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细胞外囊泡在接受 COVID-19 疫苗接种的阿达木单抗治疗的克罗恩病患者中的作用。

Role of Extracellular Vesicles in Crohn's Patients on Adalimumab Who Received COVID-19 Vaccination.

机构信息

Laboratory of Personalized Medicine, National Institute of Gastroenterology IRCCS "S. de Bellis", Research Hospital, Via Turi 27, Castellana Grotte, 70013 Bari, Italy.

Dipartimento di Ingegneria Civile, Ambientale, del Territorio, Edile e di Chimica, Politecnico di Bari, Via Orabona 4, 70126 Bari, Italy.

出版信息

Int J Mol Sci. 2024 Aug 14;25(16):8853. doi: 10.3390/ijms25168853.

Abstract

Crohn's disease (CD) is a type of inflammatory bowel disease (IBD) affecting the gastrointestinal tract that can also cause extra-intestinal complications. Following exposure to the mRNA vaccine BNT162b2 (Pfizer-BioNTech) encoding the SARS-CoV-2 Spike (S) protein, some patients experienced a lack of response to the biological drug Adalimumab and a recrudescence of the disease. In CD patients in progression, resistant to considered biological therapy, an abnormal increase in intestinal permeability was observed, more often with a modulated expression of different proteins such as Aquaporin 8 (AQP8) and in tight junctions (e.g., ZO-1, Claudin1, Claudin2, Occludin), especially during disease flares. The aim of this study is to investigate how the SARS-CoV-2 vaccine could interfere with IBD therapy and contribute to disease exacerbation. We investigated the role of the SARS-CoV-2 Spike protein, transported by extracellular vesicles (EVs), and the impact of various EVs components, namely, exosomes (EXOs) and microvesicles (MVs), in modulating the expression of molecules involved in the exacerbation of CD, which remains unknown.

摘要

克罗恩病(CD)是一种影响胃肠道的炎症性肠病(IBD),也会引起肠道外并发症。在接触编码 SARS-CoV-2 刺突(S)蛋白的 mRNA 疫苗 BNT162b2(辉瑞-生物科技)后,一些患者对生物药物阿达木单抗的反应减弱,疾病复发。在进展中的 CD 患者中,对已考虑的生物治疗产生耐药性,观察到肠道通透性异常增加,更常见的是不同蛋白质(例如水通道蛋白 8(AQP8)和紧密连接蛋白(例如 ZO-1、Claudin1、Claudin2、Occludin))的表达发生调节,尤其是在疾病发作期间。本研究旨在探讨 SARS-CoV-2 疫苗如何干扰 IBD 治疗并导致疾病恶化。我们研究了由细胞外囊泡(EVs)转运的 SARS-CoV-2 刺突蛋白的作用,以及各种 EV 成分(即外泌体(EXOs)和微泡(MVs))在调节参与 CD 恶化的分子表达方面的作用,这一点尚不清楚。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4621/11355036/56fb18f235b2/ijms-25-08853-g001.jpg

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