Upregulated Long Non-coding RNA ALMS1-IT1 Promotes Neuroinflammation by Activating NF-κB Signaling in Ischemic Cerebral Injury

2021 ◽  
Vol 27 ◽  
Author(s):  
Peng Lu ◽  
Ye Zhang ◽  
Huanjiang Niu ◽  
Yirong Wang
Keyword(s):  
Inflammatory Cytokines ◽  
Nuclear Translocation ◽  
Cell Model ◽  
Intrathecal Injection ◽  
Cerebral Injury ◽  
Aberrant Expression ◽  
Tnf Α ◽  
Neuro Inflammation ◽  
Pro Inflammatory Cytokines ◽  
Brain Tissues

Background: ALMS1-IT1, a recently identified lncRNA, has been proven to play a crucial role in regulating tumor progression and predicting the survival time of tumor patients. Data analysis from the Human Body Map (HBM) revealed that ALMS1-IT1 is expressed mainly in brain tissues. Methods: In this study, the role of ALMS1-IT in regulating neuro-inflammation and functional recovery was investigated after ischemic cerebral damage. To this end, the rat model of transient middle cerebral artery occlusion (tMCAO) was constructed, the cell model of oxygen-glucose deprivation (OGD) was established using BV2 microglial cells, and the aberrant expression of ALMS1-IT1 was assessed in brain tissues. After ALMS1-IT1 knockdown through intrathecal injection of Lv-shALMS1-IT1, neuro-inflammatory response and functional tests including a modified neurological severity score (mNSS) and a foot-fault test were assessed. Results: The level of ALMS1-IT1 was promptly enhanced at 12 hours (h) following MCAO, peaking at 48 h, and remaining high at day 14 compared to the sham group. Pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) were increased after MCAO, whereas ALMS1-IT1 inhibition suppressed the expression of IL-1β, IL-6 and TNF-α in MCAO rats. The results from mNSS and foot-fault test showed that ALMS1-IT1 knockdown significantly improved spatial learning and sensorimotor function of MCAO rats. Mechanistically, ALMS1-IT1 knockdown suppressed the activation of NF-κB signaling in vitro and in vivo, as evidenced by decreased p65 expression and p65 nuclear translocation. ALMS1-IT1 overexpression facilitated pro-inflammatory cytokines expression in microglia, whereas the effect was blocked by treatment with JSH-23 (a specific NF-κB inhibitor). Conclusions: These data demonstrated that ALMS1-IT1 inhibition improved neurological function of MCAO rats, at least in part by repressing NF-κB-dependent neuro-inflammation.

scholarly journals Lanthanum Chloride Inhibits LPS Mediated Expressions of Pro-Inflammatory Cytokines and Adhesion Molecules in HUVECs: Involvement of NF-κB-Jmjd3 Signaling

2017 ◽  
Vol 42 (5) ◽  
pp. 1713-1724 ◽  
Author(s):  
Xia Chen ◽  
Min Xiu ◽  
Juanjuan Xing ◽  
Shaoqing Yu ◽  
Dinghong Min ◽  
...  
Keyword(s):  
Dna Binding ◽  
Inflammatory Cytokines ◽  
Adhesion Molecule ◽  
Inflammatory Cytokine ◽  
Nuclear Translocation ◽  
Binding Activity ◽  
Promoter Regions ◽  
Dna Binding Activity ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Background/Aims: To investigate the regulation of LaCl3 on lipopolysaccharides (LPS)-induced pro-inflammatory cytokines and adhesion molecules in human umbilical vein endothelial cells (HUVECs). Methods: Primary cultured HUVECs were pretreated with 2.5 µM LaCl3 for 30 min followed by 1 µg/ml LPS for 2 h. Pro-inflammatory cytokine and adhesion molecule expressions were determined by real-time RT-PCR and ELISA. NF-κB/p65 nuclear translocation was examined by immunofluorescence and immuno-blot, and its DNA-binding activity was measured by chemiluminescence. Recruitment of NF-κB/p65, Jmjd3, and H3K27me3 to gene promoter regions was determined by ChIP-qPCR. Results: LaCl3 exhibited no cytotoxic effects to primary HUVECs at concentrations ≤ 50 µM. LPS-mediated TNF-α, IL-1β, IL-6, MMP-9, and ICAM-1 production, nuclear translocation, and DNA-binding activity of NF-κB/p65, as well as Jmjd3 expression, were all reduced significantly by LaCl3. Furthermore, LaCl3 treatment significantly impaired LPS-induced enrichment of NF-κB/p65 to the promoter regions of TNF-α, MMP-9, IL-1β, ICAM-1, and IL-6; and of Jmjd3 to the promoter regions of TNF-α, MMP-9, IL-1β, and IL-6. H3K27me3 abundance in the promoter regions of TNF-α and ICAM-1 increased significantly in following LaCl3 treatment. Conclusion: LaCl3 inhibits pro-inflammatory cytokine and adhesion molecule expressions induced by LPS in HUVECs. NF-κB and histone demethylase Jmjd3 are involved in this effect.

