The Pseudomonas aeruginosa HSP70-like protein DnaK induces IL-1β expression via TLR4-dependent activation of the NF-κB and JNK signaling pathways |
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| Institution: | 1. Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, Boston, Massachusetts;2. Boston University School of Public Health, Boston, Massachusetts;3. Department of Endocrinology, Diabetes, and Hypertension, Brigham and Women''s Hospital, Boston, Massachusetts;4. Department of Pharmacy, Boston Medical Center, Boston, Massachusetts.;2. Brain Korea 21 PLUS Project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Korea;1. Laboratory of Pharmaceutical Microbiology, Ghent University, Ghent, Belgium;2. Laboratory of General Biochemistry and Physical Pharmacy, Ghent University, Ghent, Belgium;3. Centre for Nano- and Biophotonics, Ghent University, Ghent, Belgium;4. Laboratory of Pharmaceutical Biotechnology, Ghent University, Ghent, Belgium;5. Research Core Unit Metabolomics, Hannover Medical School, Hannover, Germany |
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| Abstract: | IL-1β expression is increased in response to P. aeruginosa infection, but the responsible proteins have not been clearly elucidated. Here, we demonstrate for the first time that IL-1β expression is induced in response to the heat shock protein 70-like protein DnaK. Treatment with recombinant DnaK (rDnaK) increased IL-1β expression in a dose- and time-dependent manner, and the release of mature IL-1β in response to rDnaK was detected to an extent similar to that stimulated by the well-known agonists, lipopolysaccharide and nigericin. rDnaK-mediated IL-1β expression was driven by the NF-κB signaling pathway. In addition, expression was controlled by the JNK signaling pathway, although these two signaling cascades act independently upon rDnaK stimulation. Finally, rDnaK-induced IL-1β expression was initiated via the action of TLR4. Taken together, the data reveal that P. aeruginosa-derived DnaK induces expression of IL-1β via TLR4-dependent activation of the NF-κB and JNK signaling pathways. |
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| Keywords: | DnaK IL-1β JNK NF-κB TLR4 |
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