Lymphocyte Subpopulations and Cytokine Levels in Experimental Hyperhomocysteinemia

Fefelova, E. V.; Tereshkov, P.P.; Dutov, A. A.; Цыбиков, Н. Н.

doi:10.1007/s10517-015-2962-1

Cited by 6 publications

(8 citation statements)

References 9 publications

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“…The effect of homocysteine on Th17-cells in vitro confirms the in vivo study. Thus, in the study by Fefelova et al, it was shown that the treatment of experimental rats with homocysteine (0.1 μM/g) increases the IL-17A and IFN-γ plasma levels [ 78 ]. Th1- and Th17-cells play a crucial role in MS pathogenesis.…”

Section: The Role Of Homocysteine In Endothelial Dysfunction In Mumentioning

confidence: 99%

Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

et al. 2020

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Endothelial dysfunction is recognized as one of the leading factors in the pathogenesis of diseases of the central nervous system of various etiologies. Numerous studies have shown the role of hyperhomocysteinemia in the development of endothelial dysfunction and the prothrombogenic state. The most important condition in the development of multiple sclerosis (MS) is a dysregulation of the blood-brain barrier (BBB) and transendothelial leukocyte migration. It has been proven that homocysteine also contributes to the damage of neurons by the mechanism of excitotoxicity and the induction of the apoptosis of neurons. These processes can be one of the factors of neurodegenerative brain damage, which plays a leading role in the progression of MS. This review describes the pleiotropic effect of homocysteine on these processes and its role in MS pathogenesis.

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Section: The Role Of Homocysteine In Endothelial Dysfunction In Mumentioning

confidence: 99%

Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

et al. 2020

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“…In a cross-sectional study on healthy men, plasma total Hcy concentration showed positive correlation with IL-1β, TNF-α, and IL-6 [74]. In experimental rats, moderate exogenous HHcy was associated with increase in TNF-α, IFN-γ, and IL-17α concentrations in the serum and in mononuclear cells [75]. Acute administration of Hcy and chronic HHcy significantly increased proinflammatory cytokines TNF-α, IL-1β, and IL-6 in serum of rats [76,77].…”

Section: Possible Roles Of Hcy In the Immuno-pathogenesis Of Psoriasismentioning

confidence: 99%

Homocysteine and psoriasis

Lin

Meng²,

Song

2019

Bioscience Reports

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Psoriasis is caused by a complex interplay among the immune system, genetic background, autoantigens, and environmental factors. Recent studies have demonstrated that patients with psoriasis have a significantly higher serum homocysteine (Hcy) level and a higher prevalence of hyperhomocysteinaemia (HHcy). Insufficiency of folic acid and vitamin B12 can be a cause of HHcy in psoriasis. Hcy may promote the immuno-inflammatory process in the pathogenesis of psoriasis by activating Th1 and Th17 cells and neutrophils, while suppressing regulatory T cells. Moreover, Hcy can drive the immuno-inflammatory process by enhancing the production of the pro-inflammatory cytokines in related to psoriasis. Hcy can induce nuclear factor kappa B activation, which is critical in the immunopathogenesis of psoriasis. There may be a link between the oxidative stress state in psoriasis and the effect of HHcy. Hydrogen sulfide (H2S) may play a protective role in the pathogenesis of psoriasis and the deficiency of H2S in psoriasis may be caused by HHcy. As the role of Hcy in the pathogenesis of psoriasis is most likely established, Hcy can be a potential therapeutic target for the treatment of psoriasis. Systemic folinate calcium, a folic acid derivative, and topical vitamin B12 have found to be effective in treating psoriasis.

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“…Seperti yang telah dijelaskan sebelumnya, homosistein mampu menginduksi terjadinya respon inflamasi sistemik, baik yang melibatkan sistem kekebalan alami maupun adaptif. 21,26 Ternyata, beberapa penelitian juga menunjukkan bahwa homosistein, bersamasama dengan mediator inflamasi dan kondisi stres oksidatif yang disebabkannya, juga memiliki kemampuan untuk menyebabkan terjadinya disrupsi sawar darah otak, 30,31 induksi respon inflamasi di sistem saraf pusat, 32,33…”

Section: Pendahuluanunclassified

Aspek Imunologi Peran Homosistein Dalam Patogenesis Gangguan Kognitif Pasca Stroke Iskemik

Harahap

2020

JKU

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Sekitar 70% pasien stroke iskemik akut mengalami gangguan kognitif dapat terjadi akibat langsung dari stroke iskemik itu sendiri atau merupakan interaksi dari stroke iskemik dan faktor-faktor risiko yang menyertainya. Kondisi hiperhomosisteinemia merupakan salah satu faktor risiko vaskuler yang secara patofisiologik dapat menyebabkan terjadinya gangguan kognitif pasca stroke iskemik. Kondisi tersebut dapat terjadi karena peningkatan rasio SAM/SAH akibat diet tinggi kadar methionin, predisposisi genetik berupa mutasi gen pengkode enzim, dan defisiensi vitamin B6 dan asam folat. Peran homosistein dalam patogenesis terjadinya gangguan kognitif pasca stroke saat ini belum banyak diteliti. Homosistein bersifat toksik dan dapat menginduksi terjadinya respon inflamasi sistemik, disrupsi sawar darah otak, neuroinflamasi, dan kematian sel-sel neuronal yang mengarah pada proses neurodegeneratif. Proses neurodegeneratif pada struktur otak yang mengemban fungsi domain kognitif tertentu akan menyebabkan terganggunya fungsi dari domain kognitif tersebut. Pemahaman aspek imunologi peran homosistein dalam terjadinya gangguan fungsi kognitif pada pasien stroke iskemik tersebut dapat memberikan celah kemungkinan intervensi terhadap homosistein dan respon imunologis yang ditimbulkannya sebagai bagian dari tatalaksana optimal terhadap gangguan kognitif pasca stroke iskemik.

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Lymphocyte Subpopulations and Cytokine Levels in Experimental Hyperhomocysteinemia

Cited by 6 publications

References 9 publications

Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis

Homocysteine and psoriasis

Aspek Imunologi Peran Homosistein Dalam Patogenesis Gangguan Kognitif Pasca Stroke Iskemik

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