Ping-I Hsu1, Chao-Yu Pan2, John Y Kao3, Feng-Woei Tsay1, Nan-Jing Peng4, Sung-Shuo Kao1, Yan-Hua Chen1, Tzung-Jiun Tsai1, Deng-Chyang Wu5, Kuo-Wang Tsai6,7. 1. Division of Gastroenterology and Hepatology, Department of Internal Medicine, Kaohsiung Veterans General Hospital and National Yang-Ming University, Kaohsiung, Taiwan. 2. Institute of Biomedical Informatics, Academia Sinica, National Yang-Ming University and Institute of Biomedical Sciences, Taipei, Taiwan. 3. Department of Internal Medicine, Division of Gastroenterology, Michigan Medicine, University of Michigan, Ann Arbor, Michigan, USA. 4. Department of Nuclear Medicine, Kaohsiung Veterans General Hospital and National Yang-Ming University, Kaohsiung, Taiwan. 5. Division of Gastroenterology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. 6. Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan. 7. Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan.
Abstract
BACKGROUND AND AIMS: Anti-Helicobacter pylori therapy may lead to the growth of pathogenic or antibiotic-resistant bacteria in the gut. The study aimed to investigate the short-term and long-term impacts of H. pylori eradication with reverse hybrid therapy on the components and macrolide resistance of the gut microbiota. METHODS: Helicobacter pylori-related gastritis patients were administered a 14-day reverse hybrid therapy. Fecal samples were collected before treatment and at the end of week 2, week 8, and week 48. The V3-V4 region of the bacterial 16S rRNA gene in fecal specimens was amplified by polymerase chain reaction and sequenced on Illumina MiSeq platform. Additionally, amplification of erm(B) gene (encoding erythromycin resistance methylase) was performed. RESULTS: Reverse hybrid therapy resulted in decreased relative abundances of Firmicutes (from 62.0% to 30.7%; P < 0.001) and Actinobacteria (from 3.4% to 0.6%; 0.032) at the end of therapy. In contrast, the relative abundance of Proteobacteria increased from 10.2% to 49.1% (0.002). These microbiota alterations did not persist but returned to the initial levels at week 8 and week 48. The amount of erm(B) gene in fecal specimens was comparable with the pretreatment level at week 2 but increased at week 8 (0.025) and then returned to the pretreatment level by week 48. CONCLUSIONS: Helicobacter pylori eradication with reverse hybrid therapy can lead to short-term gut dysbiosis. The amount of erm(B) gene in the stool increased transiently after treatment and returned to the pretreatment level at 1-year post-treatment.
BACKGROUND AND AIMS: Anti-Helicobacter pylori therapy may lead to the growth of pathogenic or antibiotic-resistant bacteria in the gut. The study aimed to investigate the short-term and long-term impacts of H. pylori eradication with reverse hybrid therapy on the components and macrolide resistance of the gut microbiota. METHODS:Helicobacter pylori-related gastritispatients were administered a 14-day reverse hybrid therapy. Fecal samples were collected before treatment and at the end of week 2, week 8, and week 48. The V3-V4 region of the bacterial 16S rRNA gene in fecal specimens was amplified by polymerase chain reaction and sequenced on Illumina MiSeq platform. Additionally, amplification of erm(B) gene (encoding erythromycin resistance methylase) was performed. RESULTS: Reverse hybrid therapy resulted in decreased relative abundances of Firmicutes (from 62.0% to 30.7%; P < 0.001) and Actinobacteria (from 3.4% to 0.6%; 0.032) at the end of therapy. In contrast, the relative abundance of Proteobacteria increased from 10.2% to 49.1% (0.002). These microbiota alterations did not persist but returned to the initial levels at week 8 and week 48. The amount of erm(B) gene in fecal specimens was comparable with the pretreatment level at week 2 but increased at week 8 (0.025) and then returned to the pretreatment level by week 48. CONCLUSIONS:Helicobacter pylori eradication with reverse hybrid therapy can lead to short-term gut dysbiosis. The amount of erm(B) gene in the stool increased transiently after treatment and returned to the pretreatment level at 1-year post-treatment.
Authors: Evgenii I Olekhnovich; Alexander I Manolov; Andrey E Samoilov; Nikita A Prianichnikov; Maja V Malakhova; Alexander V Tyakht; Alexander V Pavlenko; Vlad V Babenko; Andrey K Larin; Boris A Kovarsky; Elizaveta V Starikova; Oksana E Glushchenko; Dilyara D Safina; Maria I Markelova; Eugenia A Boulygina; Dilyara R Khusnutdinova; Sergey Y Malanin; Sayar R Abdulkhakov; Rustam A Abdulkhakov; Tatiana V Grigoryeva; Elena S Kostryukova; Vadim M Govorun; Elena N Ilina Journal: Front Microbiol Date: 2019-08-27 Impact factor: 5.640