Azrieli Faculty of Medicine, Bar-Ilan University, Safed, 1311502, Israel.
Clinical Microbiology Laboratory, Tzafon Medical Center, Poriya, Tiberias, 1528001, Israel(1).
Microb Pathog. 2024 Nov;196:106977. doi: 10.1016/j.micpath.2024.106977. Epub 2024 Sep 23.
Helicobacter pylori (H. pylori) causes several gastrointestinal diseases. Its virulence factors contributing to disease development include biofilm formation, cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) proteins that induce host tissue damage. In addition, urease activity enables H. pylori growth in the gastric acidic environment. This work aimed to characterize bacterial factors associated with biofilm production among 89 clinical H. pylori isolates, collected from patient gastric biopsies.
Biofilm production was detected using the crystal violet method. PCR was performed to determine vacA genotype (s1m1, s1m2, s2m1 and s2m2) and cagA gene presence. Urease activity was measured via the phenol red method. Susceptibility to six antibiotics was assessed by the Etest method.
Most H. pylori isolates produced biofilm. No association was found between biofilm-formation capacity and cagA presence or vacA genotype. Urease activity levels varied across isolates; no association was found between biofilm-formation and urease activity. Clarithromycin resistance was measured in 49 % of the isolates. Isolates susceptible to tetracycline were more commonly strong biofilm producers. In contrast, a significantly higher rate of strong biofilm producers was observed among resistant isolates to amoxicillin, levofloxacin and rifampicin, compared to susceptible isolates. Non-biofilm producers were more common among isolates sensitive to rifampicin and metronidazole, compared to resistant isolates.
Further studies are needed to understand the factors that regulate biofilm production in order to search for treatments for H. pylori biofilm destruction.
幽门螺杆菌（H. pylori）可引起多种胃肠道疾病。其导致疾病发展的毒力因子包括生物膜形成、细胞毒素相关基因 A（CagA）和空泡细胞毒素 A（VacA）蛋白，这些蛋白可诱导宿主组织损伤。此外，尿素酶活性使 H. pylori能够在胃酸性环境中生长。本研究旨在分析 89 株临床 H. pylori 分离株中与生物膜形成相关的细菌因子，这些分离株均来自患者的胃活检组织。
采用结晶紫法检测生物膜的形成。通过 PCR 检测 vacA 基因型（s1m1、s1m2、s2m1 和 s2m2）和 cagA 基因的存在。采用苯酚红法检测尿素酶活性。采用 Etest 法评估对 6 种抗生素的敏感性。
大多数 H. pylori 分离株可形成生物膜。生物膜形成能力与 cagA 存在或 vacA 基因型之间没有相关性。各分离株的尿素酶活性水平存在差异；生物膜形成与尿素酶活性之间没有相关性。49%的分离株对克拉霉素耐药。对四环素敏感的分离株通常是强生物膜生产者。相比之下，与敏感株相比，对阿莫西林、左氧氟沙星和利福平耐药的分离株中强生物膜生产者的比例显著更高。与耐药株相比，对利福平和甲硝唑敏感的分离株中不产生物膜的分离株更为常见。
需要进一步研究以了解调节生物膜形成的因素，以便寻找治疗 H. pylori 生物膜破坏的方法。
