a modeling-derived hypothesis on chronicity in respiratory diseases desensitized pathogen recognition secondary to hyperactive iraktraf6 signalingmodeling-derived假说在慢性呼吸道疾病麻木的病原体识别次要活跃iraktraf6信号.pdfVIP

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a modeling-derived hypothesis on chronicity in respiratory diseases desensitized pathogen recognition secondary to hyperactive iraktraf6 signalingmodeling-derived假说在慢性呼吸道疾病麻木的病原体识别次要活跃iraktraf6信号.pdf

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a modeling-derived hypothesis on chronicity in respiratory diseases desensitized pathogen recognition secondary to hyperactive iraktraf6 signalingmodeling-derived假说在慢性呼吸道疾病麻木的病原体识别次要活跃iraktraf6信号

A Modeling-Derived Hypothesis on Chronicity in Respiratory Diseases: Desensitized Pathogen Recognition Secondary to Hyperactive IRAK/TRAF6 Signaling Tingting Zhang*, Kyung W. Song, Mohammad Hekmat-Nejad, David G. Morris, Brian R. Wong Roche Palo Alto LLC, Palo Alto, California, United States of America Abstract Several chronic respiratory diseases exhibit hyperactive immune responses in the lung: abundant inflammatory mediators; infiltrating neutrophils, macrophages, lymphocytes and other immune cells; and increased level of proteases. Such diseases include cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD) and severe/neutrophilic asthma. Paradoxically, patients with these diseases are also susceptible to detrimental bacterial infection and colonization. In this paper, we seek to explain how a positive feedback mechanism via IL-8 could lead to desensitization of epithelial cells to pathogen recognition thus perpetuating bacterial colonization and chronic disease states in the lung. Such insight was obtained from mathematical modeling of the IRAK/TRAF6 signaling module, and is consistent with existing clinical evidence. The potential implications for targeted treatment regimes for these persistent respiratory diseases are explored. Citation: Zhang T, Song KW, Hekmat-Nejad M, Morris DG, Wong BR (2009) A Modeling-Derived Hypothesis on Chronicity in Respiratory Diseases: Desensitized Pathogen Recognition Secondary to Hyperactive IRAK/TRAF6 Signaling. PLoS ONE 4(4): e5332. doi:10.1371/journal.pone.0005332 Editor: Neeraj Vij, Johns Hopkins School of Medicine, United States of America Received December 23, 2008; Accepted March 30, 2009; Published April 24, 2009 Copyright: 2009 Zhang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestric