Bacterial Pathogens Hijack the Innate Immune Response by Activation of the Reverse Transsulfuration Pathway.
Animals
Bacteria
/ immunology
Gene Silencing
Helicobacter pylori
/ genetics
Histones
/ metabolism
Humans
Immune Evasion
Immunity, Innate
Immunoglobulins
Macrophages
/ metabolism
Male
Metabolic Networks and Pathways
/ physiology
Mice
Mice, Inbred C57BL
Nitric Oxide Synthase Type II
/ metabolism
Phosphatidylinositol 3-Kinases
/ metabolism
Polyamines
/ metabolism
RAW 264.7 Cells
Spermidine
/ metabolism
Spermine
/ metabolism
Sulfur
/ metabolism
Transcription Factors
Helicobacter pylori
immune evasion
immunometabolism
innate immunity
macrophages
pathogenic bacteria
polyamines
Journal
mBio
ISSN: 2150-7511
Titre abrégé: mBio
Pays: United States
ID NLM: 101519231
Informations de publication
Date de publication:
29 10 2019
29 10 2019
Historique:
entrez:
31
10
2019
pubmed:
31
10
2019
medline:
1
5
2020
Statut:
epublish
Résumé
The reverse transsulfuration pathway is the major route for the metabolism of sulfur-containing amino acids. The role of this metabolic pathway in macrophage response and function is unknown. We show that the enzyme cystathionine γ-lyase (CTH) is induced in macrophages infected with pathogenic bacteria through signaling involving phosphatidylinositol 3-kinase (PI3K)/MTOR and the transcription factor SP1. This results in the synthesis of cystathionine, which facilitates the survival of pathogens within myeloid cells. Our data demonstrate that the expression of CTH leads to defective macrophage activation by (i) dysregulation of polyamine metabolism by depletion of
Identifiants
pubmed: 31662455
pii: mBio.02174-19
doi: 10.1128/mBio.02174-19
pmc: PMC6819659
pii:
doi:
Substances chimiques
Histones
0
Immunoglobulins
0
Polyamines
0
SP1 antigen
0
Transcription Factors
0
Spermine
2FZ7Y3VOQX
Sulfur
70FD1KFU70
Nitric Oxide Synthase Type II
EC 1.14.13.39
Nos2 protein, mouse
EC 1.14.13.39
Spermidine
U87FK77H25
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NCI NIH HHS
ID : P01 CA028842
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA190612
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI142042
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK058404
Pays : United States
Organisme : NIH HHS
ID : S10 OD023514
Pays : United States
Organisme : NCI NIH HHS
ID : P01 CA116087
Pays : United States
Organisme : BLRD VA
ID : I01 BX001453
Pays : United States
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