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Role of T cells in the pathogenesis of systemic lupus erythematous: Focus on immunometabolism dysfunctions.
Saadh, MJ, Kazemi, K, Khorramdelazad, H, Mousavi, MJ, Noroozi, N, Masoumi, M, Karami, J
International immunopharmacology. 2023;:110246
Abstract
Evidence demonstrates that T cells are implicated in developing SLE, and each of them dominantly uses distinct metabolic pathways. Indeed, intracellular enzymes and availability of specific nutrients orchestrate fate of T cells and lead to differentiation of regulatory T cells (Treg), memory T cells, helper T cells, and effector T cells. The function of T cells in inflammatory and autoimmune responses is determined by metabolic processes and activity of their enzymes. Several studies were conducted to determine metabolic abnormalities in SLE patients and clarify how these modifications could control the functions of the involved T cells. Metabolic pathways such as glycolysis, mitochondrial pathways, oxidative stress, mTOR pathway, fatty acid and amino acid metabolisms are dysregulated in SLE T cells. Moreover, immunosuppressive drugs used in treating autoimmune diseases, including SLE, could affect immunometabolism. Developing drugs to regulate autoreactive T cell metabolism could be a promising therapeutic approach for SLE treatment. Accordingly, increased knowledge about metabolic processes paves the way to understanding SLE pathogenesis better and introduces novel therapeutic options for SLE treatment. Although monotherapy with metabolic pathways modulators might not be sufficient to prevent autoimmune disease, they may be an ideal adjuvant to reduce administration doses of immunosuppressive drugs, thus reducing drug-associated adverse effects. This review summarized emerging data about T cells that are involved in SLE pathogenesis, focusing on immunometabolism dysregulation and how these modifications could affect the disease development.
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Role of T Cells in the Pathogenesis of Rheumatoid Arthritis: Focus on Immunometabolism Dysfunctions.
Masoumi, M, Alesaeidi, S, Khorramdelazad, H, Behzadi, M, Baharlou, R, Alizadeh-Fanalou, S, Karami, J
Inflammation. 2023;(1):88-102
Abstract
Evidence demonstrated that metabolic-associated T cell abnormalities could be detected in the early stage of RA development. In this context, molecular evaluations have revealed changes in metabolic pathways, leading to the aggressive phenotype of RA T cells. A growing list of genes is downregulated or upregulated in RA T cells, and most of these genes with abnormal expression fall into the category of metabolic pathways. It has been shown that RA T cells shunt glucose towards the pentose phosphate pathway (PPP), which is associated with a high level of nicotinamide adenine dinucleotide phosphate (NADPH) and intermediate molecules. An increased level of NADPH inhibits ATM activation and thereby increases the proliferation capabilities of the RA T cells. Defects in the DNA repair nuclease MRE11A cause failures in repairing mitochondrial DNA, resulting in inhibiting the fatty acid oxidation pathway and further elevated cytoplasmic lipid droplets. Accumulated lipid droplets employ to generate lipid membranes for the cell building program and are also used to form the front-end membrane ruffles that are accomplices with invasive phenotypes of RA T cells. Metabolic pathway involvement in RA pathogenesis expands the pathogenic concept of the disease beyond the common view of autoimmunity triggered by autoantigen recognition. Increased knowledge about metabolic pathways' implications in RA pathogenesis paves the way to understand better the environment/gene interactions and host/microbiota interactions and introduce potential therapeutic approaches. This review summarized emerging data about the roles of T cells in RA pathogenesis with a focus on immunometabolism dysfunctions and how these metabolic alterations can affect the disease process.
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Adolescent mental health during covid-19 pandemics: a systematic review.
