PMID- 16302095
OWN - NLM
STAT- MEDLINE
DCOM- 20060816
LR  - 20190606
IS  - 0100-879X (Print)
IS  - 0100-879X (Linking)
VI  - 38
IP  - 12
DP  - 2005 Dec
TI  - Genetic potential for an acute inflammatory response in IgA glomerulonephritis in 
      mice.
PG  - 1807-15
AB  - Mice selected on the basis of an acute inflammatory response (AIR) can provide 
      information about the immunopathological mechanisms of glomerulonephritis. We 
      studied the differences between mice selected for a maximal AIR (AIRmax that 
      attract more polymorphonuclear cells to the site of injury) or a minimal AIR 
      (AIRmin that attract more mononuclear cells) in an experimental model of IgA 
      nephropathy in order to investigate the effect of genetic background on 
      glomerular disease progression and the participation of the monocyte 
      chemoattractant protein-1 (MCP-1) chemokine. IgA nephropathy was induced by 
      intraperitoneal ovalbumin injection and bile duct ligation in AIRmax and AIRmin 
      mice. Histological changes, urinary protein/creatinine ratio, serum IgA levels, 
      immunofluorescence for IgA, IgG and complement C3 fraction, immunohistochemistry 
      for macrophages and MCP-1, and MCP-1 levels in macerated kidney were determined. 
      Mesangial IgA deposition was seen only in AIRmin mice, which presented more renal 
      lesions. Increased serum IgA levels (1.5 +/- 0.4 vs 0.3 +/- 0.1 mg/mL, P < 
      0.001), high glomerular MCP-1 expression and decreased monocyte/macrophage 
      infiltration in the interstitial area (0.3 +/- 0.3 vs 1.1 +/- 0.9 
      macrophages/field, P < 0.05) were detected in AIRmin mice compared to AIRmax 
      mice. No glomerular monocyte/macrophage infiltration was detected in either 
      strain. In spite of the absence of IgA deposition, AIRmax mice presented discrete 
      or absent mesangial proliferation. The study showed that there are differences 
      between mice selected for AIRmax and AIRmin with respect to serum IgA levels, 
      histological damage and MCP-1 chemokine production after ovalbumin injection in 
      combination with bile duct ligation.
FAU - Kurihara, R S
AU  - Kurihara RS
AD  - Laboratorio de Fisiopatologia Renal, Faculdade de Medicina, Universidade de Sao 
      Paulo, Rua Agostinho Cretella 58, 05337-040 Sao Paulo, SP, Brazil. 
      roshara@uol.com.br
FAU - Yokoo, M
AU  - Yokoo M
FAU - Domingues, W V
AU  - Domingues WV
FAU - Cabrera, W H
AU  - Cabrera WH
FAU - Ribeiro, O G
AU  - Ribeiro OG
FAU - Ibanez, O M
AU  - Ibanez OM
FAU - Malheiros, D A
AU  - Malheiros DA
FAU - Barros, R T
AU  - Barros RT
FAU - de Almeida Prado, E B
AU  - de Almeida Prado EB
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20051109
PL  - Brazil
TA  - Braz J Med Biol Res
JT  - Brazilian journal of medical and biological research = Revista brasileira de 
      pesquisas medicas e biologicas
JID - 8112917
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Acute Disease
MH  - Acute-Phase Reaction/immunology/pathology
MH  - Animals
MH  - Chemokine CCL2/*immunology
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Glomerulonephritis, IGA/*genetics/*immunology/pathology
MH  - Immunohistochemistry
MH  - Inflammation/*immunology/pathology
MH  - Macrophages/*immunology/pathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Monocytes/*immunology/physiology
MH  - Species Specificity
EDAT- 2005/11/23 09:00
MHDA- 2006/08/17 09:00
CRDT- 2005/11/23 09:00
PHST- 2005/11/23 09:00 [pubmed]
PHST- 2006/08/17 09:00 [medline]
PHST- 2005/11/23 09:00 [entrez]
AID - S0100-879X2005001200009 [pii]
AID - 10.1590/s0100-879x2005001200009 [doi]
PST - ppublish
SO  - Braz J Med Biol Res. 2005 Dec;38(12):1807-15. doi: 
      10.1590/s0100-879x2005001200009. Epub 2005 Nov 9.