAbs) to the common beta chain of the PMN beta 2 integrin 
      family (CD18), but was unaffected by mAbs to CD11a or CD11b subunits. Degradation 
      of GBM, however, was not influenced by either TNF alpha priming of PMN or 
      anti-beta 2 integrin mAbs. When PMN were incubated with GBM-anti-GBM IgG complex 
      they underwent an increase in LCL from 2.4 x 10(6) to 31.1 x 10(6). They also 
      degraded more GBM than controls (10.1% vs. 1.8%). These aspects of PMN activation 
      were Fc receptor mediated, dependent upon anti-GBM IgG being bound to GBM and 
      inhibited by mAb to the PMN Fc receptor. These studies show that TNF alpha can 
      modulate the inflammatory response of PMN in contact with GBM in a CD18 dependent 
      manner. In contrast, Fc receptor mediated events are uninfluenced by TNF alpha.
FAU - Donovan, K L
AU  - Donovan KL
AD  - Institute of Nephrology, University of Wales College of Medicine, Royal 
      Infirmary, Cardiff, United Kingdom.
FAU - Coles, G A
AU  - Coles GA
FAU - Williams, J D
AU  - Williams JD
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (CD18 Antigens)
RN  - 0 (Receptors, Fc)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9007-34-5 (Collagen)
SB  - IM
MH  - Basement Membrane/immunology/metabolism
MH  - CD18 Antigens/*physiology
MH  - Cell Adhesion
MH  - Collagen/metabolism
MH  - Glomerulonephritis/*etiology
MH  - Humans
MH  - Kidney Glomerulus/immunology/*metabolism
MH  - Neutrophils/drug effects/*physiology
MH  - Receptors, Fc/physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1995/09/01 00:00
MHDA- 1995/09/01 00:01
CRDT- 1995/09/01 00:00
PHST- 1995/09/01 00:00 [pubmed]
PHST- 1995/09/01 00:01 [medline]
PHST- 1995/09/01 00:00 [entrez]
AID - S0085-2538(15)59112-6 [pii]
AID - 10.1038/ki.1995.340 [doi]
PST - ppublish
SO  - Kidney Int. 1995 Sep;48(3):698-704. doi: 10.1038/ki.1995.340.