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ORIGINAL RESEARCH article

Front. Neurol.
Sec. Neuroinfectious Diseases
Volume 15 - 2024 | doi: 10.3389/fneur.2024.1450735

Causal relationship between Circulating inflammatory proteins and risk of different types of encephalitis：a two-sample Mendelian randomization study

Provisionally accepted
Yanwei Liu Yanwei Liu 1Xilong Wang Xilong Wang 2*Qiang Zhao Qiang Zhao 2*Jun Wei Jun Wei 1*Shiqiang Yang Shiqiang Yang 3,4*
  • 1 Neurology, First People's Hospital of Yibin, Sichuan, China
  • 2 The Five People’s Hospital of Yibin, Yibin, China
  • 3 Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China
  • 4 Neurosurgery, First People's Hospital of Yibin, Sichuan, China

The final, formatted version of the article will be published soon.

    Background Cytokines are potent molecules of the immune response. They act at the site of inflammation and circulate in the bloodstream. However, there are few studies on encephalitis and circulating inflammatory proteins.In this study, Mendelian randomization (MR) was used to explore the potential causal effect of 91 circulating inflammatory proteins on 3 different types of encephalitis. Causal effects were examined using Steiger, MR-Egger, weighted median, and inverse variance weighting (IVW) methods.IVW methods were primarily used for results interpretation. In addition, sensitivity analyses were performed, including assessment of heterogeneity, horizontal pleiotropy, and Leave-one-out techniques.We subjected 91 circulating inflammatory proteins to MR analysis of causality with each of the three types of encephalitis. The results suggested that the inflammatory factors with a potential causal relationship with viral encephalitis were caspase 8, C-X-C motif chemokine 6, interleukin-10, interleukin-15 receptor subunit alpha, interleukin-7, and TNF-beta. Inflammatory factors potentially causally associated with acute disseminated encephalomyelitis are beta-nerve growth factor, cystatin D, interleukin-7, Latency-associated peptide transforming growth factor beta 1,and neurotrophin-3.Inflammatory factors potentially causally associated with autoimmune encephalitis are C-C motif chemokine 25, hepatocyte growth factor, latency-associated peptide transforming growth factor beta 1, programmed cell death 1 ligand 1, sulfotransferase 1A1, and tumor necrosis factor.This study identifies potential causal effects of certain circulating inflammatory factors on susceptibility to three types of encephalitis. Although the exact mechanisms by which inflammatory proteins contribute to the pathogenesis of different encephalitis subtypes remain unclear, our findings provide new perspectives on these potential causal relationships.

    Keywords: Circulating inflammatory proteins, Viral Encephalitis, Acute disseminated encephalomyelitis, autoimmune encephalitis, Mendelian randomization

    Received: 20 Jun 2024; Accepted: 13 Dec 2024.

    Copyright: © 2024 Liu, Wang, Zhao, Wei and Yang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Xilong Wang, The Five People’s Hospital of Yibin, Yibin, China
    Qiang Zhao, The Five People’s Hospital of Yibin, Yibin, China
    Jun Wei, Neurology, First People's Hospital of Yibin, Sichuan, China
    Shiqiang Yang, Neurosurgery, West China Hospital, Sichuan University, Chengdu, Sichuan Province, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.