Approaching Inflammation Paradoxes-Proinflammatory Cytokine Blockages Induce Inflammatory Regulators.
inflammation
innate immune regulators
proinflammatory cytokine blockage
proinflammatory cytokines
reactive oxygen species
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
21
04
2020
accepted:
18
08
2020
entrez:
16
11
2020
pubmed:
17
11
2020
medline:
1
5
2021
Statut:
epublish
Résumé
The mechanisms that underlie various inflammation paradoxes, metabolically healthy obesity, and increased inflammations after inflammatory cytokine blockades and deficiencies remain poorly determined. We performed an extensive -omics database mining, determined the expressions of 1367 innate immune regulators in 18 microarrays after deficiencies of 15 proinflammatory cytokines/regulators and eight microarray datasets of patients receiving Mab therapies, and made a set of significant findings: 1) proinflammatory cytokines/regulators suppress the expressions of innate immune regulators; 2) upregulations of innate immune regulators in the deficiencies of IFNγ/IFNγR1, IL-17A, STAT3 and miR155 are more than that after deficiencies of TNFα, IL-1β, IL-6, IL-18, STAT1, NF-kB, and miR221; 3) IFNγ, IFNγR and IL-17RA inhibit 10, 59 and 39 proinflammatory cytokine/regulator pathways, respectively; in contrast, TNFα, IL-6 and IL-18 each inhibits only four to five pathways; 4) The IFNγ-promoted and -suppressed innate immune regulators have four shared pathways; the IFNγR1-promoted and -suppressed innate immune regulators have 11 shared pathways; and the miR155-promoted and -suppressed innate immune regulators have 13 shared pathways, suggesting negative-feedback mechanisms in their conserved regulatory pathways for innate immune regulators; 5) Deficiencies of proinflammatory cytokine/regulator-suppressed, promoted programs share signaling pathways and increase the likelihood of developing 11 diseases including cardiovascular disease; 6) There are the shared innate immune regulators and pathways between deficiency of TNFα in mice and anti-TNF therapy in clinical patients; 7) Mechanistically, up-regulated reactive oxygen species regulators such as myeloperoxidase caused by suppression of proinflammatory cytokines/regulators can drive the upregulation of suppressed innate immune regulators. Our findings have provided novel insights on various inflammation paradoxes and proinflammatory cytokines regulation of innate immune regulators; and may re-shape new therapeutic strategies for cardiovascular disease and other inflammatory diseases.
Identifiants
pubmed: 33193322
doi: 10.3389/fimmu.2020.554301
pmc: PMC7604447
doi:
Substances chimiques
Antibodies, Monoclonal
0
Cytokines
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
554301Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL138749
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL130233
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL131460
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK104116
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL147565
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK113775
Pays : United States
Informations de copyright
Copyright © 2020 Liu, Saredy, Zhang, Shao, Sun, Yang, Wang, Liu, Drummer, Johnson, Saaoud, Lu, Xu, Li, Wang, Jiang, Wang and Yang.
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