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Critical role for inflammasome-independent IL-1β production in osteomyelitis

The immune system plays an important role in the pathophysiology of many acute and chronic bone disorders, but the specific inflammatory networks that regulate individual bone disorders remain to be elucidated. Here, we characterized the osteoimmunological underpinnings of osteolytic bone disease in... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America 21 January 2014, Vol.111(3), pp.1066-71
Main Author: Lukens, John R
Other Authors: Gross, Jordan M , Calabrese, Christopher , Iwakura, Yoichiro , Lamkanfi, Mohamed , Vogel, Peter , Kanneganti, Thirumala-Devi
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; PMID: 24395792 Version:1 ; DOI: 10.1073/pnas.1318688111
Link: http://pubmed.gov/24395792
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recordid: medline24395792
title: Critical role for inflammasome-independent IL-1β production in osteomyelitis
format: Article
creator:
  • Lukens, John R
  • Gross, Jordan M
  • Calabrese, Christopher
  • Iwakura, Yoichiro
  • Lamkanfi, Mohamed
  • Vogel, Peter
  • Kanneganti, Thirumala-Devi
subjects:
  • Autoinflammation
  • Interleukin-1
  • Osteoimmunology
  • Gene Expression Regulation
  • Inflammasomes -- Metabolism
  • Interleukin-1beta -- Metabolism
  • Osteomyelitis -- Metabolism
ispartof: Proceedings of the National Academy of Sciences of the United States of America, 21 January 2014, Vol.111(3), pp.1066-71
description: The immune system plays an important role in the pathophysiology of many acute and chronic bone disorders, but the specific inflammatory networks that regulate individual bone disorders remain to be elucidated. Here, we characterized the osteoimmunological underpinnings of osteolytic bone disease in Pstpip2(cmo) mice. These mice carry a homozygous L98P missense mutation in the Pombe Cdc15 homology family phosphatase PSTPIP2 that is responsible for the development of a persistent autoinflammatory disease resembling chronic recurrent multifocal osteomyelitis in humans. We found that improper regulation of IL-1β production resulted in secondary induction of inflammatory cytokines, inflammatory cell infiltration in the bone, and unremitting bone inflammation. Aberrant Il1β expression precedes the development of osteolytic damage in young Pstpip2(cmo) mice, and genetic deletion of Il1r and Il1β, but not Il1α, rescued osteolytic bone disease in mutant mice. Intriguingly, caspase-1 and nucleotide-binding...
language: eng
source:
identifier: E-ISSN: 1091-6490 ; PMID: 24395792 Version:1 ; DOI: 10.1073/pnas.1318688111
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleCritical role for inflammasome-independent IL-1β production in osteomyelitis
creatorLukens, John R ; Gross, Jordan M ; Calabrese, Christopher ; Iwakura, Yoichiro ; Lamkanfi, Mohamed ; Vogel, Peter ; Kanneganti, Thirumala-Devi
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subjectAutoinflammation ; Interleukin-1 ; Osteoimmunology ; Gene Expression Regulation ; Inflammasomes -- Metabolism ; Interleukin-1beta -- Metabolism ; Osteomyelitis -- Metabolism
descriptionThe immune system plays an important role in the pathophysiology of many acute and chronic bone disorders, but the specific inflammatory networks that regulate individual bone disorders remain to be elucidated. Here, we characterized the osteoimmunological underpinnings of osteolytic bone disease in Pstpip2(cmo) mice. These mice carry a homozygous L98P missense mutation in the Pombe Cdc15 homology family phosphatase PSTPIP2 that is responsible for the development of a persistent autoinflammatory disease resembling chronic recurrent multifocal osteomyelitis in humans. We found that improper regulation of IL-1β production resulted in secondary induction of inflammatory cytokines, inflammatory cell infiltration in the bone, and unremitting bone inflammation. Aberrant Il1β expression precedes the development of osteolytic damage in young Pstpip2(cmo) mice, and genetic deletion of Il1r and Il1β, but not Il1α, rescued osteolytic bone disease in mutant mice. Intriguingly, caspase-1 and nucleotide-binding...
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titleCritical role for inflammasome-independent IL-1β production in osteomyelitis
descriptionThe immune system plays an important role in the pathophysiology of many acute and chronic bone disorders, but the specific inflammatory networks that regulate individual bone disorders remain to be elucidated. Here, we characterized the osteoimmunological underpinnings of osteolytic bone disease in Pstpip2(cmo) mice. These mice carry a homozygous L98P missense mutation in the Pombe Cdc15 homology family phosphatase PSTPIP2 that is responsible for the development of a persistent autoinflammatory disease resembling chronic recurrent multifocal osteomyelitis in humans. We found that improper regulation of IL-1β production resulted in secondary induction of inflammatory cytokines, inflammatory cell infiltration in the bone, and unremitting bone inflammation. Aberrant Il1β expression precedes the development of osteolytic damage in young Pstpip2(cmo) mice, and genetic deletion of Il1r and Il1β, but not Il1α, rescued osteolytic bone disease in mutant mice. Intriguingly, caspase-1 and nucleotide-binding...
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abstractThe immune system plays an important role in the pathophysiology of many acute and chronic bone disorders, but the specific inflammatory networks that regulate individual bone disorders remain to be elucidated. Here, we characterized the osteoimmunological underpinnings of osteolytic bone disease in Pstpip2(cmo) mice. These mice carry a homozygous L98P missense mutation in the Pombe Cdc15 homology family phosphatase PSTPIP2 that is responsible for the development of a persistent autoinflammatory disease resembling chronic recurrent multifocal osteomyelitis in humans. We found that improper regulation of IL-1β production resulted in secondary induction of inflammatory cytokines, inflammatory cell infiltration in the bone, and unremitting bone inflammation. Aberrant Il1β expression precedes the development of osteolytic damage in young Pstpip2(cmo) mice, and genetic deletion of Il1r and Il1β, but not Il1α, rescued osteolytic bone disease in mutant mice. Intriguingly, caspase-1 and nucleotide-binding...
doi10.1073/pnas.1318688111
pmid24395792
date2014-01-21