scholarly journals Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A

2019 ◽  
Vol 20 (18) ◽  
pp. 4559 ◽  
Author(s):  
Banabihari Giri ◽  
Kasey Belanger ◽  
Marissa Seamon ◽  
Eric Bradley ◽  
Sharad Purohit ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Molecular Mechanism ◽  
Inflammatory Cytokines ◽  
Nuclear Translocation ◽  
Raw264.7 Cells ◽  
Anti Inflammatory ◽  
Neuro Inflammation ◽  
Precise Molecular Mechanism ◽  
Pro Inflammatory Cytokines

In this study, we used macrophage RAW264.7 cells to elucidate the molecular mechanism underlying the anti-inflammatory actions of niacin. Anti-inflammatory actions of niacin and a possible role of its receptor GPR109A have been studied previously. However, the precise molecular mechanism of niacin’s action in reducing inflammation through GPR109A is unknown. Here we observed that niacin reduced the translocation of phosphorylated nuclear kappa B (p-NF-κB) induced by lipopolysaccharide (LPS) in the nucleus of RAW264.7 cells. The reduction in the nuclear translocation in turn decreased the expression of pro-inflammatory cytokines IL-1β, IL-6 in RAW264.7 cells. We observed a decrease in the nuclear translocation of p-NF-κB and the expression of inflammatory cytokines after knockdown of GPR109A in RAW264.7 cells. Our results suggest that these molecular actions of niacin are mediated via its receptor GPR109A (also known as HCAR2) by controlling the translocation of p-NF-κB to the nucleus. Overall, our findings suggest that niacin treatment may have potential in reducing inflammation by targeting GPR109A.

scholarly journals PON1 Deficiency Promotes TREM2 Pathway-Mediated Microglial Phagocytosis and Inhibits Pro-Inflammatory Cytokines Release in Vitro and in Vivo

2021 ◽  
Author(s):  
Li Zhang ◽  
Wei Dong ◽  
Yuanwu Ma ◽  
Lin Bai ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Rat Brain ◽  
Inflammatory Cytokines ◽  
Paraoxonase 1 ◽  
Primary Microglia ◽  
Microglial Phagocytosis ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines ◽  
Brain Tissues

Abstract Paraoxonase 1 (PON1) plays an anti-inflammatory role in the cardiovascular system. Levels of serum PON1 and polymorphisms in this gene were linked to Alzheimer disease (AD) and Parkinson disease (PD), but its function in the neuroimmune system and AD are not clear. To address this issue, we used PON1 knockout rats previously generated by our lab to investigate the role of PON1 in microglia. Knockout of PON1 in rat brain tissues protected against LPS-induced microglia activation. PON1 deficiency in rat primary microglia increased TREM2 (triggering receptor expressed in myeloid cells 2) expression, phagocytosis and IL-10 (M2-phenotype marker) release, but decreased production of pro-inflammatory cytokines such as IL-1β, IL-6, IL-12, IL-18 especially TNF-α (M1-phenotype markers) induced by LPS. PON1 deficiency in rat primary microglia activated TREM2 pathway but decreased LPS-induced ERK activation. The phagocytosis promoting effect of PON1 knockout could be reversed by administration of recombinant PON1 protein. The interaction between PON1 and TREM2 was verified by co-immunoprecipitation (co-IP) using rat brain tissues or over-expressed BV2 cell lysates, which might be involved in lysosomal degradation of TREM2. Furthermore, PON1 knockout may also enhance microglial phagocytosis and clearance of exogenous Aβ by an intrahippocampal injection and decrease the transcription of cytokines such as IL-1β, IL-6 and TNF-α in vivo. These results suggest an inhibitory role of PON1 in microglial phagocytosis dependent on its interaction with TREM2. These findings provide novel insights into the role of PON1 in neuroinflammation and highlight TREM2 as a potential target for Alzheimer’s disease therapy.

