Kombucha ameliorates experimental autoimmune encephalomyelitis through activation of Treg and Th2 cells

Haghmorad, Dariush; Yazdanpanah, Esmaeil; Sadighi-Moghaddam, Bizhan; Yousefi, Bahman; Sahafi, Pegah; Ghorbani, Narges; Rashidy-Pour, Ali; Kokhaei, Parviz

doi:10.1007/s13760-020-01475-3

Cited by 23 publications

(15 citation statements)

References 41 publications

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“…Clinical indications of EAE were observed and the weight of mice was evaluated was assessed daily up to 25 days after immunization. Mice were scored for clinical assessment with the following scale: 0, no symptoms; 1 = incomplete failure of tail tonicity; 2 = complete failure of tail tonicity; 3 = flaccid tail and unusual gait; 4 = hind limb paralysis; 5 = hind limb paralysis with hind body paresis; 6 = hind and foreleg paralysis; 7 = moribund or death 25,26 …”

Section: Methodsmentioning

confidence: 99%

Berberine promotes immunological outcomes and decreases neuroinflammation in the experimental model of multiple sclerosis through the expansion of Treg and Th2 cells

Tavaf

Soltanmohammadi

Zargarani

et al. 2023

Immunity Inflam & Disease

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Introduction: Among the most frequent demyelinating autoimmune disorders of the central nervous system (CNS) is multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is used as an animal model of multiple sclerosis. Berberine is an alkaloid found in some medicinal plants with anti-inflammatory effects. Methods: C57BL/6 female mice were used and divided into three groups: (1) The control group received PBS, (2) the low-dose treatment group received 10 mg/kg of berberine, and (3) The high-dose treatment group received 30 mg/kg of berberine.Myelin Oligodendrocyte Glycoprotein and complete Freund's adjuvant were subcutaneously administered to induce EAE. Mice were given intraperitoneal injections of pertussis toxin on the day of immunization and 2 days later.Histological studies showed low lymphocyte infiltration and demyelination of CNS in the treated groups. Results:The clinical scores of the treatment group with low-dose berberine (T1: 2 ± 0.13) and high-dose berberine (T2: 1.5 ± 0.14) were significantly (p < .001) lower than the control group (CTRL: 4.5 ± 0.13). Treatment groups decreased proinflammatory cytokines (IFN-γ, TNF-α, interleukin [IL]-17) (p < .001) as well as increased anti-inflammatory cytokine expression (IL-4, IL-10, IL-27, IL-33, IL-35, TGF-β) (p < .01) when compared to the CTRL group. Treatment groups with berberine reduced expression of the Th1 and Th17 cytokines and transcription factors (p < .001) and increased expression of transcription factors and Th2 and Treg cytokines (p < .01) in contrast to CTRL group. Conclusion:Berberine appears to have a protective effect on disease development and alleviating disease status in EAE, which appears to be due

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Section: Methodsmentioning

confidence: 99%

Berberine promotes immunological outcomes and decreases neuroinflammation in the experimental model of multiple sclerosis through the expansion of Treg and Th2 cells

Tavaf

Soltanmohammadi

Zargarani

et al. 2023

Immunity Inflam & Disease

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“…Daily monitoring of clinical score and body weight was performed up to 25 days according to the following criteria: 0, no detectable symptom; 1, partial limp tail; 2, complete limp tail; 3, hind legs, weakness or abnormal gait; 4, complete hind limb paralysis; 5, complete hind limb paralysis and forelimb paresis; 6, complete hind and foreleg paralysis; 7, moribund or death [ 21 , 22 ].…”

Section: Methodsmentioning

confidence: 99%

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

Haghmorad

Yousefi

Eslami

et al. 2022

CIMB

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Multiple Sclerosis (MS) is a demyelinating autoimmune disorder of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) has been widely used to determine the pathogenesis of the disease and evaluate new treatment strategies for MS. Therefore, we investigated the efficacy of oral administration of a Myelin Oligodendrocyte Glycoprotein (MOG) in the treatment of EAE. Female C57BL/6 mice were utilized in three groups (Control group, received PBS orally; prevention group, oral administration of MOG35–55 two weeks before EAE induction; treatment group, oral administration of MOG35–55 after EAE induction). MOG administration, both as prevention and treatment, significantly controlled clinical score, weight loss, CNS inflammation, and demyelination, mainly through the modulation of T cell proliferation, and reduction in pro-inflammatory cytokines and transcription factors, including TNF-α, IFN-γ, IL-17, T-bet, and ROR-γt. MOG administration, both as prevention and treatment, also induced anti-inflammatory cytokines and transcription factors, including IL-4, TGF-β, GATA-3, and Foxp3. The results showed that oral administration of MOG, both as prevention and treatment, could efficiently control EAE development. Immunomodulatory mechanisms include the induction of Th2 and Treg cells and the suppression of pro-inflammatory Th1 and Th17 cells.

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“…Daily monitoring of clinical score and body weight were performed up to 25 days according to the following criteria: 0, no detectable symptom; 1, partial limp tail; 2: complete limp tail; 3, hind legs, weakness or abnormal gait; 4, complete hind limb paralysis; 5, complete hind limb paralysis and forelimb paresis; 6, complete hind and foreleg paralysis; 7: moribund or death [19,20]. Moreover, body weight change was determined based on the weight change at the time of EAE induction until 25 days post-immunization.…”

Section: Eae Induction and Treatmentmentioning

confidence: 99%

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

Haghmorad¹,

Eslami²,

Rashidy-Pour³

et al. 2022

Preprint

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Multiple sclerosis (MS) is a demyelinating autoimmune disorder of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) has been widely used to determine the pathogenesis of the disease and evaluate new treatment strategies for MS. Therefore, we investigated the efficacy of oral administration of a Myelin Oligodendrocyte Glycoprotein (MOG) in the treatment of EAE. Female C57BL/6 mice were utilized in three groups (Control group: received PBS orally; prevention group: oral administration of MOG35-55 two weeks before EAE induction; treatment group: oral administration of MOG35-55 after EAE induction. MOG administration, both as prevention and treatment, significantly controlled clinical score, weight loss, CNS inflammation, and demyelination, mainly through the modulation of T cell proliferation, reduction of pro-inflammatory cytokines and transcription factors, including TNF-α, IFN-γ, IL-17, T-bet, and ROR-γt. MOG administration, both as prevention and treatment, also induced anti-inflammatory cytokines and transcription factors, including IL-4, TGF-β, GATA-3, and Foxp3. The results showed that oral administration of MOG, both as prevention and treatment, could efficiently control EAE development. Immunomodulatory mechanisms include the induction of Th2 and Treg cells and the suppression of pro-inflammatory Th1 and Th17 cells.

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Kombucha ameliorates experimental autoimmune encephalomyelitis through activation of Treg and Th2 cells

Cited by 23 publications

References 41 publications

Berberine promotes immunological outcomes and decreases neuroinflammation in the experimental model of multiple sclerosis through the expansion of Treg and Th2 cells

Berberine promotes immunological outcomes and decreases neuroinflammation in the experimental model of multiple sclerosis through the expansion of Treg and Th2 cells

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

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