Serum tumour necrosis factor-α and soluble tumour necrosis factor receptors levels in patients with Guillain-Barre syndrome

Radhakrishnan, V. V.; Sumi, Masaki; Reuben, S; Mathai, A; Nair, M. D.

doi:10.1034/j.1600-0404.2003.00179.x

Cited by 42 publications

(30 citation statements)

References 14 publications

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“…4A,E). The inflammatory mediator TNF-a plays a key role in the pathological processes of Guillain-Barré syndrome and CIDP (Radhakrishnan et al, 2004;Deng et al, 2008;Yang et al, 2008). TNF-a also induces cell-specific damage to Schwann cells in vitro (Boyle et al, 2005) and thus contributes to the development of inflammatory neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Peripheral nerve pericytes modify the blood–nerve barrier function and tight junctional molecules through the secretion of various soluble factors

Shimizu

Sano

Abe

et al. 2010

Journal Cellular Physiology

126

119

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The objectives of this study were to establish pure blood-nerve barrier (BNB) and blood-brain barrier (BBB)-derived pericyte cell lines of human origin and to investigate their unique properties as barrier-forming cells. Brain and peripheral nerve pericyte cell lines were established via transfection with retrovirus vectors incorporating human temperature-sensitive SV40 T antigen (tsA58) and telomerase. These cell lines expressed several pericyte markers such as α-smooth muscle actin, NG2, platelet-derived growth factor receptor β, whereas they did not express endothelial cell markers such as vWF and PECAM. In addition, the inulin clearance was significantly lowered in peripheral nerve microvascular endothelial cells (PnMECs) through the up-regulation of claudin-5 by soluble factors released from brain or peripheral nerve pericytes. In particular, bFGF secreted from peripheral nerve pericytes strengthened the barrier function of the BNB by increasing the expression of claudin-5. Peripheral nerve pericytes may regulate the barrier function of the BNB, because the BNB does not contain cells equivalent to astrocytes which regulate the BBB function. Furthermore, these cell lines expressed several neurotrophic factors such as NGF, BDNF, and GDNF. The secretion of these growth factors from peripheral nerve pericytes might facilitate axonal regeneration in peripheral neuropathy. Investigation of the characteristics of peripheral nerve pericytes may provide novel strategies for modifying BNB functions and promoting peripheral nerve regeneration.

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Section: Discussionmentioning

confidence: 99%

Peripheral nerve pericytes modify the blood–nerve barrier function and tight junctional molecules through the secretion of various soluble factors

Shimizu

Sano

Abe

et al. 2010

Journal Cellular Physiology

126

119

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“…Among the different genotypes, TNF-␣ Ϫ308 G Ͼ A and TNF-␣ Ϫ857 CϾT polymorphisms either in homozygous or heterozygous conditions, had significant association with elevated TNF-␣ serum concentration. TNF-␣ is a pro-inflammatory cytokine with a prominent role in inflammation, and has been implicated in the pathogenesis of various autoimmune and infectious diseases and correlated with severity of the disease [28,29]. Many studies AS-PCR, allele-specific polymerase chain reaction; PCR-RFLP, polymerase chain reaction-restriction fragment length polymorphism; F, forward; R, reverse; C, control.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor–α polymorphisms and expression in Guillain–Barré syndrome

et al. 2010

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“…Consistent with this thesis, we observed a rapid and marked increase in CCL2 mRNA and protein expression in PNMEC cultures responding to a TNFα challenge. The physiological concentration of TNFα in plasma of patients with GBS is reported to exceed 0.1 ng/ml (Reuben et al, 2002; Radhakrishnan et al, 2004). At this low concentration, TNFα elicited measurable increases in CCL2 mRNA content in immortalized PNMEC cultures.…”

Section: Discussionmentioning

confidence: 99%

Tumour Necrosis Factor α Enhances CCL2 and ICAM-1 Expression in Peripheral Nerve Microvascular Endoneurial Endothelial Cells

2013

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Recruitment and trafficking of autoreactive leucocytes across the BNB (blood–nerve barrier) is an early pathological insult in GBS (Guillain-Barré syndrome), an aggressive autoimmune disorder of the PNS (peripheral nervous system). Whereas the aetiology and pathogenesis of GBS remain unclear, pro-inflammatory cytokines, including TNFα (tumour necrosis factor α), are reported to be elevated early in the course of GBS and may initiate nerve injury by activating the BNB. Previously, we reported that disrupting leucocyte trafficking in vivo therapeutically attenuates the course of an established animal model of GBS. Here, PNMECs (peripheral nerve microvascular endothelial cells) that form the BNB were harvested from rat sciatic nerves, immortalized by SV40 (simian virus 40) large T antigen transduction and subsequently challenged with TNFα. Relative changes in CCL2 (chemokine ligand 2) and ICAM-1 (intercellular adhesion molecule 1) expression were determined. We report that TNFα elicits marked dose- and time-dependent increases in CCL2 and ICAM-1 mRNA and protein content and promotes secretion of functional CCL2 from immortalized and primary PNMEC cultures. TNFα-mediated secretion of CCL2 promotes, in vitro, the transendothelial migration of CCR2-expressing THP-1 monocytes. Increased CCL2 and ICAM-1 expression in response to TNFα may facilitate recruitment and trafficking of autoreactive leucocytes across the BNB in autoimmune disorders, including GBS.

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Serum tumour necrosis factor-α and soluble tumour necrosis factor receptors levels in patients with Guillain-Barre syndrome

Cited by 42 publications

References 14 publications

Peripheral nerve pericytes modify the blood–nerve barrier function and tight junctional molecules through the secretion of various soluble factors

Peripheral nerve pericytes modify the blood–nerve barrier function and tight junctional molecules through the secretion of various soluble factors

Tumor necrosis factor–α polymorphisms and expression in Guillain–Barré syndrome

Tumour Necrosis Factor α Enhances CCL2 and ICAM-1 Expression in Peripheral Nerve Microvascular Endoneurial Endothelial Cells

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