Enhanced susceptibility to immune nephritis in DBA/1 mice is contingent upon IL-1 expression

Xie, Chun; Qin, Xiangmei; Jonnala, Geetha; Gong, Yimei; Yan, Mei; Zong, Peijun; Zhou, Xin J.; Mohan, Chandra

doi:10.1016/j.clim.2007.04.002

Cited by 6 publications

(6 citation statements)

References 40 publications

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“…Consistent with reported findings, 129/SvJ kidneys developed severe proliferative glomerulonephritis (GN) including mesangial proliferation with increases in matrices, focal necrosis, destruction of capillary lumens, and crescent formation [ 12 , 13 , 25 , 28 ]. Figure 2 shows that renal disease, including GN score, percent crescent formation, and severity of tubulointerstitial (TI) disease, was markedly reduced in LP17 treated mice, commensurate with the dramatic reduction in the renal inflammatory infiltrate and interstitial macrophages in LP17-treated mice.…”

Section: Resultssupporting

confidence: 78%

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Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Zhou

et al. 2016

Inflammation

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CD354, Triggering Receptor of Myeloid Cells-1 (TREM-1), is a potent amplifier of myeloid immune responses. Our goal was to determine the expression and function of TREM-1 in immune-mediated nephritis. An anti-glomerular basement membrane antibody (anti-GBM)-induced nephritis model was employed, where mice were sensitized with rabbit IgG followed by anti-GBM serum to induce disease. Anti-GBM-treated 129x1/svJ mice developed severe nephritis whereas C57BL/6 (B6) mice were resistant to disease. Anti-GBM disease resulted in elevated renal TREM-1 messenger RNA (mRNA) and protein levels and increased urine TREM-1 levels in 129x1/svJ. TREM-1 blockade with an inhibitory peptide, LP17, inhibited proteinuria and renal disease as measured by glomerulonephritis class, severity of tubulointerstitial disease, crescent formation, and inflammatory cell infiltrates. In sum, TREM-1 is upregulated in renal inflammation and plays a vital role in driving disease. Thus, TREM-1 blockade emerges as a potential therapeutic avenue for immune-mediated renal diseases such as lupus nephritis.

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Section: Resultssupporting

confidence: 78%

“…We have previously shown that the 129/SvJ strain is susceptible to a rapid onset glomerulonephritis while C57BL/6 (B6) mice are relatively resistant to anti-GBM nephritis [ 4 , 23 , 25 , 28 ]. TREM-1 and TREM-2 were undetectable in control kidneys by immunohistochemistry (IHC) before induction of anti-GBM disease.…”

Section: Resultsmentioning

confidence: 99%

Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Zhou

et al. 2016

Inflammation

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“…BUB/BnJ, DBA/1J and 129/svJ mice developed severe proteinuria and increased BUN, indicating rapidly progressive glomerulonephritis [28]. The variable susceptibility to immune-mediated nephritis can be explained by the substantial differences in the interleukin expression profiles between mice strains, which modulate the progression of this disease [29]. …”

Section: Non-surgical Modelsmentioning

confidence: 99%

Non-Transgenic Mouse Models of Kidney Disease

Rabe¹,

Schaefer²

2016

Nephron

1,380

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Animal models are essential tools to understand the mechanisms underlying the development and progression of renal disease and to study potential therapeutic approaches. Recently, interventional models suitable to induce acute and chronic kidney disease in the mouse have become a focus of interest due to the wide availability of genetically engineered mouse lines. These models differ by their damaging mechanism (cell toxicity, immune mechanisms, surgical renal mass reduction, ischemia, hypertension, ureter obstruction etc.), functional and histomorphological phenotype and disease evolution. The susceptibility to a damaging mechanism often depends on strain and gender. The C57BL/6 strain, the most commonly used genetic background of transgenic mice, appears to be relatively resistant against developing glomerulosclerosis, proteinuria and hypertension. This review serves to provide a comprehensive overview of interventional mouse models of acute and chronic kidney disease.

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“…Our current study and several other previous studies indicate that susceptibility to anti-GBM disease is not related to the quantity or quality of xenogenic immune response to the administered rabbit sera. [15][16][17][18][19] Among the different strains studied, the NZM2410 and NZW strains exhibited the most severe renal disease following anti-GBM challenge. This is perhaps not a surprise given the fact that 75% of the NZM2410 genome is NZW-derived.…”

Section: Discussionmentioning

confidence: 99%

“…In this respect, the anti-glomerular basement membrane (GBM)-induced nephritis model is emerging as an informative experimental tool. [15][16][17][18][19][20] This may relate to the fact that anti-GBMinduced nephritis and spontaneously arising lupus nephritis share similar downstream cellular and molecular events that lead to renal pathology and dysfunction despite differing in the nature of the initial antibody deposits. 14 This powerful tool has helped to identify certain strains such as 129/sv, BUB, DBA/1, C58 and NZW as being particularly susceptible to immune-mediated nephritis and others such as A/J, AKR, BALB/c, C3H, C57BL/6, DBA/2, DDY, FVB, MRL, NOD, P/J, SB, SJL and SWR as being less susceptible.…”

Section: Introductionmentioning

confidence: 99%

Lupus-prone strains vary in susceptibility to antibody-mediated end organ disease

Xie

Kumar

et al. 2013

Genes Immun

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Renal involvement is the major cause of morbidity and mortality in lupus. Besides autoantibodies, intrinsic renal factors may contribute to the susceptibility to lupus nephritis. To determine how different mouse strains that develop spontaneous lupus fare in their susceptibility to immune mediated nephritis, mice from six lupus-prone strains and two non-lupus control strains (B6 and BALB/c) were challenged with rabbit anti-GBM sera. Among the strains tested, NZM2410 (or NZM) mice developed severe glomerulonephritis (GN), whereas BXSB and B6.lpr, NZB mice were relatively resistant to anti-GBM disease, as were the BALB/c controls. BWF1 and B6.Yaa mice exhibited intermediate degrees of GN that was comparable to the B6 controls. The severity of the renal disease in these strains did not appear to be related to the degree of the systemic immune response to the administered rabbit Ig. In addition, cytokine profiling demonstrated differential urinary excretion of several molecules in the NZM mice, compared with the controls. Together with our previous reports, our studies demonstrate that lupus-prone strains vary in their susceptibility to immune mediated nephritis, despite similar levels of circulating autoantibodies and comparable degrees of immune complex deposition in the kidneys.

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Enhanced susceptibility to immune nephritis in DBA/1 mice is contingent upon IL-1 expression

Cited by 6 publications

References 40 publications

Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Non-Transgenic Mouse Models of Kidney Disease

Lupus-prone strains vary in susceptibility to antibody-mediated end organ disease

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