Modulation of inflammatory response in mice with severe autoimmune disease by thymic peptide thymulin and an inhibitor of NF-kappaB signalling

Лунин, С. М.; Хренов, М. О.; Новоселова, Т. В.; Parfenyuk, Svetlana B.; Глушкова, О. В.; Фесенко, Е. Е.; Новоселова, Е. Г.

doi:10.1016/j.intimp.2015.01.021

Cited by 12 publications

(15 citation statements)

References 26 publications

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“…Thus, a biphasic cytokine response was observed, with an early phase characterised by an increase in plasma IL-17A and IFN-γ, and a later phase characterised by an increase only in plasma IL-17A. Therefore, our data using the rEAE model closely resembles the biphasic cytokine response recently observed in several acute EAE models, where an initial increase in IFN-γ was followed by an increase in IL-17A [10,20]. PBCA–thymulin nanoparticle administration exerted profound anti-inflammatory effects on IL-17A and IFN-γ levels, both in the early and later stages of rEAE.…”

Section: Resultssupporting

confidence: 82%

“…The aforementioned features make thymulin, either alone or in combination with other therapies, a potential treatment for diseases characterised by immune imbalances. Mechanisms of the anti-inflammatory effect of thymulin so far are not known, however, we showed its effects on different signal proteins from the NF-kappaB pathway in septic and autoimmune inflammation [5,10,11]. Along with that, recently we have shown a regulation of the NF-kappaB pathway in experimental autoimmune encephalomyelitis (EAE) via site-specific phosphorylation of a RelA/p65 protein from the NF-kappaB family.…”

Section: Introductionmentioning

confidence: 93%

“…Specifically, thymulin produced a protective effect in endotoxemic mice [9]. Moreover, we have previously observed a significant anti-inflammatory effect of thymulin in severe and mild progressive forms of autoimmune encephalomyelitis [10,11]. The aforementioned features make thymulin, either alone or in combination with other therapies, a potential treatment for diseases characterised by immune imbalances.…”

Section: Introductionmentioning

confidence: 99%

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Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice

Лунин

Хренов

Глушкова

et al. 2019

IJMS

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Relapsing–remitting experimental autoimmune encephalomyelitis (rEAE) in mice is a model that closely resembles relapsing–remitting multiple sclerosis in humans. This study aims to investigate a new approach to modulation of the inflammatory response in rEAE mice using a thymic peptide thymulin bound to polybutylcyanoacrylate (PBCA) nanoparticles. PBCA nanoparticles were used to prolong the presence of thymulin in the blood. Cytokine levels in blood were measured by ELISA; NF-κB and SAPK/JNK cascade activation, as well as Hsp72 and p53 protein expression, were measured by Western blotting. Animal health statuses were estimated using severity scores. Results showed that the cytokine response in rEAE was multi-staged: an early phase was accompanied by an increase in plasma interferon-γ, while the interleukin (IL)-17 response was markedly increased at a later stage. The stages were attributed to rEAE induction and maintenance phases. Thymulin significantly alleviated symptoms of rEAE and lowered plasma cytokine levels both in early and later stages of rEAE, and decreased NF-κB and SAPK/JNK cascade activation. Thymulin modulated NF-kappaB pathway activity via site-specific phosphorylation of RelA/p65 protein (at Ser276 and Ser536). The effect of nanoparticle-bound thymulin was more pronounced than the effect of free thymulin. Therefore, PBCA–thymulin can be considered a prospective treatment for this pathology.

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Section: Resultssupporting

confidence: 82%

Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice

Лунин

Хренов

Глушкова

et al. 2019

IJMS

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“…It has been reported that NF-κB is able to act as a messenger in the same inflammatory response syndrome in the body. At the early onset stage of local inflammation in an organism, inflammatory cytokines can be activated through NF-κB signaling (29). Thus, the TLR/NF-κB pathway serves an important role in the progression of inflammation.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory stimuli promote oxidative stress in pancreatic acinar cells via Toll-like receptor 4/nuclear factor-κB pathway

Pan

Wang

et al. 2018

Int J Mol Med

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The Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB) pathway is vital to the pathogenesis of acute pancreatitis (AP). The aim of the present study was to identify the mechanism of the activation of the TLR4/NF-κB signaling pathway in the viability of primary pancreatic cells. The cells were stimulated with lipopolysaccharide (LPS) for the activation of NF-κB signaling. Next, the reactive oxygen species (ROS) level was evaluated by detecting the concentration of malondialdehyde and glutathione peroxidase. cell viability was measured by cell counting Kit-8 and MTT assays, while the percentage of apoptosis was detected by flow cytometry. Quantitative polymerase chain reaction was used to detect TLR4, B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax) and phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1) expression levels. Western blot assay was also conducted to detect TLR4 protein expression, while the activity of NF-κB signaling was measured by determining the p65 and phosphorylated p65 protein levels. In addition, the effect of TLR4 overexpression or treatment with TLR4 antagonists in the presence of LPS stimulation was investigated. The results revealed that ROS levels were increased and cell viability was decreased in LPS-stimulated pancreatic acinar cells. TLR4, Bax and PMAIP1 levels were increased, Bcl2 expression was decreased and NF-κB signaling was activated in LPS-stimulated pancreatic acinar cells. Furthermore, pancreatic cells with TLR4 overexpression exhibited increased ROS level and decreased viability. Finally, the effect caused by LPS stimulation was partially reversed by treatment of pancreatic acinar cells with TLR4 antagonists. In conclusion, the current study investigated a novel regulatory mechanism of the TLR4/NF-κB pathway in LPS-stimulated pancreatic cells, which may contribute to pancreatitis. The damage of these cells due to increased ROS levels was observed to occur through activation of the TLR4/NF-κB pathway.

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“…Thus, more studies will be required to clarify whether or not acetylcholine receptors are involved in regulation of T cell function by NTX. NF-κB plays an essential role in lymphocyte proliferation and function [49]. It has been reported that NTX can inhibit NF-κB activation [11,24].…”

Section: Discussionmentioning

confidence: 99%

Neurotoxin from Naja naja atra venom inhibits skin allograft rejection in rats

Kou

Wang

et al. 2015

International Immunopharmacology

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Modulation of inflammatory response in mice with severe autoimmune disease by thymic peptide thymulin and an inhibitor of NF-kappaB signalling

Cited by 12 publications

References 26 publications

Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice

Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice

Inflammatory stimuli promote oxidative stress in pancreatic acinar cells via Toll-like receptor 4/nuclear factor-κB pathway

Neurotoxin from Naja naja atra venom inhibits skin allograft rejection in rats

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