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Mediators of Inflammation
Volume 2014, Article ID 708193, 10 pages
Review Article

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

1Laboratory of Mucosal Exposome and Biomodulation, Department of Microbiology and Immunology, Pusan National University School of Medicine, Yangsan 626-870, Republic of Korea
2Immunoregulatory Therapeutics Group in Brain Busan 21 Project, Busan 609-735, Republic of Korea
3Medical Research Institute, Pusan National University, Busan 609-735, Republic of Korea

Received 14 September 2013; Accepted 22 November 2013; Published 2 January 2014

Academic Editor: Eduardo López-Collazo

Copyright © 2014 Yuseok Moon. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.