scholarly journals Protection of cultured brain endothelial cells from cytokine-induced damage by α-melanocyte stimulating hormone

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4774 ◽  
Author(s):  
András Harazin ◽  
Alexandra Bocsik ◽  
Lilla Barna ◽  
András Kincses ◽  
Judit Váradi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Rat Brain ◽  
Inflammatory Cytokines ◽  
Nuclear Translocation ◽  
Brain Endothelial Cells ◽  
Melanocyte Stimulating Hormone ◽  
Brain Pericytes ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines ◽  
Stimulating Hormone

The blood–brain barrier (BBB), an interface between the systemic circulation and the nervous system, can be a target of cytokines in inflammatory conditions. Pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) induce damage in brain endothelial cells and BBB dysfunction which contribute to neuronal injury. The neuroprotective effects of α-melanocyte stimulating hormone (α-MSH) were investigated in experimental models, but there are no data related to the BBB. Based on our recent study, in which α-MSH reduced barrier dysfunction in human intestinal epithelial cells induced by TNF-α and IL-1β, we hypothesized a protective effect of α-MSH on brain endothelial cells. We examined the effect of these two pro-inflammatory cytokines, and the neuropeptide α-MSH on a culture model of the BBB, primary rat brain endothelial cells co-cultured with rat brain pericytes and glial cells. We demonstrated the expression of melanocortin-1 receptor in isolated rat brain microvessels and cultured brain endothelial cells by RT-PCR and immunohistochemistry. TNF-α and IL-1β induced cell damage, measured by impedance and MTT assay, which was attenuated by α-MSH (1 and 10 pM). The peptide inhibited the cytokine-induced increase in brain endothelial permeability, and restored the morphological changes in cellular junctions visualized by immunostaining for claudin-5 and β-catenin. Elevated production of reactive oxygen species and the nuclear translocation of NF-κB were also reduced by α-MSH in brain endothelial cells stimulated by cytokines. We demonstrated for the first time the direct beneficial effect of α-MSH on cultured brain endothelial cells, indicating that this neurohormone may be protective at the BBB.

scholarly journals PON1 deficiency promotes TREM2 pathway-mediated microglial phagocytosis and inhibits LPS-induced pro-inflammatory cytokines release

2020 ◽  
Author(s):  
lianfeng zhang ◽  
Li Zhang ◽  
Wei Dong ◽  
Yuanwu Ma ◽  
Lin Bai ◽  
...  
Keyword(s):  
Rat Brain ◽  
Inflammatory Cytokines ◽  
Paraoxonase 1 ◽  
Primary Microglia ◽  
Promoting Effect ◽  
Microglial Phagocytosis ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines ◽  
Brain Tissues

