Bacterial adherence Inhibitors for Helicobacter pylori
Affiliation
Department of Biochemistry and Bioinformatics, GITAM Institute of Science, GITAM University, Rushikonda, Visakhapatnam, Andhra Pradesh, India
Corresponding Author
Nageswara Rao Reddy Neelapu, Assistant Professor, Department of Biochemistry and Bioinformatics, School of Life Sciences, GITAM Insitute of Science, GITAM University, Rushikonda, Visakhapatnam, Andhra Pradesh, India, Tel: +91-891-2840464, Mob: +91-98495 13540; +91-93937 66612, E-mail: nrneelapu@gmail.com/ nrneelapu@gitam.edu
Citation
Neelapu, N.R.R. Bacterial adherence Inhibitors for Published Date: September 21, 2016 Helicobacter pylori (2016) J Med Chem Tox 1(1): 22- 23.
Copy rights
© 2016 Nageswara Rao Reddy, N. This is an Open access article distributed under the terms of Creative Commons Attribution 4.0 International License.
Introduction
Human pathogen Helicobacter pylori adhere to the lining of the stomach and causes gastritis (inflammation of the stomach), duodenal or peptic ulcer, and gastric cancer (stomach cancer). Adherence of the bacteria to the mucous membrane of the gastroduodenum is the necessary initial step in the infection of the gastroduodenal tissue by the bacteria. Literature review showed that H. pylori uses adhesion molecules like AlpA, AlpB, BabA, HopZ, OipA and SabA to adhere to the epithelial lining of the stomach[1-4]. Reports showed that a class of sulfated glycolipids act as receptors for adherence of H. pylori[5-11].
Slomiany et al.[5] identified and reported sulfated glyceroglucolipids and its related compounds in the lipid extract of the human gastric content. The human gastric content was from the alimentary tract. Sulfated glyceroglucolipids and its related compounds are probably involved in the attachment of the organisms to the gut mucosa[6]. Slomiany et al[11] reported that H. pylori adhere to triglucosyl monoalkyl-monoacyl glycerol sulfate. Lingwood et al[10] also reported that gastric glyceroglucolipid acts as a receptor for bacterial adherence in H. pylori. Thus, these studies demonstrate that sulfated glycolipids of the gastric mucosa have a role in adherence of H. pylori.
Medicinal chemistry can be applied to synthesize the analogues for sulfated glycolipids without changing the pharmacological properties of the compound[12]. Several groups have attempted to synthesize the analogues of sulfated glycerogluco-lipids[13-15]. Gigg[13] synthesized seminolipid [3-O-(β-D-galactopyranosyl-3-sulfate)-2-O-hexadecanpyl-1-O-hexadecyl-L-glcerol] an analogue for sulfated glycerogalactolipid. Ogawa and Horisaki[14] synthesized 2-O-hexadecanpyl-1-O-hexadecyl-[α- Glc-6SO3Na-(1-6)-α-Glc(1-6)-α-Glc-(1-3)]-sn-glycerol an homologue for trisaccharide sulfated glyceroglucolipid.
Randall and Leunk[15] synthesized sulfated gylceroglucolipids with various R, R′ groups, where R or R′ is of hydrogen or C1-C24 acyl or alkyl and M+ is a cationic moiety. The pools of synthesized compounds were tested for adherence of H. pylori by two methods. First method tested the ability of H. pylori to adhere to the HeLa cells in the presence or absence of sulfated glyceroglycolipids. Second method tested the ability of H. pylori to establish infection in the neonatal gnotobiotic piglets. The sulfated glyceroglucolipids in combination with antimicrobials/anti ulcer medications were tested. Pharmaceutical component inhibited the adherence of H. pylori to the mucosal surface of the upper gastrointestinal tract. These sulfated glyceroglucolipids can be modified to improve the binding affinities so that these compounds act as a good inhibitor for adherence of H. pylori. Further, sulfated glyceroglucolipids can be encapsulated in nanocarrier using nanotechnology that acts as a gastrorententive delivery system for site specific delivery, slow release of drug with more half life and also bringing the stability to the compound[16].
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