Helicobacter Pylori & Adhesion to Endothelial cells

 Helicobacter Pylori & Adhesion to Endothelial cells
Helicobacter pylori infection is one of the most common human diseases and the main risk factor for peptic ulcer and gastric cancer. Virulence agents are three antigens, Vaccinate A cytotoxin (ACA), cytotoxin-related antigen (GagA), and neutrophil-activating Helicobacter pylori protein (HPNAP).

HPNAP attracts and activates neutrophils, monocytes, and mast cells, resulting in the release of pro-inflammatory mediators. The same molecule promotes the immune response, and it has also been reported that the C terminal region of HPNAP stimulates neutrophil activation indicated by the production of active oxygen intermediates after activation of the adenine nicotinamide phosphate dinucleotide phosphate oxidase.

In this study, there is evidence that the C-terminal region of HPNAP is essential for the attachment of neutrophils to endothelial cells, a necessary step for inflammation of Helicobacter pylori. Also, it appears that arabinogalactan (AGPs) proteins, which derive from Chios mastic, the natural resin from the Pistacia lentiscus, inhibit the activation of neutrophils in vitro.

Human neutrophils were separately incubated with pre-linked endothelial cells with HPNAP-6xHis, HPNAP-6xHis (N-terminal region), and HPNAP-6xHis (C-terminal region) and their adhesion were quantitated using the myeloperoxidase assay MPO). Also, neutrophils were incubated in the same way as the neutrophil peptide stimulant (fMLP) to test for their bioactivity. The HPNAP-6xHis and the C-terminal region display almost the same potential for promoting neutrophil adhesion to endothelial cells, while the N-terminal region, on the other hand, has a remarkable lack of this ability.

Considering the presence of liposaccharides and their involvement in activation, it is clear that even after their removal the activation effect did not change significantly. These results are consistent with previous data, indicating that the HPNAP protein domain is the critical component of neutrophils for uptake, activation and subsequent adhesion to endothelial cells, leading to oxidative burst and inflammation in Helicobacter pylori infection.

The inhibition of neutrophil adhesion by arabinogalactan protein (AGPs) of Chios mastic and its derivatives has been used extensively in traditional medicine to ease the suffering of patients suffering from gastric pain. In vitro antibacterial properties against a wide variety of bacteria have been demonstrated. In this study, they proved that AGPs extracted from Chios mastiha inhibit neutrophil adhesion to endothelial cells caused by neutrophil-activated Helicobacter pylori protein and its C-terminal region.

Summarizing the results of this laboratory study, appears that the broad C-terminal region of HPNAR stimulates neutrophil adhesion and that AGPs from Chios mastitis disrupt HPNAP-mediated neutrophil-endothelial cell binding, a result that needs to be further investigated and to be used for the anti-inflammatory treatment of patients with Helicobacter pylori.

Kottakis F, Befani C, Asiminas A, Kontou M, Koliakos G, Choli-Papadopoulou T. The C-terminal region of HPNAP activates neutrophils and promotes their adhesion to endothelial cells. Helicobacter 2009;14:177-179.

Related product: L-Glutamine & Chios Mastic
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