Growth Characteristics and Influence of Antibiotics on Rough/Smooth Phenotypic Variants of Helicobacter pylori

Bertram-Drogatz, P. A.; Sobek-Klocke, Ingeborg; Wingbermühle, D; Beil, Winfried; Sewing, Karl–Friedrich; Manns, Michael P.; Wagner, Siegfried

doi:10.1007/s100960050329

Cited by 3 publications

(1 citation statement)

References 15 publications

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“…This was caused by two independent mutations in wapH (PP4943 ), a gene involved in lipopolysaccharide (LPS) biosynthesis (Hansen et al, 2007). Rough/smooth phenotype variants due to altered LPS composition were also observed for Hp , yet its association with biofilm formation and virulence is unclear (Bertram-Drogatz et al, 1999).…”

Section: Functional and Morphological Changes Associated With Biofilmmentioning

confidence: 99%

Potential Role of Biofilm Formation in the Development of Digestive Tract Cancer With Special Reference to Helicobacter pylori Infection

et al. 2019

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Bacteria are highly social organisms that communicate via signaling molecules and can assume a multicellular lifestyle to build biofilm communities. Until recently, complications from biofilm-associated infection have been primarily ascribed to increased bacterial resistance to antibiotics and host immune evasion, leading to persistent infection. In this theory and hypothesis article we present a relatively new argument that biofilm formation has potential etiological role in the development of digestive tract cancer. First, we summarize recent new findings suggesting the potential link between bacterial biofilm and various types of cancer to build the foundation of our hypothesis. To date, evidence has been particularly convincing for colorectal cancer and its precursor, i.e., polyps, pointing to several key individual bacterial species, such as Bacteroides fragilis, Fusobacterium nucleatum , and Streptococcus gallolyticus subsp. Gallolyticus. Then, we further extend this hypothesis to one of the most common bacterial infection in humans , Helicobacter pylori ( Hp ), which is considered a major cause of gastric cancer. Thus far, there has been no direct evidence linking in vivo Hp gastric biofilm formation to gastric carcinogenesis. Yet, we synthesize the information to support an argument that biofilm associated- Hp is potentially more carcinogenic, summarizing biological characteristics of biofilm-associated bacteria. We also discuss mechanistic pathways as to how Hp or other biofilm-associated bacteria control biofilm formation and highlight recent findings on Hp genes that influence biofilm formation, which may lead to strain variability in biofilm formation. This knowledge may open a possibility of developing targeted intervention. We conclude, however, that this field is still in its infancy. To test the hypothesis rigorously and to link it ultimately to gastric pathologies (e.g., premalignant lesions and cancer), studies are needed to learn more about Hp biofilms, such as compositions and biological properties of extracellular polymeric substance (EPS), presence of non- Hp microbiome and geographical distribution of biofilms in relation to gastric gland types and structures. Identification of specific Hp strains with enhanced biofilm formation would be helpful not only for screening patients at high risk for sequelae from Hp infection, but also for development of new antibiotics to avoid resistance, regardless of its association with gastric cancer.

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Section: Functional and Morphological Changes Associated With Biofilmmentioning

confidence: 99%

Potential Role of Biofilm Formation in the Development of Digestive Tract Cancer With Special Reference to Helicobacter pylori Infection

et al. 2019

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Antimicrobial resistance in Helicobacter pylori

Argila

Rafael

Baquero

2001

Reviews in Medical Microbiology

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Phase Variation in the Helicobacter pylori Phospholipase A Gene and Its Role in Acid Adaptation

et al. 2001

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Previously, we have shown that Helicobacter pylori can spontaneously and reversibly change its membrane lipid composition, producing variants with low or high content of lysophospholipids. The "lyso" variant contains a high percentage of lysophospholipids, adheres better to epithelial cells, and releases more proteins such as urease and VacA, compared to the "normal" variant, which has a low content of lysophospholipids. Prolonged growth of the normal variant at pH 3.5, but not under neutral conditions, leads to enrichment of lyso variant colonies, suggesting that the colony switch is relevant to acid adaptation. In this study we show that the change in membrane lipid composition is due to phase variation in the pldA gene. A change in the (C) tract length of this gene results in reversible frameshifts, translation of a full-length or truncated pldA, and the production of active or inactive outer membrane phospholipase A (OMPLA). The role of OMPLA in determining the colony morphology was confirmed by the construction of an OMPLA-negative mutant. Furthermore, variants with an active OMPLA were able to survive acidic conditions better than variants with the inactive form. This explains why the lyso variant is selected at low pH. Our studies demonstrate that phase variation in the pldA gene, resulting in an active form of OMPLA, is important for survival under acidic conditions. We also demonstrated the active OMPLA genotype in fresh isolates of H. pylori from patients referred to gastroscopy for dyspepsia.

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Growth Characteristics and Influence of Antibiotics on Rough/Smooth Phenotypic Variants of Helicobacter pylori

Cited by 3 publications

References 15 publications

Potential Role of Biofilm Formation in the Development of Digestive Tract Cancer With Special Reference to Helicobacter pylori Infection

Potential Role of Biofilm Formation in the Development of Digestive Tract Cancer With Special Reference to Helicobacter pylori Infection

Antimicrobial resistance in Helicobacter pylori

Phase Variation in the Helicobacter pylori Phospholipase A Gene and Its Role in Acid Adaptation

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