PMID- 2002624
OWN - NLM
STAT- MEDLINE
DCOM- 19910417
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 39
IP  - 1
DP  - 1991 Jan
TI  - Glomerular interleukin 1 production is dependent on macrophage infiltration in 
      anti-GBM glomerulonephritis.
PG  - 103-10
AB  - Both macrophages and glomerular mesangial cells have the potential to synthesize 
      interleukin 1 (IL-1), however, their respective contributions to IL-1 production 
      in anti-GBM glomerulonephritis (GN) are unknown. To address this problem, IL-1 
      production by glomeruli from rabbits with macrophage-associated anti-GBM GN 
      (passive autologous anti-GBM GN [PAGBMGN]) and macrophage independent 
      (heterologous phase) anti-GBM GN was studied. Macrophage-infiltrated nephritic 
      glomeruli produced IL-1 bioactivity which was inhibitable by an anti-IL-1 
      antibody, and had a molecular weight consistent with rabbit IL-1. Glomerular IL-1 
      production in PAGBMGN was markedly augmented (1.43 +/- 0.79 U/10(3) glomeruli 
      [gloms]/24 hr) compared to normal glomeruli (0.13 +/- 0.06 U/10(3) gloms/24 hr, P 
      less than 0.05) or glomeruli from rabbits with macrophage independent GN (0.11 
      +/- 0.07 U/10(3) gloms/24 hr, P less than 0.05). IL-1 production by glomeruli 
      from leukocyte depleted rabbits with PAGBMGN (0.16 +/- 0.07 U/10(3) gloms/24 hr) 
      was not significantly elevated compared to normal glomeruli. Glomerular 
      macrophages from rabbits with PAGBMGN produced more IL-1 (3.62 +/- 1.63 U/10(3) 
      cells/24 hr) than blood monocytes (0.51 +/- 0.30 U/10(3) cells/24 hr) or alveolar 
      macrophages (0.24 +/- 0.12 U/10(3) cells/24 hr) from the same animals. These 
      results show that in experimental anti-GBM GN where injury is macrophage 
      dependent, IL-1 production is also macrophage dependent and infiltrating 
      glomerular macrophages are the major source of IL-1. Further, as glomerular IL-1 
      production was not significantly augmented in GN in the absence of macrophages, 
      glomerular deposition of immunoglobulin and complement alone do not stimulate 
      significant IL-1 production by intrinsic glomerular cells in experimental 
      anti-GBM GN.
FAU - Tipping, P G
AU  - Tipping PG
AD  - Department of Medicine, Monash University, Prince Henry's Hospital, Melbourne, 
      Australia.
FAU - Lowe, M G
AU  - Lowe MG
FAU - Holdsworth, S R
AU  - Holdsworth SR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Antibodies)
RN  - 0 (Autoantibodies)
RN  - 0 (Interleukin-1)
RN  - 0 (antiglomerular basement membrane antibody)
SB  - IM
MH  - Animals
MH  - Antibodies/*immunology
MH  - Autoantibodies
MH  - Glomerulonephritis/*immunology
MH  - Interleukin-1/*biosynthesis
MH  - Kidney Glomerulus/*immunology/metabolism
MH  - Macrophages/*immunology
MH  - Rabbits
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
AID - S0085-2538(15)57094-4 [pii]
AID - 10.1038/ki.1991.13 [doi]
PST - ppublish
SO  - Kidney Int. 1991 Jan;39(1):103-10. doi: 10.1038/ki.1991.13.