NDLI: Cellular stress amplifies TLR3/4-induced CXCL1/2 gene transcription in mononuclear phagocytes via RIPK1.

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Cellular stress amplifies TLR3/4-induced CXCL1/2 gene transcription in mononuclear phagocytes via RIPK1.

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Cellular stress amplifies TLR3/4-induced CXCL1/2 gene transcription in mononuclear phagocytes via RIPK1.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Datta, Shyamasree Hamilton, Thomas A. Pavicic, Paul G. Sun, Dongxu Novotny, Michael Zhao, Chenyang
Description	Author Affiliation: Zhao C ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195.); Pavicic PG ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195.); Datta S ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195.); Sun D ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195.); Novotny M ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195.); Hamilton TA ( Department of Immunology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195 hamiltt@ccf.org.)
Abstract	The impact of environmental stressors on the magnitude of specific chemokine gene expression was examined in mouse bone marrow-derived macrophages stimulated through various TLRs. Levels of TLR-stimulated CXCL1 and CXCL2 but not CXCL10 or CCL5 mRNAs were selectively enhanced (>10-fold) in stressed macrophages. The amplification was also manifested for other proinflammatory cytokines, including TNF- , IL-1 , and IL-6. Responses through TLR3 and TLR4 exhibited the greatest sensitivity, reflecting a requirement for Toll/IL-IR domain-containing adaptor-inducing IFN-ß (TRIF), the adaptor protein selectively associated with these TLRs. IFN regulatory factor 3, a transcription factor that is downstream of TLR4/TRIF signaling, was not required for sensitivity to stress-induced chemokine amplification. c/EBP homologous protein and X box binding protein 1 have been reported to enhance inflammatory cytokine responses but are not required for amplification of TLR3/4-induced CXCL1 expression. Rather, receptor-interacting protein kinase 1, a kinase also linked with TLR3/4/TRIF signaling, is required and involves a stress-dependent increase in its abundance and ubiquitination. Whereas NF-κB activation is necessary for TLR-induced chemokine gene transcription, this factor does not appear to be the primary mechanistic target of environmental stress. The application of stress also enhanced chemokine expression in macrophages infiltrating the peritoneal cavity but was not observed in the resident peritoneal cells or in the liver. These findings identify novel mechanisms for modulating the magnitude and duration of selective TLR-induced chemokine and cytokine gene expression and further establish the importance of cell stress pathways in coordinating the outcomes of cellular and tissue injury.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1303396
Journal	The Journal of Immunology
Issue Number	2
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chemokine Cxcl1 Genetics Chemokine Cxcl2 Macrophages Metabolism Receptor-interacting Protein Serine-threonine Kinases Toll-like Receptor 3 Toll-like Receptor 4 Adaptor Proteins, Vesicular Transport Animals Blotting, Western Cell Line Cells, Cultured Cytokines Dna-binding Proteins Dimethyl Sulfoxide Pharmacology Gene Expression Drug Effects Lipopolysaccharides Mice Mice, Inbred C57bl Mice, Knockout Myeloid Cells Rna Interference Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Stress, Physiological Transcription Factors Tunicamycin Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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