Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID‐19–associated Guillain‐Barré syndrome

Li, Zheng; Huang, Ziheng; Li, Xingye; Huang, Cheng; Shen, Jianxiong; Li, Shugang; Zhang, Lin; Wong, Sunny H.; Chan, Matthew T. V.; Wu, William Ka Kei

doi:10.1111/cpr.13024

Cited by 21 publications

(19 citation statements)

References 58 publications

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“…It should also be considered that group 3 innate lymphoid cells (ILC3s) and mucosal-associated invariant T (MAIT) cells are highly activated in patients with COVID-19, irrespective of the course of the disease, and express high levels of proinflammatory cytokines such as IL-17A, suggesting their possible involvement in COVID-19 immunopathogenesis [61] , [62] . Finally, bioinformatic analyses to delineate the potential genetic crosstalk between COVID-19 and Guillain-Barré syndrome have suggested that aberrant Th17 cell differentiation could represent a possible mechanism by which SARS-COV-2 can increase the risk of the autoimmune peripheral nervous disease [63 ] . Taken together, these findings underline a key role of IL-17A in COVID-19 and likely could pave the way to novel therapeutic approaches based upon IL-17A blockage by biological drugs that are already available [19] , [64] .…”

Section: Il-17a As a Rheostat Of Covid-19 Immune Responsementioning

confidence: 99%

Interleukin-17A (IL-17A): A silent amplifier of COVID-19

Μaione

Casillo

Raucci

et al. 2021

Biomedicine & Pharmacotherapy

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One of the hallmarks of COVID-19 is the cytokine storm that provokes primarily pneumonia followed by systemic inflammation. Emerging evidence has identified a potential link between elevated interleukin-17A (IL-17A) levels and disease severity and progression. Considering that per se , IL-17A can activate several inflammatory pathways, it is plausible to hypothesize an involvement of this cytokine in COVID-19 clinical outcomes. Thus, IL-17A could represent a marker of disease progression and/or a target to develop therapeutic strategies. This hypothesis paper aims to propose this “unique” cytokine as a silent amplifier of the COVID-19 immune response and (potentially) related therapy.

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Section: Il-17a As a Rheostat Of Covid-19 Immune Responsementioning

confidence: 99%

Interleukin-17A (IL-17A): A silent amplifier of COVID-19

Μaione

Casillo

Raucci

et al. 2021

Biomedicine & Pharmacotherapy

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“…Th17 cells are known to play an important role in the pathogenesis of various immune-mediated diseases such as rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease ( 29 ). In a recent bioinformatics analysis; Th17 cell differentiation and cytokine response was identified as an important process connecting COVID-19 to GBS ( 30 ). In our study, transferrin and albumin levels, which are negative acute phase reactants, were found to be significantly lower in the post-COVID-19 GBS group compared to the non-COVID-19 GBS group; D-dimer levels were found to be high.…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Acute Phase Reactants and Disability in Guillian-Barré Syndrome During the COVID-19 Pandemic

Yevgi

2022

Archives of Medical Research

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Backround Guillain-Barré syndrome (GBS) is an immune-mediated disease that affects the peripheral nervous system and may occur after some bacterial-viral infections. Aim The aim of this study is to determine and compare the epidemiological, clinical and laboratory characteristics of the patients followed up in our clinic with the diagnosis of GBS in the 15 month periods before and after March 2020. At the same time, we aimed to examine the importance of these markers as prognostic indicators by investigating the relationship of D-dimer, CRP, albumin and transferrin levels with Hughes functional grading scale score (HFGSS). Material and Methods The medical files of the patients who were followed up with the diagnosis of GBS between December 2018 and May 2021 were retrospectively analyzed. The patients were divided into groups as pandemic, pre-pandemic, post-COVID-19 and non-COVID-19. Epidemiological and clinical characteristics of GBS patients and plasma D-dimer, serum albumin, CRP and transferrin levels were recorded. Results No significant difference was found between the pandemic and pre-pandemic periods in terms of age, gender, GBS subtype, seasonal distribution and treatment characteristics of GBS patients. PostCOVID-19 GBS patients had significantly higher HFGSS both at admission and at discharge ( p <0.05). In post-COVID-19 GBS patients good-excellent negative correlation between transferrin and albumin levels and HFGSS at hospital admission and discharge, positive correlations with CRP levels were observed. Conclusion Post-COVID-19 GBS patients had worse HFGSS at both admission and discharge. CRP was positively correlated with HFGSS whereas transferrin and albumin showed negative correlation with HFGSS.

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“…The cytokine storm resulting from viral disturbance of the immune system could be why patients with COVID-19 are predisposed to neuropathies like GBS. In particular, Li et al recently revealed the underlying pathophysiology of GBS in COVID-19 by conducting bioinformatics analyses [ 93 ]. The genetic crosstalk between COVID-19 and GBS they observed shows the pivotal role of Th17 cells in increasing the risk of GBS in COVID-19 patients [ 93 ].…”

Section: Indirect Systemic Damagementioning

confidence: 99%

A Review of Neurological Involvement in Patients with SARS-CoV-2 Infection

Kang

2021

Med Sci Monit

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of the recent pandemic of coronavirus disease 19 (COVID-19). As the infection spreads, there is increasing evidence of neurological and psychiatric involvement in COVID-19. Headache, impaired consciousness, and olfactory and gustatory dysfunctions are common neurological manifestations described in the literature. Studies demonstrating more specific and more severe neurological involvement such as cerebrovascular insults, encephalitis and Guillain-Barré syndrome are also emerging. Respiratory failure, a significant condition that leads to mortality in COVID-19, is hypothesized to be partly due to brainstem impairment. Notably, some of these neurological complications seem to persist long after infection. This review aims to provide an update on what is currently known about neurological involvement in patients with COVID-19 due to SARS-CoV-2 infection. In this review, we demonstrate invasion routes of SARS-CoV-2, provide evidence to support the neurotropism hypothesis of the virus, and investigate the pathological mechanisms that underlie neurological complications associated with SARS-CoV-2.

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Bioinformatic analyses hinted at augmented T helper 17 cell differentiation and cytokine response as the central mechanism of COVID‐19–associated Guillain‐Barré syndrome

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 21 publications

References 58 publications

Interleukin-17A (IL-17A): A silent amplifier of COVID-19

Interleukin-17A (IL-17A): A silent amplifier of COVID-19

Relationship Between Acute Phase Reactants and Disability in Guillian-Barré Syndrome During the COVID-19 Pandemic

A Review of Neurological Involvement in Patients with SARS-CoV-2 Infection

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