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

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

doi:10.1016/j.clim.2007.04.002

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

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

Internal Medicine

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

The DBA/1 mouse strain is particularly sensitive to experimental immune-mediated nephritis. Previous studies have indicated that various chemokines/cytokines are elevated in strains of mice susceptible to immune-mediated glomerulonephritis. One of the many elevated cytokines is IL-1. This study was designed to determine if IL-1 is essential for the development of immune-mediated nephritis in the DBA/1 mouse strain that is particularly sensitive to this disease. Both male and female DBA/1 mice and DBA/1.IL-1R1^-/- mice were challenged with anti-GBM sera. We then compared DBA/1 mice to DBA/1.IL-1R1^-/- mice to determine the influence of IL-1 on immune-mediated nephritis. Compared to DBA/1 mice, DBA/1.IL-1R1^-/- mice excreted significantly less protein post anti-GBM serum challenge. None of the DBA/1.IL-1R1^-/- mice, male or female, had a BUN higher than 22 mg/dl post-challenge whereas wild-type DBA/1 mice had significantly elevated BUN. Wild-type DBA/1 mice exhibited pronounced glomerulonephritis, with crescent formation, as well as tubulo-interstitial disease compared to DBA/1.IL1R1^-/- mice. These findings indicate that IL-1 is necessary for the development of nephritis in DBA/1 mice and suggest that the elevated IL-1 levels in these mice may be one reason why the DBA/1 strain is particularly sensitive to multiple end organ diseases.

Original language	English (US)
Pages (from-to)	49-56
Number of pages	8
Journal	Clinical Immunology
Volume	124
Issue number	1
DOIs	https://doi.org/10.1016/j.clim.2007.04.002
State	Published - Jul 2007

Keywords

DBA/1
Genetics
IL-1
Lupus

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1016/j.clim.2007.04.002

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

abstract = "The DBA/1 mouse strain is particularly sensitive to experimental immune-mediated nephritis. Previous studies have indicated that various chemokines/cytokines are elevated in strains of mice susceptible to immune-mediated glomerulonephritis. One of the many elevated cytokines is IL-1. This study was designed to determine if IL-1 is essential for the development of immune-mediated nephritis in the DBA/1 mouse strain that is particularly sensitive to this disease. Both male and female DBA/1 mice and DBA/1.IL-1R1-/- mice were challenged with anti-GBM sera. We then compared DBA/1 mice to DBA/1.IL-1R1-/- mice to determine the influence of IL-1 on immune-mediated nephritis. Compared to DBA/1 mice, DBA/1.IL-1R1-/- mice excreted significantly less protein post anti-GBM serum challenge. None of the DBA/1.IL-1R1-/- mice, male or female, had a BUN higher than 22 mg/dl post-challenge whereas wild-type DBA/1 mice had significantly elevated BUN. Wild-type DBA/1 mice exhibited pronounced glomerulonephritis, with crescent formation, as well as tubulo-interstitial disease compared to DBA/1.IL1R1-/- mice. These findings indicate that IL-1 is necessary for the development of nephritis in DBA/1 mice and suggest that the elevated IL-1 levels in these mice may be one reason why the DBA/1 strain is particularly sensitive to multiple end organ diseases.",

keywords = "DBA/1, Genetics, IL-1, Lupus",

author = "Chun Xie and Xiangmei Qin and Geetha Jonnala and Yimei Gong and Mei Yan and Peijun Zong and Zhou, {Xin J.} and Chandra Mohan",

year = "2007",

month = jul,

doi = "10.1016/j.clim.2007.04.002",

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AU - Xie, Chun

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AU - Yan, Mei

AU - Zong, Peijun

AU - Zhou, Xin J.

AU - Mohan, Chandra

PY - 2007/7

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AB - The DBA/1 mouse strain is particularly sensitive to experimental immune-mediated nephritis. Previous studies have indicated that various chemokines/cytokines are elevated in strains of mice susceptible to immune-mediated glomerulonephritis. One of the many elevated cytokines is IL-1. This study was designed to determine if IL-1 is essential for the development of immune-mediated nephritis in the DBA/1 mouse strain that is particularly sensitive to this disease. Both male and female DBA/1 mice and DBA/1.IL-1R1-/- mice were challenged with anti-GBM sera. We then compared DBA/1 mice to DBA/1.IL-1R1-/- mice to determine the influence of IL-1 on immune-mediated nephritis. Compared to DBA/1 mice, DBA/1.IL-1R1-/- mice excreted significantly less protein post anti-GBM serum challenge. None of the DBA/1.IL-1R1-/- mice, male or female, had a BUN higher than 22 mg/dl post-challenge whereas wild-type DBA/1 mice had significantly elevated BUN. Wild-type DBA/1 mice exhibited pronounced glomerulonephritis, with crescent formation, as well as tubulo-interstitial disease compared to DBA/1.IL1R1-/- mice. These findings indicate that IL-1 is necessary for the development of nephritis in DBA/1 mice and suggest that the elevated IL-1 levels in these mice may be one reason why the DBA/1 strain is particularly sensitive to multiple end organ diseases.

KW - DBA/1

KW - Genetics

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

Abstract

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