Alamolhoda, SH, Zare, E, Atena HakimZadeh, , Zalpour, A, Vakili, F, Razie Mohammadi Chermahini, , Ebadifard, R, Masoumi, M, Niayesh Khaleghi, , Malihe Nasiri,
International journal of adolescent medicine and health. 2023;(1):41-60
Abstract
OBJECTIVES The outbreak of the COVID-19 pandemic has had wide-ranging outcomes on adolescents' well-being. However, less attention has been paid to the adolescent's mental health during the pandemic. The pandemic may impair adolescents' mental health through stress spillover from other family members, contextual and policy changes, and the disruption of everyday life routines. Therefore, our research is motivated by a need to address the relative scarcity of research examining adolescent mental health during the pandemic. CONTENT This systematic review was conducted through the medical database, Web of Science, Scopus, Medline, Embase, Google Scholar, and Cochrane databases for peer-reviewed, cross-sectional, cohort studies assessing the mental health status of adolescents during the Covid-19 virus pandemic from May 2020 till Dec 2022 without language restriction. Keywords were selected based on the Mesh terms and Emtree. SUMMARY Studies on coronavirus have revealed many significant psychological effects on teens of all ages. The most commom problems were on the stress and anxiety, sleep disorders, depression, post-traumatic stress disorder. Risk factors were concidered as prior mental health problem, female sexuality, fear of covid-19, nutrition, physical activity and listening the covid 19 news. OUTLOOK Considering the critical age of teenagers, the role of parents is vital. Health policy maker should support parents as a key factors to approprate care for adolescent. Parents should be educated on parenting methods during the covid pandemic to avoid irreparable damage of adolescent's mental health.
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The regulation of Niemann-Pick C1-Like 1 (NPC1L1) gene expression in opposite direction by Bacteroides spp. and related outer membrane vesicles in Caco-2 cell line.
Badi, SA, Motahhary, A, Bahramali, G, Masoumi, M, Khalili, SFS, Ebrahimzadeh, N, Nouri, P, Rahimi, A, Masotti, A, Moshiri, A, et al
Journal of diabetes and metabolic disorders. 2020;(1):415-422
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Abstract
PURPOSE The intestine has substantial role in cholesterol homeostasis due to the presence of various cholesterol transporters and gut microbiota. Bacteroides spp. are important members of gut microbiota that employ outer membrane vesicles (OMVs) to interact with host. In this regard, we evaluated the effect of Bacteroides fragilis, Bacteroides thetaiotaomicron and related OMVs on the gene expression of important cholesterol transporters, Niemann-Pick C1-Like 1 (NPC1L1), ATP-binding cassette (ABCA1), and liver X receptors (LXRs) in Caco-2 cells. METHODS OMVs were isolated from overnight brain heart infusion (BHI) broth of bacterial standard strains using deoxycholate and assessed by Scanning electron microscopy (SEM). The relative change in genes expression was assessed by Quantitative reverse transcription PCR (RT-qPCR) based on SYBR Green and 2-∆∆ct method in Caco-2 cells that were treated with bacteria and OMVs. Data were statistically analyzed with GraphPad Prism software. Finally, pathway enrichment based on the studied genes was performed using Cytoscape plugin ClueGO. RESULTS B. fragilis (P value = 0.002) and B. thetaiotaomicron (P value = 0.001) significantly reduced NPC1L1 gene expression in Caco-2 cells. Interestingly, NPC1L1 transcripts were significantly increased by both OMVs(P value = 0.04) (P value = 0.01). Also, LXRβ was significantly down regulated by B. thetaiotaomicron (P value = 0.02). ClueGO analysis on the studied genes demonstrated several functional groups which involve in lipid and cholesterol metabolism. CONCLUSION The opposite effect of B. fragilis, B. thetaiotaomicron and related OMVs on the NPC1L1 gene expression was observed in Caco-2 cells. Interestingly, these effects partially were in line with the alternation of LXRs expression. However, based on pathway enrichment analysis, further molecular investigations are required to elaborate in details the specific association between Bacteroides spp. and OMVs with regulation of cholesterol signaling pathways including cholesterol transport, lipid storage, lipid homeostasis and cholesterol homeostasis.