Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation

Ribosomal inactivation damages 28S ribosomal RNA by interfering with its functioning during gene translation, leading to stress responses linked to a variety of inflammatory disease processes. Although the primary effect of ribosomal inactivation in cells is the functional inhibition of global prote...

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Main Author: Yuseok Moon
Format: Article
Language:English
Published: Hindawi Limited 2014-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2014/708193
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spelling doaj-f2818ce2aa4c4dd1b71ac9f85e33a8822020-11-25T01:19:13ZengHindawi LimitedMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/708193708193Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal InactivationYuseok Moon0Laboratory of Mucosal Exposome and Biomodulation, Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan 626-870, Republic of KoreaRibosomal inactivation damages 28S ribosomal RNA by interfering with its functioning during gene translation, leading to stress responses linked to a variety of inflammatory disease processes. Although the primary effect of ribosomal inactivation in cells is the functional inhibition of global protein synthesis, early responsive gene products including proinflammatory cytokines are exclusively induced by toxic stress in highly dividing tissues such as lymphoid tissue and epithelia. In the present study, ribosomal inactivation-related modulation of cytokine production was reviewed in leukocyte and epithelial pathogenesis models to characterize mechanistic evidence of ribosome-derived cytokine induction and its implications for potent therapeutic targets of mucosal and systemic inflammatory illness, particularly those triggered by organellar dysfunctions.http://dx.doi.org/10.1155/2014/708193
collection DOAJ
language English
format Article
sources DOAJ
author Yuseok Moon
spellingShingle Yuseok Moon
Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation
Mediators of Inflammation
author_facet Yuseok Moon
author_sort Yuseok Moon
title Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation
title_short Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation
title_full Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation
title_fullStr Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation
title_full_unstemmed Ribosomal Alteration-Derived Signals for Cytokine Induction in Mucosal and Systemic Inflammation: Noncanonical Pathways by Ribosomal Inactivation
title_sort ribosomal alteration-derived signals for cytokine induction in mucosal and systemic inflammation: noncanonical pathways by ribosomal inactivation
publisher Hindawi Limited
series Mediators of Inflammation
issn 0962-9351
1466-1861
publishDate 2014-01-01
description Ribosomal inactivation damages 28S ribosomal RNA by interfering with its functioning during gene translation, leading to stress responses linked to a variety of inflammatory disease processes. Although the primary effect of ribosomal inactivation in cells is the functional inhibition of global protein synthesis, early responsive gene products including proinflammatory cytokines are exclusively induced by toxic stress in highly dividing tissues such as lymphoid tissue and epithelia. In the present study, ribosomal inactivation-related modulation of cytokine production was reviewed in leukocyte and epithelial pathogenesis models to characterize mechanistic evidence of ribosome-derived cytokine induction and its implications for potent therapeutic targets of mucosal and systemic inflammatory illness, particularly those triggered by organellar dysfunctions.
url http://dx.doi.org/10.1155/2014/708193
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