Only in Titles

           Search results for: Helicobacter pylori antibody, Monoclonal Antibodies, Host Mouse, Isotype IgG1   

paperclip

#15806982   2005/04/05 Save this To Up

Augmentation of Helicobacter pylori urease activity by its specific IgG antibody: implications for bacterial colonization enhancement.

Gastric colonization of Helicobacter pylori (H. pylori) occurs in a very early age via infected mothers having H. pylori-specific IgG antibodies that would be transplacentally transferred to infants. In addition, H. pylori urease-specific IgG was associated with chronic gastric atrophy and post-immunization gastritis is usually correlated with a strong local IgG response. These findings indicate that H. pylori-specific IgG antibodies, in particular its urease-specific IgG, may induce unfavorable influence on host resistance against H. pylori. Here, we show that we have found a unique H. pylori urease-specific IgG monoclonal antibody (MAb), termed S3, recognizing the conformational structure of the small subunit Ure-A, which enhanced the urease enzymatic activity. Such enhancement of the H. pylori urease activity induced by 1 microg of S3 was almost completely cancelled by simultaneously added the same amount of L2 MAb, which has a strong and specific inhibitory activity against H. pylori urease and recognizes a liner epitope of 8-mer peptide (F8: SIKEDVQF) within its large subunit Ure-B (Infect. Immun. 69: 6597, 2001). Intravenous pre-administration of purified S3 into BALB/c mice showed significant augmentation for gastric colonization with the susceptible strain Sydney Strain-1 (SS-1). To our knowledge, this is the first demonstration that a H. pylori urease-specific IgG MAb induced an augmentation of their gastric colonization in vivo.

1462 related Products with: Augmentation of Helicobacter pylori urease activity by its specific IgG antibody: implications for bacterial colonization enhancement.

MOUSE ANTI BOVINE ROTAVIR Helicobacter pylori antib Helicobacter pylori antib MOUSE ANTI BORRELIA BURGD RABBIT ANTI GSK3 BETA (pS MOUSE ANTI CANINE DISTEMP MOUSE ANTI HUMAN CD19 RPE MOUSE ANTI APAAP COMPLEX, Infection diseases: Heli Rabbit Anti-Nkx2.5 Cardia Rabbit Anti-Nkx2.5 Cardia Rabbit Anti-Nkx2.5 Cardia

Related Pathways

paperclip

#12126911   2002/07/19 Save this To Up

Serum-derived IgG1-mediated immune exclusion as a mechanism of protection against H. pylori infection.

The induction of protective immunity against Helicobacter challenge in a murine model was found to correlate with the magnitude of IgG (serum and gastric lavage) responsiveness to intra-nasal (i.n.) immunisation. IgG1-secreting hybridoma backpacks in Helicobacter pylori (H. pylori)-infected mice revealed serum transudation into the stomach. A Lpp20-specific monoclonal antibody was associated with significantly reduced H. pylori colonisation. Histology revealed aggregates of the remaining H. pylori in these mice, suggesting a role for IgG1-mediated immune exclusion of the bacteria. In vitro immunogold electron microscopy supported this hypothesis, but also suggested that a threshold of H. pylori-specific antibody needs to be maintained if immune exclusion by the host is to overcome immune evasion by the bacteria.

1989 related Products with: Serum-derived IgG1-mediated immune exclusion as a mechanism of protection against H. pylori infection.

Human Serum Albumin antib Human Serum Albumin antib Astrovirus antibody, Mono Helicobacter pylori antib Helicobacter pylori antib Mouse anti-chick type II Mouse anti chick type II Mouse anti-chick type II Mouse anti-bovine type II Mouse anti bovine type II Mouse anti-porcine type I Mouse anti porcine type I

Related Pathways

paperclip

#1561526   1992/05/14 Save this To Up

IgG subclass response to Helicobacter pylori in patients with chronic active gastritis and duodenal ulcer.

The IgG subclass response is determined by the type of bacteria producing the infection and by genetic factors of the host. Patients with a Helicobacter pylori infection develop a specific immune response that is mainly of the IgA and IgG class. We measured the IgG subclass response in 20 patients with chronic active gastritis without a history of duodenal ulcer and 20 patients with chronic active gastritis and duodenal ulcer diagnosed by endoscopy and histology. A control group included 20 H. pylori-negative patients and 60 H. pylori-positive blood transfusion donors. Systemic IgG subclass response was measured with a modified enzyme-linked immunosorbent assay technique, using as antigen a sonicate of six different H. pylori strains. Mouse monoclonal antibodies against each of the four human IgG subclasses (IgG1, IgG2, IgG3, and IgG4) were used. The total IgG anti-H. pylori antibody titres were equal in all three H. pylori-positive groups and significantly different from that of the negative control group (p less than 0.01). The IgG subclass response in persons infected with H. pylori involved all four subclasses but was predominantly of the IgG1 and IgG2 subclasses. All of the groups with H. pylori infection had significantly higher levels of IgG1 than the negative control group, but no differences were detected among the three groups. However, the duodenal ulcer group had a significantly higher IgG2 response than the gastritis group (mean optical density +/- SEM, 0.382 +/- 0.047 versus 0.200 +/- 0.025, respectively; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

2605 related Products with: IgG subclass response to Helicobacter pylori in patients with chronic active gastritis and duodenal ulcer.

Infection diseases: Heli Helicobacter pylori antib Helicobacter pylori antib Infection diseases: Heli CAR,CAR,Constitutive acti Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl HIV1 integrase antibody, Shiga Toxin 1 antibody, M

Related Pathways