Publication
Title
NLRP3/Caspase-1-Independent IL-1β production mediates diesel exhaust particle-induced pulmonary inflammation
Author
Abstract
Inhalation of diesel exhaust particles (DEP) induces an inflammatory reaction in the lung; however, the mechanisms are largely unclear. IL-1 beta/IL-1RI signaling is crucial in several lung inflammatory responses. Typically, caspase-1 is activated within the NLRP3 inflammasome that recognizes several damage-associated molecular patterns, which results in cleavage of pro-IL-1 beta into mature IL-1 beta. In this study, we hypothesized that the NLRP3/caspase-1/IL-1 beta pathway is critical in DEP-induced lung inflammation. Upon DEP exposure, IL-1RI knockout mice had reduced pulmonary inflammation compared with wild-type mice. Similarly, treatment with rIL-1R antagonist (anakinra) and IL-1 beta neutralization impaired the DEP-induced lung inflammatory response. Upon DEP exposure, NLRP3 and caspase-1 knockout mice, however, showed similar IL-1 beta levels and comparable pulmonary inflammation compared with wild-type mice. In conclusion, these data show that the DEP-induced pulmonary inflammation acts through the IL-1 beta/IL-1RI axis. In addition, DEP initiates inflammation independent of the classical NLRP3/caspase-1 pathway, suggesting that other proteases might be involved. The Journal of Immunology, 2011, 187: 3331-3337.
Language
English
Source (journal)
The journal of immunology. - Baltimore, Md
Publication
Baltimore, Md : 2011
ISSN
0022-1767 [Print]
1550-6606 [Online]
Volume/pages
187 :6 (2011) , p. 3331-3337
ISI
000295034200052
Full text (Publisher's DOI)
UAntwerpen
Publication type
Subject
External links
Web of Science
Record
Identification
Creation 18.10.2018
Last edited 06.09.2021