Cyclic stretch induced IL-33 production through HMGB1/TLR-4 signaling pathway in murine respiratory epithelial cells

Interleukin 33 (IL-33), an inflammatory and mechanically responsive cytokine, is an important component of a TLR4-dependent innate immune process in mucosal epithelium. Although TLR4 also plays a role in sensing biomechanical stretch, a pathway of stretch-induced TLR4-dependent IL-33 biosynthesis ha...

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Bibliographic Details
Published in:PloS one 2017-09, Vol.12 (9), p.e0184770
Main Authors: Chang, Jing, Xia, Yuefeng, Wasserloos, Karla, Deng, Meihong, Blose, Kory J, Vorp, David A, Turnquist, Heth R, Billiar, Timothy R, Pitt, Bruce A, Zhang, Ma-Zhong, Zhang, Li-Ming
Format: Article
Language:English
Subjects:
Allergies
Anesthesiology
Animals
Bioengineering
Biology and life sciences
Biomechanics
Biosynthesis
Cardiomyocytes
Cell Line
Cellular signal transduction
Conditioned stimulus
Conditioning
Cytokines
Epithelial cells
Epithelium
Gene expression
Genetic aspects
HMGB1 protein
HMGB1 Protein - metabolism
Immunology
Inflammation
Interleukin-33 - genetics
Interleukin-33 - metabolism
Interleukins
Ligands
Mechanotransduction, Cellular
Medicine
Medicine and Health Sciences
Mice
Molecular biology
Mucosal immunity
Occupational health
Physiological aspects
Physiology
Public health
Receptors
Research and Analysis Methods
Respiratory Mucosa - metabolism
Respiratory tract
Rodents
Second Messenger Systems
Signal transduction
Stress, Mechanical
Surgery
TLR4 protein
Toll-Like Receptor 4 - metabolism
Toll-like receptors
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Summary:Interleukin 33 (IL-33), an inflammatory and mechanically responsive cytokine, is an important component of a TLR4-dependent innate immune process in mucosal epithelium. Although TLR4 also plays a role in sensing biomechanical stretch, a pathway of stretch-induced TLR4-dependent IL-33 biosynthesis has not been revealed. In the current study, we show that short term (6 h) cyclic stretch (CS) of cultured murine respiratory epithelial cells (MLE-12) increased intracellular IL-33 expression in a TLR4 dependent fashion. There was no detectable IL-33 in conditioned media in this interval. CS, however, increased release of the notable alarmin, HMGB1, and a neutralizing antibody (2G7) to HMGB1 completely abolished the CS mediated increase in IL-33. rHMGB1 increased IL-33 synthesis and this was partially abrogated by silencing TLR4 suggesting additional receptors for HMGB1 are involved in its regulation of IL-33. Collectively, these data reveal a HMGB1/TLR4/IL-33 pathway in the response of respiratory epithelium to mechanical stretch.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0184770