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Prevention of cold-associated acute inflammation in familial cold autoinflammatory syndrome by interleukin-1 receptor antagonist

Familial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterised by recurrent episodes of rash, arthralgia, and fever after cold exposure. The genetic basis of this disease has been elucidated. Cryopyrin, the protein that is altered in FCAS, is one of the adaptor protei... Full description

Journal Title: The Lancet (British edition) 2004, Vol.364 (9447), p.1779-1785
Main Author: Hoffman, Hal M
Other Authors: Rosengren, Sanna , Boyle, David L , Cho, Jae Y , Nayar, Jyothi , Mueller, James L , Anderson, Justin P , Wanderer, Alan A , Firestein, Gary S
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: London: Elsevier Ltd
ID: ISSN: 0140-6736
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4321997
title: Prevention of cold-associated acute inflammation in familial cold autoinflammatory syndrome by interleukin-1 receptor antagonist
format: Article
creator:
  • Hoffman, Hal M
  • Rosengren, Sanna
  • Boyle, David L
  • Cho, Jae Y
  • Nayar, Jyothi
  • Mueller, James L
  • Anderson, Justin P
  • Wanderer, Alan A
  • Firestein, Gary S
subjects:
  • Abridged Index Medicus
  • Acute Disease
  • Aged
  • Apoprotein
  • Arthralgia
  • Article
  • Autoimmune diseases
  • Biological and medical sciences
  • Care and treatment
  • Carrier Proteins - genetics
  • Carrier Proteins - physiology
  • Clinical trials
  • Cold Temperature - adverse effects
  • Colds
  • Control
  • Cytokines - metabolism
  • Development and progression
  • Dosage and administration
  • Exanthema
  • Female
  • Fever
  • General aspects
  • Genetic aspects
  • Genetic disorders
  • Health aspects
  • Human viral diseases
  • Humans
  • Immunohistochemistry
  • Infectious diseases
  • Inflammation
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Interleukin-1 - metabolism
  • Interleukin-6 - blood
  • Leukocyte Count
  • Male
  • Medical disorders
  • Medical sciences
  • Medical treatment
  • Middle Aged
  • Mutation
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Physiological aspects
  • Prevention
  • Proteins
  • Receptors, Interleukin-1 - antagonists & inhibitors
  • Sialoglycoproteins - therapeutic use
  • Skin - metabolism
  • Syndrome
  • Urticaria - genetics
  • Urticaria - metabolism
  • Urticaria - prevention & control
  • Viral diseases
  • Viral diseases of the respiratory system and ent viral diseases
ispartof: The Lancet (British edition), 2004, Vol.364 (9447), p.1779-1785
description: Familial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterised by recurrent episodes of rash, arthralgia, and fever after cold exposure. The genetic basis of this disease has been elucidated. Cryopyrin, the protein that is altered in FCAS, is one of the adaptor proteins that activate caspase 1, resulting in release of interleukin 1. An experimental cold challenge protocol was developed to study the acute inflammatory mechanisms occurring after a general cold exposure in FCAS patients and to investigate the effects of pretreatment with an antagonist of interleukin 1 receptor (IL-1Ra). ELISA, real-time PCR, and immunohistochemistry were used to measure cytokine responses. After cold challenge, untreated patients with FCAS developed rash, fever, and arthralgias within 1–4 h. Significant increases in serum concentrations of interleukin 6 and white-blood-cell counts were seen 4–8 h after cold challenge. Serum concentrations of interleukin 1 and cytokine mRNA in peripheral-blood leucocytes were not raised, but amounts of interleukin 1 protein and mRNA were high in affected skin. IL-1Ra administered before cold challenge blocked symptoms and increases in white-blood-cell counts and serum interleukin 6. The ability of IL-1Ra to prevent the clinical features and haematological and biochemical changes in patients with FCAS indicates a central role for interleukin 1β in this disorder. Involvement of cryopyrin in activation of caspase 1 and NF-κB signalling suggests that it might have a role in many chronic inflammatory diseases. These findings support a new therapy for a disorder with no previously known acceptable treatment. They also offer insights into the role of interleukin 1β in more common inflammatory diseases.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0140-6736
fulltext: fulltext
issn:
  • 0140-6736
  • 1474-547X
url: Link


