Cholesterol‐α‐glucosyltransferase gene is present in most Helicobacter species including gastric non‐Helicobacter pylori helicobacters obtained from Japanese patients

Abstract

Background Non‐Helicobacter pylori helicobacters (NHPHs) besides H. pylori infect human stomachs and cause chronic gastritis and mucosa‐associated lymphoid tissue lymphoma. Cholesteryl‐α‐glucosides have been identified as unique glycolipids present in H. pylori and some Helicobacter species. Cholesterol‐α‐glucosyltransferase (αCgT), a key enzyme for the biosynthesis of cholesteryl‐α‐glucosides, plays crucial roles in the pathogenicity of H. pylori. Therefore, it is important to examine αCgTs of NHPHs. Materials and Methods Six gastric NHPHs were isolated from Japanese patients and maintained in mouse stomachs. The αCgT genes were amplified by PCR and inverse PCR. We retrieved the αCgT genes of other Helicobacter species by BLAST searches in GenBank. Results αCgT genes were present in most Helicobacter species and in all Japanese isolates examined. However, we could find no candidate gene for αCgT in the whole genome of Helicobacter cinaedi and several enterohepatic species. Phylogenic analysis demonstrated that the αCgT genes of all Japanese isolates show high similarities to that of a zoonotic group of gastric NHPHs including Helicobacter suis, Helicobacter heilmannii, and Helicobacter ailurogastricus. Of 6 Japanese isolates, the αCgT genes of 4 isolates were identical to that of H. suis, and that of another 2 isolates were similar to that of H. heilmannii and H. ailurogastricus. Conclusions All gastric NHPHs examined showed presence of αCgT genes, indicating that αCgT may be beneficial for these helicobacters to infect human and possibly animal stomachs. Our study indicated that NHPHs could be classified into 2 groups, NHPHs with αCgT genes and NHPHs without αCgT genes.

Helicobacter pylori Virulence Factors—Mechanisms of Bacterial Pathogenicity in the Gastric Microenvironment

“…Thus, it was proposed that greater levels of αCgT might induce stronger immune responses that eventually lead to more severe H. pyloriinduced inflammation, especially during the early stages of infection. Furthermore, αCgT also seems to be crucial for proper bacterial growth [306]. As an example, showed that H. pylori strains deficient in αCgT result in inhibited growth or even enhanced bacterial lethality [307].…”

Acute gastric mucosal lesions caused by acute infection of non‐HelicobacterpyloriHelicobacter: a case report

“…In order to search the existence of NHPH, a polymerase chain reaction (PCR) analysis using a formalin‐fixed paraffin‐embedded tissue sample was also performed. However, neither urease gene 1 nor cholesterol‐α‐glucosyltransferase (αCgT) gene 2 were successfully detected.…”

Antimicrobial Susceptibility Pattern of Helicobacter heilmannii and Helicobacter ailurogastricus Isolates

“…For assay (1), E. coli and S. aureus were cultured in the biphasic conditions at pH 5, as described for H. heilmannii and H. ailurogastricus. For assay (2), unsupplemented Mueller-Hinton broth at pH 7 was used according to the CLSI guidelines. Additionally, positive (i.e., wells containing agar, broth, and bacteria but free of the tested antimicrobials) and negative (i.e., wells containing agar and broth free of the tested antimicrobials and reference bacteria) controls were included.…”

“…Helicobacter species colonize the gastrointestinal tract of both humans and animals which may result in the development of gastrointestinal disorders such as inflammation, ulceration, and cancer. Helicobacter pylori is the best-studied and most prevalent Helicobacter species colonizing the stomach of human patients with gastric disorders [ 1 , 2 , 3 , 4 , 5 , 6 ]. Other gastric, spiral-shaped non- H. pylori helicobacters (NHPHs) have also been associated with the development of gastric disorders in humans [ 1 , 7 , 8 , 9 ].…”