Abstract Background Paraoxonase 1 (PON1), an HDL-associated enzyme, plays an anti-inflammatory role in the cardiovascular system. Levels of serum PON1 and polymorphisms in this gene were linked to Alzheimer disease (AD) and Parkinson disease (PD), but its function in the neuroimmune system and AD are not clear. Methods PON1 knockout rats previously generated by our lab were used to investigate the role of PON1 in microglia. Wild type (WT) rats and PON1 knockout (KO) rats were injected with lipopolysaccharide (LPS, 5 or 20 mg/kg) and the survival rates were compared. Microglia on the sections of rat brain tissues were immunostained with anti-Iba1 antibody and the microglia morphology was compared. The phagocytosis, cytokines release and transcriptome of primary microglia cells treated with or without LPS were analyzed. The interactions between PON1 and TREM2 were detected by co-immunoprecipitation (co-IP) using rat brain tissues or over-expressed BV2 cell lysates. Results The expression of PON1 was detected in human and rat brain tissues and rat primary microglia. Knockout of PON1 in rat brain tissues protected against LPS-induced lethality by decreasing TNF-α expression. PON1 knockout in microglia increased TREM2 (triggering receptor expressed in myeloid cells 2) expressing and phagocytosis, but decreased production of pro-inflammatory cytokines such as IL-1β, IL-6, IL-12, IL-18 especially TNF-α (M1-phenotype markers) and increased IL-10 (M2-phenotype marker) release induced by LPS. PON1 knockout activated TREM2 pathway but decreased LPS-induced ERK activation. The phagocytosis promoting effect was reversed by administration of recombinant PON1 protein. The interaction between PON1 and TREM2 was verified and was associated with the localization of TREM2 in lysosomes. Conclusions These results suggest an inhibitory role of PON1 in microglial phagocytosis dependent on its interaction with TREM2. These findings provide novel insights into the role of PON1 in neuroinflammation and highlight TREM2 as a potential target for Alzheimer’s disease therapy.

scholarly journals PON1 Deficiency Promotes TREM2 Pathway-Mediated Microglial Phagocytosis and Inhibits Pro-Inflammatory Cytokines Release in Vitro and in Vivo

2021 ◽  
Author(s):  
Li Zhang ◽  
Wei Dong ◽  
Yuanwu Ma ◽  
Lin Bai ◽  
Xu Zhang ◽  
...  
Keyword(s):  
Rat Brain ◽  
Inflammatory Cytokines ◽  
Paraoxonase 1 ◽  
Primary Microglia ◽  
Microglial Phagocytosis ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines ◽  
Brain Tissues

Abstract Background: Paraoxonase 1 (PON1), an HDL-associated enzyme, plays an anti-inflammatory role in the cardiovascular system. Levels of serum PON1 and polymorphisms in this gene were linked to Alzheimer disease (AD) and Parkinson disease (PD), but its function in the neuroimmune system and AD are not clear.Methods: PON1 knockout rats previously generated by our lab were used to investigate the role of PON1 in microglia. Wild type (WT) rats and PON1 knockout (KO) rats were injected with lipopolysaccharide (LPS, 5 or 20 mg/kg) and the survival rates were compared. Microglia on the sections of rat brain tissues were immunostained with anti-Iba1 antibody and the microglia morphology was compared. The phagocytosis, cytokines release and transcriptome of rat primary microglia cells treated with or without LPS were analyzed. The interactions between PON1 and TREM2 were detected by co-immunoprecipitation (co-IP) using rat brain tissues or over-expressed BV2 cell lysates. The effects of PON1 on microglial phagocytosis in vivo were investigated in a rat model of AD produced by an intrahippocampal injection of Aβ1-42.Results: The expression of PON1 was detected in human and rat brain tissues and rat primary microglia. Knockout of PON1 in rat brain tissues protected against LPS-induced lethality by decreasing TNF-α expression. PON1 knockout in microglia increased TREM2 (triggering receptor expressed in myeloid cells 2) expressing and phagocytosis, but decreased production of pro-inflammatory cytokines such as IL-1β, IL-6, IL-12, IL-18 especially TNF-α (M1-phenotype markers) and increased IL-10 (M2-phenotype marker) release induced by LPS. PON1 knockout activated TREM2 pathway but decreased LPS-induced ERK activation. The phagocytosis promoting effect was reversed by administration of recombinant PON1 protein. The interaction between PON1 and TREM2 was verified and might be involved in lysosomal degradation of TREM2. Further, PON1 knockout may also enhance microglial phagocytosis and clearance of exogenous Aβ and decrease the transcription of cytokines such as IL-1β, IL-6 and TNF-α in vivo.Conclusions: These results suggest an inhibitory role of PON1 in microglial phagocytosis dependent on its interaction with TREM2. These findings provide novel insights into the role of PON1 in neuroinflammation and highlight TREM2 as a potential target for Alzheimer’s disease therapy.

