Can we assess severity of Guillain‐Barré syndrome using absolute monocyte count?

Li, X.; Li, W.; Luo, Yue; Qin, Liuqun; Su, Qingde; Mo, W.

doi:10.1111/ijlh.12845

Cited by 10 publications

(7 citation statements)

References 23 publications

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“…Similar to many other localized autoimmune disorders where essential pathology is restricted to a specific organ/tissue, in addition to inflammatory damage in peripheral nerve, many GBS patients experience systemic inflammation. The number of neutrophils [31] and monocytes [32] in GBS patients are higher than healthy controls. Blood cytokine levels are found altered, with a significant increase of TNF-α, IL-1β, IL-6, IFN-γ, and Creactive protein in GBS patients [33,34].…”

Section: Discussionmentioning

confidence: 80%

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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Section: Discussionmentioning

confidence: 80%

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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“…Thirty of the 60 studies were excluded after reading the full text because they lacked the necessary data ( n = 7); lack of a control group ( n = 9); reported ex vivo cytokine data ( n = 4); single case reports ( n = 2), and blood or CSF cytokines were analyzed in less than three studies ( n = 8). Thus, a total of 30 studies comprising 1,302 patients with GBS and 1,073 healthy individuals were included in the meta-analysis (Sharief et al, 1993; Exley et al, 1994; Sindern et al, 1996; Creange et al, 1998; Hohnoki et al, 1998; Ossege et al, 2000; Press et al, 2001; Radhakrishnan et al, 2003, 2004; Deng et al, 2008; Nyati et al, 2010, 2011; Sainaghi et al, 2010; Li et al, 2012, 2013, 2014, 2018a,b; Liang et al, 2012; Wang et al, 2012; Han et al, 2014; Beppu et al, 2015; Du et al, 2015; Chang et al, 2016; Doncel-Perez et al, 2016; Zhang et al, 2016; Kharwar et al, 2017; Debnath et al, 2018a,b; Ethemoglu and Calik, 2018) (Flowchart see Figure 1).…”

Section: Resultsmentioning

confidence: 99%

Peripheral Blood and Cerebrospinal Fluid Cytokine Levels in Guillain Barré Syndrome: A Systematic Review and Meta-Analysis

et al. 2019

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Background: Guillain Barré Syndrome (GBS) is an autoimmune disorder caused by the immune-mediated damage of the peripheral nervous system. Increasing evidence suggests that inflammatory cytokines are important mediators for the onset and progression of GBS. A number of clinical studies have demonstrated elevated levels of T helper-1 (Th1-), Th2-, and Th17-related cytokines in patients with GBS; however, the results were inconsistent across studies. Methods: We performed a systematic review and a meta-analysis of studies comparing the levels of inflammatory cytokines in the cerebrospinal fluid and peripheral blood between patients with GBS and healthy individuals, using Comprehensive Meta-Analysis Version 2 software. A database search identified 30 studies comprising 1,302 patients with GBS and 1,073 healthy controls. Results: The random-effects meta-analysis demonstrated that peripheral blood tumor necrosis factor-α (Hedges g, 1.544; 95% confidence interval (CI), 0.923–2.165; p < 0.001), interleukin-1β (IL-1β; Hedges g, 0.678; 95% CI, 0.183–1.172; p = 0.007), IL-6 (Hedges g, 0.630; 95% CI, 0.100–1.160; p = 0.02), IL-4 (Hedges g, 0.822; 95% CI, 0.220–1.423; p = 0.007), IL-17 (Hedges g, 1.452; 95% CI, 0.331–2.573; p = 0.011), interferon-γ (Hedges g, 1.104; 95% CI, 0.490–1.719; p < 0.001), and C-reactive protein (Hedges g, 0.909; 95% CI, 0.453–1.365; p < 0.001) levels were significantly increased in patients with GBS when compared with healthy controls. Contrastingly, the blood IL-10 and transforming growth factor-β levels were not significantly associated with GBS. Furthermore, the meta-analysis found that cerebrospinal fluid IL-17 levels were significantly associated with GBS (Hedges g, 1.882; 95% CI, 0.104–3.661; p = 0.038). Conclusion: Altogether, our results clarified the circulating inflammatory cytokine profile in patients with GBS, and revealed that Th1-, Th2-, and Th17-related cytokines were highly elevated in the GBS patients, suggesting the potential use of these cytokines as biomarkers for GBS.

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“…Although GBS is an organ/tissue specific autoimmune disorder, systemic inflammation has been seen in patients (27) and in experimental animals, e.g., EAN (28). Compared with healthy control, the number of monocytes is higher in GBS patients (29). An enhanced CCR2 expression has been observed in the blood of both GBS patients and EAN rats (8,9,12).…”

Section: Discussionmentioning

confidence: 99%

CX3CR1 But Not CCR2 Expression Is Required for the Development of Autoimmune Peripheral Neuropathy in Mice

et al. 2021

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One hallmark of Guillain-Barre syndrome (GBS), a prototypic autoimmune peripheral neuropathy (APN) is infiltration of leukocytes (macrophages and T cells) into peripheral nerves, where chemokines and their receptors play major roles. In this study, we aimed to understand the potential contribution of chemokine receptors CCR2 and CX3CR1 in APN by using a well-established mouse model, B7.2 transgenic (L31) mice, which possesses a predisposed inflammatory background. We crossbred respectively CCR2KO and CX3CR1KO mice with L31 mice. The disease was initiated by partial ligation on one of the sciatic nerves. APN pathology and neurological function were evaluated on the other non-ligated sciatic nerve/limb. Our results revealed that L31/CX3CR1KO but not L31/CCR2KO mice were resistant to APN. CX3CR1 is needed for maintaining circulating monocyte and CD8+ T cell survival. While migration of a significant number of activated CD8+ T cells to peripheral nerves is essential in autoimmune response in nerve, recruitment of monocytes into PNS seems optional. Disease onset is independent of CCR2 mediated blood-derived macrophage recruitment, which can be replaced by compensatory proliferation of resident macrophages in peripheral nerve. CX3CR1 could also contribute to APN via its critical involvement in maintaining nerve macrophage phagocytic ability. We conclude that blockade of CX3CR1 signaling may represent an interesting anti-inflammatory strategy to improve therapeutic management for GBS patients.

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Can we assess severity of Guillain‐Barré syndrome using absolute monocyte count?

Abstract: Our findings demonstrated that elevated monocyte count is independently associated with GBS patients, and suggested monocyte count is positively associated with disease severity of GBS.

Cited by 10 publications

References 23 publications

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

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

Peripheral Blood and Cerebrospinal Fluid Cytokine Levels in Guillain Barré Syndrome: A Systematic Review and Meta-Analysis

CX3CR1 But Not CCR2 Expression Is Required for the Development of Autoimmune Peripheral Neuropathy in Mice

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