Glomerular interleukin 1 production is dependent on macrophage infiltration in anti-GBM glomerulonephritis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1991-01

AUTHORS

P G Tipping, M G Lowe, S R Holdsworth

ABSTRACT

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. More... »

PAGES

103-110

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ki.1991.13

DOI

http://dx.doi.org/10.1038/ki.1991.13

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1020616087

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/2002624


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