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descriptionFamilial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterised by recurrent episodes of rash, arthralgia, and fever after cold exposure. The genetic basis of this disease has been elucidated. Cryopyrin, the protein that is altered in FCAS, is one of the adaptor proteins that activate caspase 1, resulting in release of interleukin 1. An experimental cold challenge protocol was developed to study the acute inflammatory mechanisms occurring after a general cold exposure in FCAS patients and to investigate the effects of pretreatment with an antagonist of interleukin 1 receptor (IL-1Ra). ELISA, real-time PCR, and immunohistochemistry were used to measure cytokine responses. After cold challenge, untreated patients with FCAS developed rash, fever, and arthralgias within 1–4 h. Significant increases in serum concentrations of interleukin 6 and white-blood-cell counts were seen 4–8 h after cold challenge. Serum concentrations of interleukin 1 and cytokine mRNA in peripheral-blood leucocytes were not raised, but amounts of interleukin 1 protein and mRNA were high in affected skin. IL-1Ra administered before cold challenge blocked symptoms and increases in white-blood-cell counts and serum interleukin 6. The ability of IL-1Ra to prevent the clinical features and haematological and biochemical changes in patients with FCAS indicates a central role for interleukin 1β in this disorder. Involvement of cryopyrin in activation of caspase 1 and NF-κB signalling suggests that it might have a role in many chronic inflammatory diseases. These findings support a new therapy for a disorder with no previously known acceptable treatment. They also offer insights into the role of interleukin 1β in more common inflammatory diseases.
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subjectAbridged Index Medicus ; Acute Disease ; Aged ; Apoprotein ; Arthralgia ; Article ; Autoimmune diseases ; Biological and medical sciences ; Care and treatment ; Carrier Proteins - genetics ; Carrier Proteins - physiology ; Clinical trials ; Cold Temperature - adverse effects ; Colds ; Control ; Cytokines - metabolism ; Development and progression ; Dosage and administration ; Exanthema ; Female ; Fever ; General aspects ; Genetic aspects ; Genetic disorders ; Health aspects ; Human viral diseases ; Humans ; Immunohistochemistry ; Infectious diseases ; Inflammation ; Interleukin 1 Receptor Antagonist Protein ; Interleukin-1 ; Interleukin-1 - metabolism ; Interleukin-6 - blood ; Leukocyte Count ; Male ; Medical disorders ; Medical sciences ; Medical treatment ; Middle Aged ; Mutation ; NLR Family, Pyrin Domain-Containing 3 Protein ; Physiological aspects ; Prevention ; Proteins ; Receptors, Interleukin-1 - antagonists & inhibitors ; Sialoglycoproteins - therapeutic use ; Skin - metabolism ; Syndrome ; Urticaria - genetics ; Urticaria - metabolism ; Urticaria - prevention & control ; Viral diseases ; Viral diseases of the respiratory system and ent viral diseases
ispartofThe Lancet (British edition), 2004, Vol.364 (9447), p.1779-1785
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descriptionFamilial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterised by recurrent episodes of rash, arthralgia, and fever after cold exposure. The genetic basis of this disease has been elucidated. Cryopyrin, the protein that is altered in FCAS, is one of the adaptor proteins that activate caspase 1, resulting in release of interleukin 1. An experimental cold challenge protocol was developed to study the acute inflammatory mechanisms occurring after a general cold exposure in FCAS patients and to investigate the effects of pretreatment with an antagonist of interleukin 1 receptor (IL-1Ra). ELISA, real-time PCR, and immunohistochemistry were used to measure cytokine responses. After cold challenge, untreated patients with FCAS developed rash, fever, and arthralgias within 1–4 h. Significant increases in serum concentrations of interleukin 6 and white-blood-cell counts were seen 4–8 h after cold challenge. Serum concentrations of interleukin 1 and cytokine mRNA in peripheral-blood leucocytes were not raised, but amounts of interleukin 1 protein and mRNA were high in affected skin. IL-1Ra administered before cold challenge blocked symptoms and increases in white-blood-cell counts and serum interleukin 6. The ability of IL-1Ra to prevent the clinical features and haematological and biochemical changes in patients with FCAS indicates a central role for interleukin 1β in this disorder. Involvement of cryopyrin in activation of caspase 1 and NF-κB signalling suggests that it might have a role in many chronic inflammatory diseases. These findings support a new therapy for a disorder with no previously known acceptable treatment. They also offer insights into the role of interleukin 1β in more common inflammatory diseases.
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38Medical treatment
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40Mutation
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42Physiological aspects
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44Proteins
45Receptors, Interleukin-1 - antagonists & inhibitors
46Sialoglycoproteins - therapeutic use
47Skin - metabolism
48Syndrome
49Urticaria - genetics
50Urticaria - metabolism
51Urticaria - prevention & control
52Viral diseases
53Viral diseases of the respiratory system and ent viral diseases
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titlePrevention of cold-associated acute inflammation in familial cold autoinflammatory syndrome by interleukin-1 receptor antagonist
authorHoffman, Hal M ; Rosengren, Sanna ; Boyle, David L ; Cho, Jae Y ; Nayar, Jyothi ; Mueller, James L ; Anderson, Justin P ; Wanderer, Alan A ; Firestein, Gary S
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abstractFamilial cold autoinflammatory syndrome (FCAS) is an autosomal dominant disorder characterised by recurrent episodes of rash, arthralgia, and fever after cold exposure. The genetic basis of this disease has been elucidated. Cryopyrin, the protein that is altered in FCAS, is one of the adaptor proteins that activate caspase 1, resulting in release of interleukin 1. An experimental cold challenge protocol was developed to study the acute inflammatory mechanisms occurring after a general cold exposure in FCAS patients and to investigate the effects of pretreatment with an antagonist of interleukin 1 receptor (IL-1Ra). ELISA, real-time PCR, and immunohistochemistry were used to measure cytokine responses. After cold challenge, untreated patients with FCAS developed rash, fever, and arthralgias within 1–4 h. Significant increases in serum concentrations of interleukin 6 and white-blood-cell counts were seen 4–8 h after cold challenge. Serum concentrations of interleukin 1 and cytokine mRNA in peripheral-blood leucocytes were not raised, but amounts of interleukin 1 protein and mRNA were high in affected skin. IL-1Ra administered before cold challenge blocked symptoms and increases in white-blood-cell counts and serum interleukin 6. The ability of IL-1Ra to prevent the clinical features and haematological and biochemical changes in patients with FCAS indicates a central role for interleukin 1β in this disorder. Involvement of cryopyrin in activation of caspase 1 and NF-κB signalling suggests that it might have a role in many chronic inflammatory diseases. These findings support a new therapy for a disorder with no previously known acceptable treatment. They also offer insights into the role of interleukin 1β in more common inflammatory diseases.
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