Tissue proteases convert CCL23 into potent monocyte chemoattractants in patients with chronic rhinosinusitis

Because trypsin-like serine proteases have a major role in the truncation of CCL23 in NPs and inhibitors of neutrophil elastase (SSR69071) and matrix metalloproteinases (MMPs; marimastat), which are known to cleave CCL23,8,9 did not block the truncation (Fig 1, C), we focused on the mast cell trypsi...

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Published in:Journal of allergy and clinical immunology 2016-04, Vol.137 (4), p.1274-1277.e9
Main Authors: Poposki, Julie A., MS, Keswani, Anjeni, MD, Kim, Julie K., MD, Klingler, Aiko I., PhD, Suh, Lydia A., BS, Norton, James, MS, Carter, Roderick G., BS, Peters, Anju T., MD, Hulse, Kathryn E., PhD, Grammer, Leslie C., MD, Tan, Bruce K., MD, Conley, David B., MD, Jaen, Juan C., PhD, Schall, Thomas J., PhD, Kern, Robert C., MD, Kato, Atsushi, PhD
Format: Article
Language:English
Subjects:
Allergy and Immunology
Biomarkers - metabolism
Blotting, Western
Chemokines, CC - immunology
Chemokines, CC - metabolism
Chronic Disease
Humans
Infrared imaging systems
Mass spectrometry
Molecular weight
Monocytes - immunology
Monocytes - metabolism
Nasal Polyps - etiology
Nasal Polyps - immunology
Peptide Hydrolases - immunology
Peptide Hydrolases - metabolism
Protein Processing, Post-Translational
Proteins
Rhinitis - complications
Rhinitis - immunology
Scientific imaging
Sinusitis - complications
Sinusitis - immunology
Software
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Summary:Because trypsin-like serine proteases have a major role in the truncation of CCL23 in NPs and inhibitors of neutrophil elastase (SSR69071) and matrix metalloproteinases (MMPs; marimastat), which are known to cleave CCL23,8,9 did not block the truncation (Fig 1, C), we focused on the mast cell trypsin-like serine protease tryptase. Importantly, the CCR1 antagonist CCX8960 completely blocked NP-treated CCL23-dependent but not CCL2 (a CCR2 ligand)-dependent migration of THP-1 cells, indicating that truncation of CCL23 by NP extracts results in increased CCR1-dependent migration of THP-1 cells (see Fig E3, B). Because previously known active truncated forms of CCL23 are formed by N-terminal truncations, we initially assessed N-terminal protein sequences.
ISSN:0091-6749
1097-6825
DOI:10.1016/j.jaci.2015.09.029