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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
Human Peripheral Nerve Pericyte, supplied by ScienCell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
Biomimetic Peripheral Nerves, supplied by BioMimetic Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
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merkin peripheral neuropathy and nerve regeneration center  (Johns Hopkins HealthCare)
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(A) Immunostaining of human <t>peripheral</t> nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and <t>pericytes.</t> (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.
Merkin Peripheral Neuropathy And Nerve Regeneration Center, supplied by Johns Hopkins HealthCare, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) Immunostaining of human peripheral nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and pericytes. (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.

Journal: Neurology® Neuroimmunology & Neuroinflammation

Article Title: Small Nuclear Ribonucleoprotein Autoantibody Associated With Blood-Nerve Barrier Breakdown in Guillain-Barré Syndrome

doi: 10.1212/NXI.0000000000200405

Figure Lengend Snippet: (A) Immunostaining of human peripheral nerve microvascular endothelial cells (PnMECs) for snRNPs. Nuclear snRNP expression in monolayer PnMECs decreased after incubation with GBS-IgG with snRNP antibodies or anti-snRNP monoclonal antibody compared with after cont-IgG or cont-Ab. GBS-IgG: IgG purified from serum samples of 20 patients with U1-snRNP autoantibody–positive GBS; cont-IgG: IgG purified from serum samples of 10 healthy controls; RNP antibody: commercial snRNP monoclonal antibody; cont-Ab: commercial anti-rabbit IgG. Scale bar, 50 μm. (B) Incubation of GBS-IgG with snRNP antibodies or anti-snRNP antibody caused a significant increase in 10-kDa dextran permeability, compared with that with cont-IgG or cont-Ab, using a monolayer coculture model consisting of FH-BNB cells and pericytes. (C) GBS-IgG with anti-snRNP antibody induced a significant increase in the permeability of FH-BNB compared with cont-IgG, GBS-IgG without anti-snRNP antibody, or GBS-IgG after the reduction of U1-snRNP antibody from GBS-IgG with U1-snRNP antibody. (D) Incubation with GBS-IgG or snRNP antibodies leads to a decrease in claudin-5 and an increase in 10-kDa dextran permeability compared with cont-IgG using the spheroid model, which consists of both FH-BNB cells and pericytes (Left). Scale bar, 50 μm. Permeability of 20-kDa dextran increased after exposure to GBS-IgG or snRNP antibodies compared with cont-IgG using a microfluidic in vitro BNB coculture model (Right). Scale bar, 100 μm. BNB = blood-nerve barrier; U1-snRNP = U1-small nuclear ribonucleoprotein.

Article Snippet: After loading the cell suspension with human peripheral nerve pericyte (2.5 × 10 6 cells/mL) in collagen I gel (2 μL) into the middle channel, PnMECs were seeded and cultured in the top channel to establish a BNB microfluidic coculture model. CB medium and fresh Sciencell pericyte medium were used to assess their influence on barrier function.

Techniques: Immunostaining, Expressing, Incubation, Purification, Permeability, In Vitro