Journal
KIDNEY INTERNATIONAL
Volume 86, Issue 6, Pages 1174-1186Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ki.2014.205
Keywords
chronic kidney disease; fibrosis; immunology and pathology; macrophages; obstructive nephropathy
Categories
Funding
- National Science Council [NSC97-2320-B010-032-MY2, NSC99-2320-B10-003-MY3, NSC102-2320-B -010-015, NSC 99-2314-B-010-004-MY3, NSC 102-2314-B-010-004-MY3]
- Taipei Veterans General Hospital [V97S5-001, V98S5-008, V99S5-002, V100E4-003, V101E4-001, V102E4-001]
- Yen Tjing Ling Medical Foundation [CI-100-10]
- Ministry of Education, Aim for the Top University Plan in Taiwan [98A-C-D117]
- Bureau of Health Promotion, Department of Health [DOH98-HP-1110]
- Canadian Institute of Health Research
- Leukemia Lymphoma Society
- Terry Fox Cancer Research Foundation
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Chronic kidney disease (CKD) is an emerging worldwide public health problem. Inflammatory cell infiltration and activation during the early stages in injured kidneys is a common pathologic feature of CKD. Here, we determined whether an important inflammatory regulator, triggering receptor expressed on myeloid cells (TREM)-1, is upregulated in renal tissues collected from mouse ureteral obstruction-induced nephritis. TREM-1 is crucial for modulating macrophage polarization, and has a pivotal role in mediating tubular injury and interstitial collagen deposition in obstructive nephritis. Lysates from nephritic kidneys triggered a TREM-1-dependent M1 polarization ex vivo, consistent with the observation that granulocyte-macrophage colony-stimulating factor (GM-CSF)-derived M1 macrophages express higher levels of TREM-1 in comparison with M-CSF-derived cells. Moreover, agonistic TREM-1 crosslink significantly strengthens the inductions of iNOS and GMCSF in M1 cells. These observations are validated by a strong clinical correlation between infiltrating TREM-1-expressing/iNOS-positive macrophages and renal injury in human obstructive nephropathy. Thus, TREM-1 may be a potential diagnostic and therapeutic target in human kidney disease.
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