Toll‐like receptor‐4 299Gly allele is associated with Guillain‐Barré syndrome in Bangladesh

Jahan, Israt; Ahammad, Rijwan Uddin; Khalid, Mir M.; Rahman, Mohammad Imtiazur; Hayat, Shoma; Islam, Badrul; Mohammad, Quazi Deen; Islam, Zhahirul

doi:10.1002/acn3.744

Cited by 13 publications

(16 citation statements)

References 39 publications

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“…[5][6][7][8][9] However, in certain pathogens such as Hepatitis E virus, this association has not been established globally, as it was only reported in Netherlands and Bangladesh. 104 Therefore, immunogenicity of COVID-19 in the development of GBS should consider the variations between different populations, [105][106][107][108] as epidemiologic studies involving certain populations might introduce bias in reporting results.…”

Section: Discussionmentioning

confidence: 99%

Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review

Aladawi

Elfil

Abu-Esheh

et al. 2021

Can. J. Neurol. Sci.

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Background: In January 2020, the first case of Guillain Barre syndrome (GBS) due to COVID-19 was documented in China. GBS is known to be postinfectious following several types of infections. Although causality can only be proven through large epidemiological studies, we intended to study this association by a thorough review of the literature. Methods: We searched PubMed, EMBASE, and Google scholar and included all papers with English or Spanish full text and original data of patients with GBS and recent COVID infection. Variables of interest were demographics, diagnostic investigations, and the latency between arboviral and neurological symptoms. Further variables were pooled to identify GBS clinical and electrophysiological variants, used treatments, and outcomes. The certainty of GBS diagnosis was verified using Brighton criteria. Results: We identified a total of 109 GBS cases. Ninety-nine cases had confirmed COVID-19 infection with an average age of 56.07 years. The average latency period between the arboviral symptoms and neurologic manifestations for confirmed COVID-19 cases was 12.2 d. The predominant GBS clinical and electromyography variants were the classical sensorimotor GBS and acute demyelinating polyneuropathy respectively. Forty cases required intensive care, 33 cases required mechanical ventilation, and 6 cases were complicated by death. Conclusions: Studies on COVID-19-related GBS commonly reported sensorimotor demyelinating GBS with frequent facial palsy. The time between the onset of infectious and neurological symptoms suggests a postinfectious mechanism. Early diagnosis of GBS in COVID-19 patients is important as it might be associated with a severe disease course requiring intensive care and mechanical ventilation.

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Section: Discussionmentioning

confidence: 99%

Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review

Aladawi

Elfil

Abu-Esheh

et al. 2021

Can. J. Neurol. Sci.

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“…Increased expression of TLR4 in GBS patients have been repeatedly reported [ 9 , 24 ]. TLR4 299Gly polymorphisms were associated with an increased susceptibility to GBS [ 25 , 26 ]. While GBS has been considered as a post-infectious neuropathy, a strong response to TLR4 stimulation has been suggested as a critical host condition for Campylobacter jejuni triggered GBS [ 27 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of TLR4 signaling protects mice from sensory and motor dysfunction in an animal model of autoimmune peripheral neuropathy

Oladiran

Shi

Yang

et al. 2021

J Neuroinflammation

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Background While the etiology remains elusive, macrophages and T cells in peripheral nerves are considered as effector cells mediating autoimmune peripheral neuropathy (APN), such as Guillain-Barre syndrome. By recognizing both pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) signals, TLRs play a central role in the initiation of both innate and adaptive immune responses. In this study, we aimed to understand the involvement of TLR4 in the pathogenesis of APN and explore the potential of TLR4 as a drug target for therapeutic use. Methods APN was induced by a partial ligation on one of the sciatic nerves in B7.2 (L31) transgenic mice which possess a predisposed inflammatory background. APN pathology and neurological function were evaluated on the other non-injured sciatic nerve. Results TLR4 and its endogenous ligand HMGB1 were highly expressed in L31 mice, in circulating immune cells and in peripheral nerves. Enhanced TLR4 signaling was blocked with TAK 242, a selective TLR4 inhibitor, before and after disease onset. Intraperitoneal administration of TAK 242 not only inhibited monocyte, macrophage and CD8+ T cell activation, but also reduced the release of pro-inflammatory cytokines. TAK 242 protected mice from severe myelin and axonal loss, resulting in a remarkable improvement in mouse motor and sensory functions. TAK 242 was effective in alleviating the disease in both preventive and reversal paradigms. Conclusion The study identified the critical contribution of TLR4-mediated macrophage activation in disease course and provided strong evidence to support TLR4 as a useful drug target for treating inflammatory autoimmune neuropathy.

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“…Interestingly, previous studies reported increased expression of TLR4 in GBS patients [ 148 ]. Moreover, TLR4 299Gly polymorphisms were associated with an increased susceptibility to GBS [ 149 , 150 ]. All this observations provide evidence to support TLR4 as a useful drug target for treating GBS, but trials using this therapeutic strategy are not yet planned.…”

Section: Guillain-barré Syndromementioning

confidence: 99%

Novel Immunological and Therapeutic Insights in Guillain-Barré Syndrome and CIDP

Querol

Lleixà

2021

Neurotherapeutics

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Inflammatory neuropathies are a heterogeneous group of rare diseases of the peripheral nervous system that include acute and chronic diseases, such as Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). The etiology and pathophysiological mechanisms of inflammatory neuropathies are only partly known, but are considered autoimmune disorders in which an aberrant immune response, including cellular and humoral components, is directed towards components of the peripheral nerve causing demyelination and axonal damage. Therapy of these disorders includes broad-spectrum immunomodulatory and immunosuppressive treatments, such as intravenous immunoglobulin, corticosteroids, or plasma exchange. However, a significant proportion of patients do not respond to any of these therapies, and treatment selection is not optimized according to disease pathophysiology. Therefore, research on disease pathophysiology aiming to reveal clinically and functionally relevant disease mechanisms and the development of new treatment approaches are needed to optimize disease outcomes in CIDP and GBS. This topical review describes immunological progress that may help guide therapeutic strategies in the future in these two disorders. Supplementary Information The online version contains supplementary material available at 10.1007/s13311-021-01117-3.

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Toll‐like receptor‐4 299Gly allele is associated with Guillain‐Barré syndrome in Bangladesh

Cited by 13 publications

References 39 publications

Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review

Guillain Barre Syndrome as a Complication of COVID-19: A Systematic Review

Inhibition of TLR4 signaling protects mice from sensory and motor dysfunction in an animal model of autoimmune peripheral neuropathy

Novel Immunological and Therapeutic Insights in Guillain-Barré Syndrome and CIDP

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