Inflammatory and immunometabolic consequences of gut dysfunction in HIV: Parallels with IBD and implications for reservoir persistence and non-AIDS comorbidities.
Animals
Cell Membrane Permeability
Comorbidity
Dysbiosis
Energy Metabolism
Fatty Acids
/ metabolism
Gastrointestinal Diseases
/ etiology
Gastrointestinal Microbiome
/ immunology
HIV
/ immunology
HIV Infections
/ complications
Humans
Inflammatory Bowel Diseases
/ immunology
Intestinal Mucosa
/ immunology
Macrophages
/ immunology
Monocytes
/ immunology
HIV cure
Immunometabolism, microbiome
Inflammation
Inflammatory bowel disease
Macrophage metabolism
Journal
EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039
Informations de publication
Date de publication:
Aug 2019
Aug 2019
Historique:
received:
29
03
2019
revised:
07
07
2019
accepted:
09
07
2019
pubmed:
23
7
2019
medline:
16
1
2020
entrez:
23
7
2019
Statut:
ppublish
Résumé
The gastrointestinal mucosa is critical for maintaining the integrity and functions of the gut. Disruption of this barrier is a hallmark and a risk factor for many intestinal and chronic inflammatory diseases. Inflammatory bowel disease (IBD) and HIV infection are characterized by microbial translocation and systemic inflammation. Despite the clinical overlaps between HIV and IBD, significant differences exist such as the severity of gut damage and mechanisms of immune cell homeostasis. Studies have supported the role of metabolic activation of immune cells in promoting chronic inflammation in HIV and IBD. This inflammatory response persists in HIV+ persons even after long-term virologic suppression by antiretroviral therapy (ART). Here, we review gut dysfunction and microbiota changes during HIV infection and IBD, and discuss how this may induce metabolic reprogramming of monocytes, macrophages and T cells to impact disease outcomes. Drawing from parallels with IBD, we highlight how factors such as lipopolysaccharides, residual viral replication, and extracellular vesicles activate biochemical pathways that regulate immunometabolic processes essential for HIV persistence and non-AIDS metabolic comorbidities. This review highlights new mechanisms and support for the use of immunometabolic-based therapeutics towards HIV remission/cure, and treatment of metabolic diseases.
Identifiants
pubmed: 31327693
pii: S2352-3964(19)30462-1
doi: 10.1016/j.ebiom.2019.07.027
pmc: PMC6710907
pii:
doi:
Substances chimiques
Fatty Acids
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
522-531Subventions
Organisme : NIAID NIH HHS
ID : R21 AI129636
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI143385
Pays : United States
Informations de copyright
Copyright © 2019. Published by Elsevier B.V.
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