Abstract

Ulcerative Colitis (UC) is a form of inflammatory bowel disease (IBD) characterized by damage of large bowel mucosa and frequent extra-intestinal autoimmune comorbidities. The role played in IBD pathogenesis by molecular chaperones known to interact with components of the immune system involved in inflammation is unclear. We previously demonstrated that mucosal HSP60 decreases in UC patients treated with conventional therapies (mesalazine, probiotics), suggesting that this chaperonin could be a reliable biomarker useful for monitoring response to treatment, and that it might play a role in pathogenesis. In the present work we investigated three other heat sock protein/molecular chaperones:HSP10, HSP70; and HSP90. We found that the levels of these proteins are increased in UC patients at the time of diagnosis and decrease after therapy, supporting the notion that these proteins deserve attention in the study of the mechanism that promote the development and maintenance of IBD, and as biomarkers of this disease (c.g., to monitor response to treatment at the histological level).
Lingua originaleEnglish
pagine (da-a)210-214
Numero di pagine5
RivistaDefault journal
Volume55
Stato di pubblicazionePublished - 2011

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Ulcerative Colitis
Inflammatory Bowel Diseases
Molecular Chaperones
Biomarkers
Chaperonins
Mesalamine
Proteins
Probiotics
Therapeutics
Comorbidity
Immune System
Mucous Membrane
Hot Temperature
Maintenance
Inflammation

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Histology
  • Cell Biology

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@article{2251d3a3a44a45349065447e2e07728e,
title = "HSP10,HSP70 AND HSP90 IMMUNOHISTOCHEMICAL LEVELS CHANGE IN ULCERATIVE COLITIS AFTER THERAPY",
abstract = "Ulcerative Colitis (UC) is a form of inflammatory bowel disease (IBD) characterized by damage of large bowel mucosa and frequent extra-intestinal autoimmune comorbidities. The role played in IBD pathogenesis by molecular chaperones known to interact with components of the immune system involved in inflammation is unclear. We previously demonstrated that mucosal HSP60 decreases in UC patients treated with conventional therapies (mesalazine, probiotics), suggesting that this chaperonin could be a reliable biomarker useful for monitoring response to treatment, and that it might play a role in pathogenesis. In the present work we investigated three other heat sock protein/molecular chaperones:HSP10, HSP70; and HSP90. We found that the levels of these proteins are increased in UC patients at the time of diagnosis and decrease after therapy, supporting the notion that these proteins deserve attention in the study of the mechanism that promote the development and maintenance of IBD, and as biomarkers of this disease (c.g., to monitor response to treatment at the histological level).",
author = "Francesca Rappa and Giovanni Tomasello and Monica Zerilli and Carmelo Sciume' and Felicia Farina and {De Luca}, Rossella and Francesco Cappello and Anna Martorana and Giovanni Zummo and Vito Rodolico and Marcello Romeo and Giuseppe Cicero and Giuseppe Modica and Giuseppe Bonaventura and Romeo and Cappello and {Conway De Macario} and Macario, {Alberto J.L.}",
year = "2011",
language = "English",
volume = "55",
pages = "210--214",
journal = "Default journal",

}

TY - JOUR

T1 - HSP10,HSP70 AND HSP90 IMMUNOHISTOCHEMICAL LEVELS CHANGE IN ULCERATIVE COLITIS AFTER THERAPY

AU - Rappa, Francesca

AU - Tomasello, Giovanni

AU - Zerilli, Monica

AU - Sciume', Carmelo

AU - Farina, Felicia

AU - De Luca, Rossella

AU - Cappello, Francesco

AU - Martorana, Anna

AU - Zummo, Giovanni

AU - Rodolico, Vito

AU - Romeo, Marcello

AU - Cicero, Giuseppe

AU - Modica, Giuseppe

AU - Bonaventura, Giuseppe

AU - Romeo, null

AU - Cappello, null

AU - Conway De Macario, null

AU - Macario, Alberto J.L.

PY - 2011

Y1 - 2011

N2 - Ulcerative Colitis (UC) is a form of inflammatory bowel disease (IBD) characterized by damage of large bowel mucosa and frequent extra-intestinal autoimmune comorbidities. The role played in IBD pathogenesis by molecular chaperones known to interact with components of the immune system involved in inflammation is unclear. We previously demonstrated that mucosal HSP60 decreases in UC patients treated with conventional therapies (mesalazine, probiotics), suggesting that this chaperonin could be a reliable biomarker useful for monitoring response to treatment, and that it might play a role in pathogenesis. In the present work we investigated three other heat sock protein/molecular chaperones:HSP10, HSP70; and HSP90. We found that the levels of these proteins are increased in UC patients at the time of diagnosis and decrease after therapy, supporting the notion that these proteins deserve attention in the study of the mechanism that promote the development and maintenance of IBD, and as biomarkers of this disease (c.g., to monitor response to treatment at the histological level).

AB - Ulcerative Colitis (UC) is a form of inflammatory bowel disease (IBD) characterized by damage of large bowel mucosa and frequent extra-intestinal autoimmune comorbidities. The role played in IBD pathogenesis by molecular chaperones known to interact with components of the immune system involved in inflammation is unclear. We previously demonstrated that mucosal HSP60 decreases in UC patients treated with conventional therapies (mesalazine, probiotics), suggesting that this chaperonin could be a reliable biomarker useful for monitoring response to treatment, and that it might play a role in pathogenesis. In the present work we investigated three other heat sock protein/molecular chaperones:HSP10, HSP70; and HSP90. We found that the levels of these proteins are increased in UC patients at the time of diagnosis and decrease after therapy, supporting the notion that these proteins deserve attention in the study of the mechanism that promote the development and maintenance of IBD, and as biomarkers of this disease (c.g., to monitor response to treatment at the histological level).

UR - http://hdl.handle.net/10447/62452

M3 - Article

VL - 55

SP - 210

EP - 214

JO - Default journal

JF - Default journal

ER -