Roles of Cholesteryl-α-Glucoside Transferase and Cholesteryl Glucosides in Maintenance of Helicobacter pylori Morphology, Cell Wall Integrity, and Resistance to Antibiotics

Qaria, Majjid A.; Kumar, Naveen; Hussain, Arif; Qumar, Shamsul; Doddam, Sankara Narayana; P, Sepe, Ludovico; Ahmed, Niyaz

doi:10.1128/mbio.01523-18

Cited by 28 publications

(29 citation statements)

References 35 publications

(43 reference statements)

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“…However, MC H pylori showed occurrence of higher amount of cholesterol (54 181 ppm) compared with NM (19 155 ppm). It has been demonstrated that accumulation of cholesterol in H pylori cell membrane increases bacterial resistance to antibiotics and reduction in cholesterol leads to susceptibility to antibiotics . Accumulation of cholesterol in H pylori cell membrane might affect bacterial cell surface properties by increasing hydrophobicity, decreasing negative charge, decreasing fluidity, and altering LPS and proteins.…”

Section: Discussionmentioning

confidence: 99%

“…24 However, MC H pylori showed occurrence of higher amount of cholesterol (54 181 ppm) compared with NM (19 155 ppm). It has been demonstrated that accumulation of cholesterol in H pylori cell membrane increases bacterial resistance to antibiotics 25 and reduction in cholesterol leads to susceptibility to antibiotics. 43 Furthermore, MC exhibited resistance to all the used antibiotics.…”

Section: Discussionmentioning

confidence: 99%

“…CGs occur in three types: cholesteryl‐α‐D‐glucopyranoside (CGL), cholesteryl‐6‐ 0 ‐tetradecanoyl‐α‐D‐glucopyranoside (CAG), and cholesteryl‐6‐ 0 ‐phosphatidyl‐α‐D‐glucopyranoside (CPG) . CGs appear to play important roles in the maintenance of H pylori spiral shape, membrane permeability, resistance to antimicrobial uptake and pathogenicity, and cell division …”

Section: Introductionmentioning

confidence: 99%

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Mucoid and coccoid Helicobacter pylori with fast growth and antibiotic resistance

2019

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Background In this study, one Helicobacter pylori isolate, from gastric biopsy of a dyspeptic patient that turned into mucoid‐coccoid (MC) form upon consecutive subcultures, was identified. The culturability, antibiotic resistance, and lipid contents of MC were compared with those of non‐mucoid (NM) spiral H pylori. Materials and Methods Mucoid‐coccoid and NM H pylori were subcultured on Brucella blood agar (BBA) and incubated under aerobic and microaerobic atmospheres at 37°C. Cultures were examined for colony characteristics and bacterial morphology after 1‐3 days. The isolates were identified by biochemical tests and detection of H pylori‐16S rDNA. Antibiogram was performed with currently used antibiotics for H pylori eradication. Cellular lipid contents were extracted and analyzed by gas chromatography. Results Compared with pin‐pointed and glistening colonies of NM H pylori that appeared under microaerobic conditions, MC H pylori grew well in consecutive subcultures under aerobic and microaerobic atmospheres and produced white patches of mucoid colonies. MC exhibited coccoid and NM spiral morphology. Both isolates were catalase, oxidase, and urease positive and contained 16S rDNA. Compared with NM that was susceptible to almost all the antibiotics, MC was resistant to all the antibiotics. Lipid analyses showed high frequency of unsaturated fatty acids and cholesterol in MC. Conclusions Coccoid forms with high fatty acid and cholesterol contents that show resistance to antibiotics might resist against other stressful conditions such as gastric acidity and immune response. Moreover, mucoid property may enhance resistance of coccoids to stresses. With mucoid‐coccoid lifestyle, H pylori may establish a chronic infection refractory to antimicrobial therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mucoid and coccoid Helicobacter pylori with fast growth and antibiotic resistance

2019

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“…H. pylori harboring CGT, inhibits interferon gamma-induced signaling, which avoids host inflammatory responses [46]. Noticeably, CGs also contribute to cell wall integrity, morphology, and antibiotic resistance [47]. Collectively, these findings highlight the multiple strategies employed by H. pylori for persistent colonization.…”

Section: Cholesterol-α-glucosyltransferase (Cgt)mentioning

confidence: 92%

Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate

Sit

Chen

et al. 2020

Seminars in Cell & Developmental Biology

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A B S T R A C THelicobacter pylori colonizes human stomach mucosa and its infection causes gastrointestinal diseases with variable severity. Bacterial infection stimulates autophagy, which is a part of innate immunity used to eliminate intracellular pathogens. Several intracellular bacteria have evolved multipronged strategies to circumvent this conserved system and thereby enhance their chance of intracellular survival. Nonetheless, studies on H. pylori have produced inconsistent results, showing either elevated or reduced clearance efficiency of intracellular bacteria through autophagy. In this review, we summarize recent studies on the mechanisms involved in autophagy induced by H. pylori and the fate of intracellular bacteria.

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“…Cholesterol and cholesteryl glucosides have no influence on the stability of the cell membrane conformation of H. pylori, and rather these steroidal compounds serve to strengthen the membrane lipid barrier of the bacteria on the limitation of the permeability of lipophilic compounds. A recent study by other group has demonstrated that cholesteryl glucosides are responsible for the morphological maintenance of H. pylori, for the acquirement of resistance to antibiotics such as polymyxin B, colistin, and tetracycline, and for the promotion of biofilm formation [47]. This suggests that cholesteryl glucosides of H. pylori play an important role to limit the membrane permeability of various low-molecular-weight compounds.…”

Section: Bactericidal Mechanism Of the Indene Compound Speciesmentioning

confidence: 99%

Development of a Novel Antibacterial Medicine that Targets a Characteristic Lipid of the Cell Membranes ofHelicobacter pylori

Wanibuchi¹,

Masui²,

Takahashi³

et al. 2019

Gastritis - New Approaches and Treatments

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Helicobacter pylori is one of the most prevalent causes of gastritis. This pathogen colonizes for many years human stomach and asymptomatically leads the persons to chronic gastritis. The eradication of H. pylori from human stomach is, therefore, important in order to prevent the digestive diseases including peptic ulcers and gastric cancer that develop via chronic atrophic gastritis. Wide-spectrum antibiotics such as amoxicillin and metronidazole are used for the treatment for H. pylori infectious diseases. However, the H. pylori strains resistant to these antibiotics are increasing year by year around the world. On this basis, we need urgently to develop the antibacterial medicines that act on H. pylori with a novel mechanism. Recent studies by our group have demonstrated that H. pylori shows susceptibility to the bactericidal action of indene compounds derived from decomposition of vitamin D. The bactericidal action of indene compounds is selective not against commonplace bacteria but against H. pylori. The indene compounds turned out to target the H. pylori's phosphatidylethanolamine that retains a myristic acid as the saturated fatty acid side chain. These findings will contribute to the development of new antibacterial medicines specialized to the treatment for H. pylori infectious diseases.

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Roles of Cholesteryl-α-Glucoside Transferase and Cholesteryl Glucosides in Maintenance of Helicobacter pylori Morphology, Cell Wall Integrity, and Resistance to Antibiotics

Cited by 28 publications

References 35 publications

Mucoid and coccoid Helicobacter pylori with fast growth and antibiotic resistance

Mucoid and coccoid Helicobacter pylori with fast growth and antibiotic resistance

Cellular evasion strategies of Helicobacter pylori in regulating its intracellular fate

Development of a Novel Antibacterial Medicine that Targets a Characteristic Lipid of the Cell Membranes ofHelicobacter pylori

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