Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1996-8-16
|
| pubmed:abstractText |
The lpr mutation on the MRL background accelerates autoimmune nephritis in which macrophage (M phi) accumulation is prominent. Renal disease is absent in other strains with lpr. TNF-alpha and CSF-1 are increased in the kidney of MRL-lpr mice with loss of renal function. We have established that CSF-1 can incite renal injury in mice with the lpr mutation, and M phi from the MRL strain hyper-respond to this growth factor. We hypothesized that TNF-alpha enhanced the M phi response to CSF-1 in MRL-lpr mice. We now report that TNF-alpha enhanced CSF-1-induced bone marrow M phi proliferation in MRL-lpr mice, and not in congenic MRL +/+, normal C3H +/+, and BALB/c, or another strain with lpr (C3H-lpr). Using a gene transfer approach to deliver CSF-1 together with TNF-alpha into the kidney, we evaluated the impact on renal injury. Tubular epithelial cells genetically modified to produce CSF-1 (CSF-1-TEC) and TNF-alpha (TNF-TEC) placed under the renal capsule caused a greater accumulation of M phi in the implant site than CSF-1-TECs alone in MRL-lpr, but not MRL +/+ mice. We noted in tissues adjacent but not distal to the implanted TECs, an increase in M phi in the interstitium and surrounding glomeruli of MRL-lpr but not MRL +/+ mice. This indicated that CSF-1 and TNF-alpha released by TECs were responsible for promoting renal pathology. Taken together, these data suggest that the simultaneous expression of TNF-alpha and CSF-1 in the MRL-lpr kidney fosters M phi accumulation. We speculate that the increase in M phi in the kidney in response to CSF-1 and TNF-alpha is responsible for the rapid tempo of autoimmune renal injury in MRL-lpr mice.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
157
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
427-32
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:8683148-Adjuvants, Immunologic,
pubmed-meshheading:8683148-Animals,
pubmed-meshheading:8683148-Bone Marrow,
pubmed-meshheading:8683148-Cell Division,
pubmed-meshheading:8683148-Colony-Forming Units Assay,
pubmed-meshheading:8683148-Epithelium,
pubmed-meshheading:8683148-Female,
pubmed-meshheading:8683148-Gene Transfer Techniques,
pubmed-meshheading:8683148-Kidney Glomerulus,
pubmed-meshheading:8683148-Kidney Tubules,
pubmed-meshheading:8683148-Lupus Nephritis,
pubmed-meshheading:8683148-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:8683148-Macrophages,
pubmed-meshheading:8683148-Mice,
pubmed-meshheading:8683148-Mice, Inbred BALB C,
pubmed-meshheading:8683148-Mice, Inbred C3H,
pubmed-meshheading:8683148-Mice, Mutant Strains,
pubmed-meshheading:8683148-Tumor Necrosis Factor-alpha
|
| pubmed:year |
1996
|
| pubmed:articleTitle |
TNF-alpha enhances colony-stimulating factor-1-induced macrophage accumulation in autoimmune renal disease.
|
| pubmed:affiliation |
Immunogenetics and Transplantation, Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|