PMID- 7542490
OWN - NLM
STAT- MEDLINE
DCOM- 19950830
LR  - 20210518
IS  - 1046-6673 (Print)
IS  - 1046-6673 (Linking)
VI  - 5
IP  - 11
DP  - 1995 May
TI  - Role of macrophages and colony-stimulating factor-1 in murine antiglomerular 
      basement membrane glomerulonephritis.
PG  - 1903-9
AB  - Macrophages have been shown to mediate glomerular injury in antiglomerular 
      basement membrane (anti-GBM) glomerulonephritis in rats and rabbits. To evaluate 
      the role of macrophages and the macrophage-related cytokines, colony stimulating 
      factor-1 (CSF-1), monocyte chemoattractant protein-1 (MCP-1) and RANTES, 
      accelerated anti-GBM nephritis was studied in op/op mutant mice, which lack CSF-1 
      and are severely macrophage deficient, and in heterozygous op/+ control mice. 
      Observations were made 24 h and 3 days after the injection of rabbit anti-mouse 
      GBM antibody in mice preimmunized with rabbit immunoglobulin G. Proteinuria rose 
      progressively in both groups but did not differ between them (urine 
      protein/creatinine ratio at 3 days: 1.01 +/- 0.38 in op/op versus 1.45 +/- 0.43 
      in op/+; P, not significant). In both op/op and op/+ mice, anti-GBM nephritis was 
      associated with renal expression of mRNA for RANTES and MCP-1 and barely 
      detectable levels of mRNA for CSF-1. In contrast, these cytokines were not 
      expressed in sham-injected mice. Morphologic lesions appeared earlier in op/op 
      mice but were comparable by Day 3. Glomerular injury consisted of capillary 
      thrombosis and endothelial cell damage associated with mild to moderate leukocyte 
      infiltration. Despite enhanced expression of mRNA for RANTES and MCP-1, 
      glomerular macrophage infiltration was not increased in op/+ mice. It was 
      concluded that, in mice, in contrast to rats and rabbits, accelerated anti-GBM 
      nephritis may develop in the absence of both CSF-1 and macrophage infiltration.
FAU - Neugarten, J
AU  - Neugarten J
AD  - Department of Medicine, Albert Einstein College of Medicine, Bronx, NY 10461, 
      USA.
FAU - Feith, G W
AU  - Feith GW
FAU - Assmann, K J
AU  - Assmann KJ
FAU - Shan, Z
AU  - Shan Z
FAU - Stanley, E R
AU  - Stanley ER
FAU - Schlondorff, D
AU  - Schlondorff D
LA  - eng
GR  - 5R01DK22036/DK/NIDDK NIH HHS/United States
GR  - CA 32551/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Am Soc Nephrol
JT  - Journal of the American Society of Nephrology : JASN
JID - 9013836
RN  - 0 (Antibodies)
RN  - 0 (Autoantibodies)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Colony-Stimulating Factors)
RN  - 0 (Cytokines)
RN  - 0 (Lymphokines)
RN  - 0 (Monocyte Chemoattractant Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (antiglomerular basement membrane antibody)
SB  - IM
MH  - Animals
MH  - Antibodies
MH  - Autoantibodies
MH  - Basement Membrane/immunology
MH  - Chemokine CCL5
MH  - Chemotactic Factors/genetics/physiology
MH  - Colony-Stimulating Factors/genetics/*physiology
MH  - Cytokines/genetics/physiology
MH  - Disease Models, Animal
MH  - Fluorescent Antibody Technique
MH  - Glomerulonephritis/*pathology
MH  - Kidney Glomerulus/immunology/pathology
MH  - Lymphokines/genetics
MH  - Macrophages/*physiology
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Monocyte Chemoattractant Proteins
MH  - RNA, Messenger/analysis
MH  - T-Lymphocytes/metabolism
EDAT- 1995/05/01 00:00
MHDA- 1995/05/01 00:01
CRDT- 1995/05/01 00:00
PHST- 1995/05/01 00:00 [pubmed]
PHST- 1995/05/01 00:01 [medline]
PHST- 1995/05/01 00:00 [entrez]
AID - 10.1681/ASN.V5111903 [doi]
PST - ppublish
SO  - J Am Soc Nephrol. 1995 May;5(11):1903-9. doi: 10.1681/ASN.V5111903.