anti mcherry mouse monoclonal antibody novus  (Hycult Biotech)

Journal: PLoS ONE

Article Title: Complement and the Alternative Pathway Play an Important Role in LPS/D-GalN-Induced Fulminant Hepatic Failure

doi: 10.1371/journal.pone.0026838

Figure Lengend Snippet: Wt C57BL/6 mice were injected i.p. with LPS/D-GalN and euthanized at 0, 1, 4 and 8 hours after the injection. (A–L) Immunohistochemical staining for C3, C3aR and C5aR in liver sections after the LPS/D-GalN injection. (M–N) The relative C3aR mRNA and C5aR mRNA expression levels were determined in live tissue at the indicated time points after the LPS/D-GalN injection. The mRNA expression was determined by relative quantitative real-time PCR analysis. The results are expressed as the means±SEM relative to GAPDH expression. (O) The serum concentrations of C3a at the indicated times after the LPS/D-GalN injection. ** and *** indicate p <0.01 and p <0.001, respectively. n = 6–7 per group. The original magnification for C3 of stained images: ×200; for C3aR and C5aR of stained images: ×800.

Article Snippet: Monoclonal antibody to mouse C5aR (HM1076) was purchased from Hycult Biotechnology B.V (Hycult Biotechnology, The Netherlands).

Techniques: Injection, Immunohistochemical staining, Staining, Expressing, Real-time Polymerase Chain Reaction

Journal: PLoS ONE

Article Title: Complement and the Alternative Pathway Play an Important Role in LPS/D-GalN-Induced Fulminant Hepatic Failure

doi: 10.1371/journal.pone.0026838

Figure Lengend Snippet: (A–F) C3aR antagonist group mice displayed reduced liver damage (A–B, D–E) and decreased C3 deposition (C, F) 8 hours after LPS/D-GalN injection. (G–H) C3aR mRNA expression decreased at 8 hours compared with that of the saline group, whereas C5aR mRNA expression decreased from 4 to 8 hours (n = 4–5). (I) The different response patterns of ALT concentration in the C3aR antagonist group mice and the wt mice (n = 4–5). (J–L) The concentrations of TNF-α and IL-6 in the C3aR antagonist mice were lower than in the saline group. There was a delayed increase in MCP-1 in the C3aR antagonist group (n = 4–5). (M) Treatment with the C3aR antagonist increased the survival rate of the mice after LPS/D-GalN injection (n = 8). *, **and *** indicate p <0.05, p <0.01 and p <0.001, respectively, relative to the saline group. The means±SEM are shown. Magnification of the H&E and immunohistochemically stained images: ×200. The results are representative of 3 separate experiments.

Article Snippet: Monoclonal antibody to mouse C5aR (HM1076) was purchased from Hycult Biotechnology B.V (Hycult Biotechnology, The Netherlands).

Techniques: Injection, Expressing, Concentration Assay, Staining

Journal: PLoS ONE

Article Title: Complement and the Alternative Pathway Play an Important Role in LPS/D-GalN-Induced Fulminant Hepatic Failure

doi: 10.1371/journal.pone.0026838

Figure Lengend Snippet: (A–I) Both C5aRmAb and CR2-fH groups displayed reduced liver damage (A–B, D–E, G–H) and decreased C3 deposition (C, F, I) 8 hours after LPS/D-GalN injection. (J) The different response patterns of ALT concentration in the C3aR antagonist mice and the wt mice (n = 4–5). (J–K) Treatment with the C5aR antagonist or CR2-fH increased the survival rate of the mice after LPS/D-GalN injection (n = 8). ** and *** indicate p <0.01 and p <0.001, respectively, relative to the saline group. The means±SEM are shown. Magnification of the H&E and immunohistochemically stained images: ×200. The results are representative of 3 separate experiments.

Article Snippet: Monoclonal antibody to mouse C5aR (HM1076) was purchased from Hycult Biotechnology B.V (Hycult Biotechnology, The Netherlands).

