Nicotine induces TIPE2 upregulation and Stat3 phosphorylation contributes to cholinergic anti-inflammatory effect

Sui, Hua; Ke, Shi; Xu, Dan; Lü, Nan; Wang, Yi Nan; Zhang, Yue Hua; Gao, Feng

doi:10.3892/ijo.2017.4080

Cited by 9 publications

(7 citation statements)

References 39 publications

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“…Interestingly, nicotine can both promote and reduce inflammation. By acting through nAChRs on immune cells, nicotine inhibits the function of the transcription factor nuclear factor-κβ (NF-κB) by increasing the phosphorylation of signal transducer and activator of transcription 3 (STAT3) [123,124]. Conversely, nicotine can activate immune cells by increasing their chemotactic activity, migration, and interaction with endothelial cells, resulting in a heightened inflammatory response [125].…”

Section: Inflammationmentioning

confidence: 99%

Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health

Traboulsi

Cherian

Rjeili

et al. 2020

IJMS

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E-cigarettes have a liquid that may contain flavors, solvents, and nicotine. Heating this liquid generates an aerosol that is inhaled into the lungs in a process commonly referred to as vaping. E-cigarette devices can also contain cannabis-based products including tetrahydrocannabinol (THC), the psychoactive component of cannabis (marijuana). E-cigarette use has rapidly increased among current and former smokers as well as youth who have never smoked. The long-term health effects are unknown, and emerging preclinical and clinical studies suggest that e-cigarettes may not be harmless and can cause cellular alterations analogous to traditional tobacco smoke. Here, we review the historical context and the components of e-cigarettes and discuss toxicological similarities and differences between cigarette smoke and e-cigarette aerosol, with specific reference to adverse respiratory outcomes. Finally, we outline possible clinical disorders associated with vaping on pulmonary health and the recent escalation of acute lung injuries, which led to the declaration of the vaping product use-associated lung injury (EVALI) outbreak. It is clear there is much about vaping that is not understood. Consequently, until more is known about the health effects of vaping, individual factors that need to be taken into consideration include age, current and prior use of combustible tobacco products, and whether the user has preexisting lung conditions such as asthma and chronic obstructive pulmonary disease (COPD).

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Section: Inflammationmentioning

confidence: 99%

Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health

Traboulsi

Cherian

Rjeili

et al. 2020

IJMS

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“…Co-Immunoprecipitation (Co-IP) was performed according to previous description [ 21 ]. Briefly, BMPC conferred with above treatments was harvested and lysed in the buffer of Pierce™ Co-Immunoprecipitation Kit (Cat.…”

Section: Methodsmentioning

confidence: 99%

“…Whole cellular lysates or the output of Co-IP was subjected to 7–10% SDS polyacrylamide gel electrophoresis (SDS-PAGE) according to previous description [ 21 ]. Briefly, proteins were electrophoretically transferred onto a PVDF membrane (Millipore).…”

Section: Methodsmentioning

confidence: 99%

Akt+ IKKα/β+ Rab5+ Signalosome Mediate the Endosomal Recruitment of Sec61 and Contribute to Cross-Presentation in Bone Marrow Precursor Cells

You

et al. 2020

Vaccines

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Cross-presentation in dendritic cells (DC) requires the endosomal relocations of internalized antigens and the endoplasmic reticulum protein Sec61. Despite the fact that endotoxin-containing pathogen and endotoxin-free antigen have different effects on protein kinase B (Akt) and I-kappa B Kinase α/β (IKKα/β) activation, the exact roles of Akt phosphorylation, IKKα or IKKβ activation in endotoxin-containing pathogen-derived cross-presentation are poorly understood. In this study, endotoxin-free ovalbumin supplemented with endotoxin was used as a model pathogen. We investigated the effects of endotoxin-containing pathogen and endotoxin-free antigen on Akt phosphorylation, IKKα/β activation, and explored the mechanisms that the endotoxin-containing pathogen orchestrating the endosomal recruitment of Sec61 of the cross-presentation in bone marrow precursor cells (BMPC). We demonstrated that endotoxin-containing pathogen and endotoxin-free antigen efficiently induced the phosphorylation of Akt-IKKα/β and Akt-IKKα, respectively. Endotoxin-containing pathogen derived Akt+ IKKα/β+ Rab5+ signalosome, together with augmented the recruitment of Sec61 toward endosome, lead to the increased cross-presentation in BMPC. Importantly, the endosomal recruitment of Sec61 was partly mediated by the formation of Akt+ IKKα/β+ signalosome. Thus, these data suggest that Akt+ IKKα/β+ Rab5+ signalosome contribute to endotoxin-containing pathogen-induced the endosomal recruitment of Sec61 and the superior efficacy of cross-presentation in BMPC.

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“…In addition to the above 2 models, another study showed that nonphosphorylated STAT3 might compete with NF-κB. The inhibition of STAT3 protein expression could enhance cytokine production and eliminate α7nAChR signaling [40]. Furthermore, other studies have found that nicotine increases the level of IL-1 receptor-related kinase M in macrophages, which depends on JAK2, STAT3, and PI3K [47].…”

Section: Color Version Available Onlinementioning

confidence: 99%

“…Nevertheless, studies have shown that nicotine can induce IKK to inhibit the phosphorylation of I-kappa B and the transcriptional activity of NF-κB [32]. Nicotine treatment has been also shown to increase STAT3 phosphorylation and reduce LPS-induced p65 translocation [39,40].…”

Section: Nf-κb Pathwaysmentioning

confidence: 99%

Advances in the Treatment of Cholinergic Anti-Inflammatory Pathways in Gastrointestinal Diseases by Electrical Stimulation of Vagus Nerve

Lei

Duan

2019

Digestion

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Background: The cholinergic anti-inflammatory pathway (CAIP) has been proposed as a key mechanism by which the brain, through the vagus nerve (VN), modulates the immune system in the body. Recent studies of VN stimulation (VNS) in vivo systems have shown that it plays an anti-inflammatory role through CAIP. Inflammatory diseases in the gastrointestinal tract are frequent and difficult to treat. Summary: The mechanism of the anti-inflammatory effect of VNS through CAIP is not fully known. The current review covers anatomy, molecular mechanisms, and the application in gastrointestinal diseases of the vagal CAIP. Key Messages: CAIP bridges immune and nervous systems and plays pleiotropic roles in modulating inflammation in animal models by targeting different immune, proinflammatory, epithelial and endothelial cells, and signaling pathways. Numerous animal studies have shown beneficial effects of stimulation of this pathway in models of inflammatory diseases, either through (electrical) stimulation of the VN or pharmacological approaches. In this review, we focus on the anti-inflammatory benefits of VNS as a means of providing new insights into treating inflammation-related gastrointestinal diseases, as exemplified by those described herein.

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Nicotine induces TIPE2 upregulation and Stat3 phosphorylation contributes to cholinergic anti-inflammatory effect

Cited by 9 publications

References 39 publications

Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health

Inhalation Toxicology of Vaping Products and Implications for Pulmonary Health

Akt+ IKKα/β+ Rab5+ Signalosome Mediate the Endosomal Recruitment of Sec61 and Contribute to Cross-Presentation in Bone Marrow Precursor Cells

Advances in the Treatment of Cholinergic Anti-Inflammatory Pathways in Gastrointestinal Diseases by Electrical Stimulation of Vagus Nerve

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