Cigarette smoke promotes inflammasome-independent activation of caspase-1 and -4 leading to gasdermin D cleavage in human macrophages.
Caspase 1
/ metabolism
Caspases
/ metabolism
Caspases, Initiator
/ metabolism
Cigarette Smoking
Humans
Inflammasomes
/ metabolism
Inflammation
/ metabolism
Intracellular Signaling Peptides and Proteins
/ metabolism
Lipopolysaccharides
/ metabolism
Macrophages
/ metabolism
NLR Family, Pyrin Domain-Containing 3 Protein
/ metabolism
Phosphate-Binding Proteins
/ metabolism
Pore Forming Cytotoxic Proteins
/ metabolism
Nicotiana
/ metabolism
alveolar macrophages
caspase
cigarette smoke
inflammasome
lung
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
revised:
02
08
2022
received:
06
06
2022
accepted:
17
08
2022
entrez:
25
8
2022
pubmed:
26
8
2022
medline:
27
8
2022
Statut:
ppublish
Résumé
Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)-associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase-1, -8, and -4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs ranging from cell hyperactivation to pyroptosis. We have previously reported that in human monocyte-derived macrophages CS extract (CSE) inhibits the NLRP3 inflammasome and shifts the response to lipopolysaccharide (LPS) towards the TLR4-TRIF axis leading to activation of caspase-8, which, in turn, activates caspase-1. In the present work, we investigated whether other ASC-dependent inflammasomes could be involved in caspase activation by CSE and whether caspase activation led to GSDMD cleavage and other downstream effects. Presented results demonstrate that CSE promoted ASC-independent activation of caspase-1 leading to GSDMD cleavage and increased cell permeability, in the absence of cell death. GSDMD cleavage was strongly enhanced upon stimulation with LPS+CSE, suggesting a synergistic effect between the two stimuli. Noteworthy, CSE promoted LPS internalization leading to caspase-4 activation, thus contributing to increased GSDMD cleavage. Caspase-dependent GSDMD cleavage was associated with mitochondrial superoxide generation. Increased cleaved GSDMD was found in lung macrophages of smokers compared to ex-smokers and non-smoking controls. Our findings revealed that ASC-independent activation of caspase-1, -4, and -8 and GSDMD cleavage upon exposure to CS may contribute to macrophage dysfunction and feed the chronic inflammation observed in the smokers' lung.
Identifiants
pubmed: 36004615
doi: 10.1096/fj.202200837R
doi:
Substances chimiques
GSDMD protein, human
0
Inflammasomes
0
Intracellular Signaling Peptides and Proteins
0
Lipopolysaccharides
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Phosphate-Binding Proteins
0
Pore Forming Cytotoxic Proteins
0
CASP4 protein, human
EC 3.4.22.-
Caspases
EC 3.4.22.-
Caspases, Initiator
EC 3.4.22.-
Caspase 1
EC 3.4.22.36
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e22525Informations de copyright
© 2022 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.
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