Techniques: Injection, Concentration Assay, Staining

Journal: The Journal of General Virology

Article Title: MERS-CoV infection causes brain damage in human DPP4-transgenic mice through complement-mediated inflammation

doi: 10.1099/jgv.0.001667

Figure Lengend Snippet: Anti-C5aR1 antibody treatment decreased inflammation and viral spread in brains of hDPP4-transgenic mice. Representative images of immunohistochemical staining of cleaved caspase-3 ( a, b ), phosphorylated P38 ( c, d ), IBA-1 ( e, f ), and antiviral NP ( g, h ) in similar regions of cerebral cortex in brains of hDPP4 transgenic mice 7 days after infection with MERS-CoV and treatment with anti-C5aR1 monoclonal antibody. Fewer immunopositive cells were detected in the anti-C5aR1 antibody treatment group ( n =3 per group).

Article Snippet: Mice were treated intravenously (600 µg kg −1 ) with a monoclonal antibody (mAb) to the mouse C5a receptor (C5aR1, HM1076; Hycult Biotech, PB Uden, The Netherlands) for complement inhibition immediately after virus challenge or with the same volume of isotype antibody (HI4041, Hycult Biotech, PB Uden, The Netherlands) as a control.

Techniques: Transgenic Assay, Immunohistochemical staining, Staining, Infection

Journal: The Journal of General Virology

Article Title: MERS-CoV infection causes brain damage in human DPP4-transgenic mice through complement-mediated inflammation

doi: 10.1099/jgv.0.001667

Figure Lengend Snippet: Anti-C5aR1 antibody treatment decreased brain damage in hDPP4 transgenic mice. ( a, b ) Representative images of H&E staining of brain sections of hDPP4-transgenic mice 7 days after infection with MERS-CoV and treatment with anti-C5aR1 or sham control. The representative image of the brains in anti-C5aR1 treatment mice showed less oedema, fewer infiltrating inflammatory cells, especially around vessels in the cerebellum compared to those receiving sham treatment. ( c, d ) Evans blue staining of mice brain on day 7. The brain of a MERS-CoV-infected mouse appeared blue compared with that of a mouse treated with anti-C5aR1 antibody. ( e–h ) Representative images of immunohistochemical staining for neutrophil infiltration ( e, f ) and NF-κB localization ( g, h ). ( i, j ) Semiquantitative analysis of brain damage via H&E scores ( i ) and neutrophil infiltration ( j ). #, Undetectable; ** P <0.01 (Student’s t -test with Welch’s correction)

Article Snippet: Mice were treated intravenously (600 µg kg −1 ) with a monoclonal antibody (mAb) to the mouse C5a receptor (C5aR1, HM1076; Hycult Biotech, PB Uden, The Netherlands) for complement inhibition immediately after virus challenge or with the same volume of isotype antibody (HI4041, Hycult Biotech, PB Uden, The Netherlands) as a control.

Techniques: Transgenic Assay, Staining, Infection, Immunohistochemical staining

Journal: The Journal of General Virology

Article Title: MERS-CoV infection causes brain damage in human DPP4-transgenic mice through complement-mediated inflammation

doi: 10.1099/jgv.0.001667

Figure Lengend Snippet: Diagram illustrating damage to brain tissues in human DPP4-transgenic mice. Neurons infected by MERS-CoV secrete complement components which could activate microglia, which, in turn, could also secrete complement components in brain. Excessive complement activation could activate the endothelial cells of BBB, enhancing the infiltration of inflammatory cells, such as neutrophils and macrophages, into brain parenchyma. The infiltrated inflammatory cells secrete proinflammatory cytokines which could further enhance neuronal damage. However, the inhibition of C5a-C5aR1 interaction could inhibit BBB damage and decrease second damage owing to the excessive inflammatory response.

Article Snippet: Mice were treated intravenously (600 µg kg −1 ) with a monoclonal antibody (mAb) to the mouse C5a receptor (C5aR1, HM1076; Hycult Biotech, PB Uden, The Netherlands) for complement inhibition immediately after virus challenge or with the same volume of isotype antibody (HI4041, Hycult Biotech, PB Uden, The Netherlands) as a control.

Techniques: Transgenic Assay, Infection, Activation Assay, Inhibition