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells

2020 ◽  
Vol 90 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Michael J. Haas ◽  
Marilu Jurado-Flores ◽  
Ramadan Hammoud ◽  
Victoria Feng ◽  
Krista Gonzales ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Coronary Artery ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Culture Media ◽  
Cytokine Secretion ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract. Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.5 mM dextrose for 24-hours and interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF α) levels were measured by enzyme immunoassays. To determine the effect of antioxidants on inflammatory cytokine secretion, cells were also treated with α-tocopherol, ascorbic acid, and the glutathione peroxidase mimetic ebselen. Only the concentration of IL-1β in culture media from cells exposed to 27.5 mM dextrose increased relative to cells maintained in 5.5 mM dextrose. Treatment with α-tocopherol (10, 100, and 1,000 μM) and ascorbic acid (15, 150, and 1,500 μM) at the same time that the dextrose was added reduced IL-1β, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1β, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. However, ebselen treatment reduced IL-1β, IL-6, and IL-8 levels in cells maintained in either 5.5 or 27.5 mM dextrose. IL-2 and TNF α concentrations in culture media were below the limit of detection under all experimental conditions studied suggesting that these cells may not synthesize detectable quantities of these cytokines. These results suggest that dextrose at certain concentrations may increase IL-1β levels and that antioxidants have differential effects on suppressing the secretion of pro-inflammatory cytokines in HCAEC.

scholarly journals Punicalagin Prevents Inflammation in LPS-Induced RAW264.7 Macrophages by Inhibiting FoxO3a/Autophagy Signaling Pathway

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2794 ◽  
Author(s):  
Cao ◽  
Chen ◽  
Ren ◽  
Zhang ◽  
Tan ◽  
...  
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Inflammatory Responses ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Autophagy Inhibition ◽  
Pro Inflammatory Cytokines

Punicalagin, a hydrolysable tannin of pomegranate juice, exhibits multiple biological effects, including inhibiting production of pro-inflammatory cytokines in macrophages. Autophagy, an intracellular self-digestion process, has been recently shown to regulate inflammatory responses. In this study, we investigated the anti-inflammatory potential of punicalagin in lipopolysaccharide (LPS) induced RAW264.7 macrophages and uncovered the underlying mechanisms. Punicalagin significantly attenuated, in a concentration-dependent manner, LPS-induced release of NO and decreased pro-inflammatory cytokines TNF-α and IL-6 release at the highest concentration. We found that punicalagin inhibited NF-κB and MAPK activation in LPS-induced RAW264.7 macrophages. Western blot analysis revealed that punicalagin pre-treatment enhanced LC3II, p62 expression, and decreased Beclin1 expression in LPS-induced macrophages. MDC assays were used to determine the autophagic process and the results worked in concert with Western blot analysis. In addition, our observations indicated that LPS-induced releases of NO, TNF-α, and IL-6 were attenuated by treatment with autophagy inhibitor chloroquine, suggesting that autophagy inhibition participated in anti-inflammatory effect. We also found that punicalagin downregulated FoxO3a expression, resulting in autophagy inhibition. Overall these results suggested that punicalagin played an important role in the attenuation of LPS-induced inflammatory responses in RAW264.7 macrophages and that the mechanisms involved downregulation of the FoxO3a/autophagy signaling pathway.

scholarly journals Modulation of ACE-2 mRNA by inflammatory cytokines in human thyroid cells: a pilot study

Endocrine ◽  
2021 ◽  
Author(s):  
Francesca Coperchini ◽  
Gianluca Ricci ◽  
Laura Croce ◽  
Marco Denegri ◽  
Rubina Ruggiero ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Combination Treatment ◽  
Primary Cultures ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Mrna Levels ◽  
Thyroid Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Pro Inflammatory Cytokines

Abstract Introduction Angiotensin-converting-enzyme-2 (ACE-2) was demonstrated to be the receptor for cellular entry of SARS-CoV-2. ACE-2 mRNA was identified in several human tissues and recently also in thyroid cells in vitro. Purpose Aim of the present study was to investigate the effect of pro-inflammatory cytokines on the ACE-2 mRNA levels in human thyroid cells in primary cultures. Methods Primary thyroid cell cultures were treated with IFN-γ and TNF-α alone or in combination for 24 h. ACE-2 mRNA levels were measured by RT-PCR. As a control, the levels of IFN-γ inducible chemokine (CXCL10) were measured in the respective cell culture supernatants. Results The mean levels of ACE-2 mRNA increased after treatment with IFN-γ and TNF-α in all the thyroid cell preparations, while the combination treatment did not consistently synergically increase ACE-2-mRNA. At difference, CXCL10 was consistently increased by IFN-γ and synergically further increased by the combination treatment with IFN-γ + TNF-α, with respect to IFN-γ alone. Conclusions The results of the present study show that IFN-γ and, to a lesser extent TNF-α consistently increase ACE-2 mRNA levels in NHT primary cultures. More interestingly, the combined stimulation (proven to be effective according to the synergic effect registered for CXCL10) produces different responses in terms of ACE-2 mRNA modulation. These results would suggest that elevated levels of pro-inflammatory cytokines could facilitate the entering of the virus in cells by further increasing ACE-2 expression and/or account for the different degree of severity of SARS-COV-2 infection. This hypothesis deserves to be confirmed by further specific studies.

scholarly journals Effects of 14-weeks betaine supplementation on pro-inflammatory cytokines and hematology status in professional youth soccer players during a competition season: a double blind, randomized, placebo-controlled trial

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Hadi Nobari ◽  
Jason M. Cholewa ◽  
Jorge Pérez-Gómez ◽  
Alfonso Castillo-Rodríguez
Keyword(s):  
Inflammatory Cytokines ◽  
Blood Cells ◽  
Well Being ◽  
Soccer Players ◽  
Mean Corpuscular Hemoglobin ◽  
Significant Group ◽  
Youth Soccer ◽  
Tnf Α ◽  
Betaine Supplementation ◽  
Pro Inflammatory Cytokines

Abstract Objective Systemic elevations in pro-inflammatory cytokines are a marker of non-functional over reaching, and betaine has been shown to reduce the secretion of pro-inflammatory cytokines in vitro. The aim of this study was to investigate the effects of betaine supplementation on tumor necrosis factor alpha (TNF-α), interleukins-1 beta (IL-1β), − 6 (IL-6) and the complete blood cell (CBC) count in professional youth soccer players during a competitive season. Methods Twenty-nine soccer players (age, 15.5 ± 0.3 years) were randomly divided into two groups based on playing position: betaine group (BG, n = 14, 2 g/day) or placebo group (PG, n = 15). During the 14-week period, training load was matched and well-being indicators were monitored daily. The aforementioned cytokines and CBC were assessed at pre- (P1), mid- (P2), and post- (P3) season. Results Significant (p < 0.05) group x time interactions were found for TNF-α, IL-1β, and IL-6. These variables were lower in the BG at P2 and P3 compared to P1, while IL-1β was greater in the PG at P3 compared to P1 (p = 0.033). The CBC count analysis showed there was significant group by time interactions for white blood cells (WBC), red blood cells (RBC), hemoglobin (Hb), and mean corpuscular hemoglobin concentration (MCHC). WBC demonstrated increases at P3 compared to P2 in PG (p = 0.034); RBC was less at P3 compared to P1 in BG (p = 0.020); Hb was greater at P2 compared to P1, whilst it was less at P3 compared to P3 for both groups. MCHC was greater at P3 and P2 compared to P1 in BG, whereas MCHC was significantly lower at P3 compared to P2 in the PG (p = 0.003). Conclusion The results confirmed that 14 weeks of betaine supplementation prevented an increase in pro-inflammatory cytokines and WBC counts. It seems that betaine supplementation may be a useful nutritional strategy to regulate the immune response during a fatiguing soccer season.

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