Статья

Inflammatory Bowel Disease–Associated Changes in the Gut: Focus on Kazan Patients

G. Sasso, L. Khachatryan, A. Kondylis, J. Battey, N. Sierro, N. Danilova, T. Grigoryeva, M. Markelova, D. Khusnutdinova, A. Laikov, I. Salafutdinov, Y. Romanova, M. Siniagina, I. Vasiliev, E. Boulygina, V. Solovyeva, E. Garanina, K. Kitaeva, K. Ivanov, D. Chulpanova, K. Kletenkov, A. Valeeva, A. Odintsova, M. Ardatskaya, R. Abdulkhakov, N. Ivanov, M. Peitsch, J. Hoeng, S. Abdulkhakov,
2020

BACKGROUND: Several studies have highlighted the role of host-microbiome interactions in the pathogenesis of inflammatory bowel disease (IBD), resulting in an increasing amount of data mainly focusing on Western patients. Because of the increasing prevalence of IBD in newly industrialized countries such as those in Asia, the Middle East, and South America, there is mounting interest in elucidating the gut microbiota of these populations. We present a comprehensive analysis of several IBD-related biomarkers and gut microbiota profiles and functions of a unique population of patients with IBD and healthy patients from Kazan (Republic of Tatarstan, Russia). METHODS: Blood and fecal IBD biomarkers, serum cytokines, and fecal short-chain fatty acid (SCFA) content were profiled. Finally, fecal microbiota composition was analyzed by 16S and whole-genome shotgun sequencing. RESULTS: Fecal microbiota whole-genome sequencing confirmed the presence of classic IBD dysbiotic features at the phylum level, with increased abundance of Proteobacteria, Actinobacteria, and Fusobacteria and decreased abundance of Firmicutes, Bacteroidetes, and Verrucomicrobia. At the genus level, the abundance of both fermentative (SCFA-producing and hydrogen (H2)-releasing) and hydrogenotrophic (H2-consuming) microbes was affected in patients with IBD. This imbalance was confirmed by the decreased abundance of SCFA species in the feces of patients with IBD and the change in anaerobic index, which mirrors the redox status of the intestine. CONCLUSIONS: Our analyses highlighted how IBD-related dysbiotic microbiota-which are generally mainly linked to SCFA imbalance-may affect other important metabolic pathways, such as H2 metabolism, that are critical for host physiology and disease development.

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  • 1. Version of Record от 2020-08-07

Метаданные

Об авторах
  • G. Sasso
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • L. Khachatryan
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • A. Kondylis
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • J. Battey
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • N. Sierro
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • N. Danilova
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • T. Grigoryeva
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • M. Markelova
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • D. Khusnutdinova
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • A. Laikov
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • I. Salafutdinov
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • Y. Romanova
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • M. Siniagina
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • I. Vasiliev
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • E. Boulygina
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • V. Solovyeva
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • E. Garanina
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • K. Kitaeva
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • K. Ivanov
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • D. Chulpanova
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • K. Kletenkov
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
  • A. Valeeva
    Department of Clinical Immunology and Allergology, Kazan State Medical University, Kazan, Tatarstan, Russian Federation
  • A. Odintsova
    Department of Gastroenterology, Republican Clinical Hospital of Tatarstan Republic, Kazan, Tatarstan, Russian Federation
  • M. Ardatskaya
    Central State Medical Academy of Administrative Department of the President of the Russian Federation, Moscow, Russian Federation
  • R. Abdulkhakov
    Department of Clinical Immunology and Allergology, Kazan State Medical University, Kazan, Tatarstan, Russian Federation
  • N. Ivanov
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • M. Peitsch
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • J. Hoeng
    Philip Morris International Research and Development, Philip Morris Products S.A., Neuchâtel, Switzerland
  • S. Abdulkhakov
    Kazan Federal University, Institute of Fundamental Medicine and Biology, Kazan, Tatarstan, Russian Federation
Название журнала
  • Inflammatory Bowel Diseases
Том
  • 27
Выпуск
  • 3
Страницы
  • izaa188-
Издатель
  • Oxford University Press (OUP)
Тип документа
  • journal article
Тип лицензии Creative Commons
  • CC BY
Правовой статус документа
  • Свободная лицензия
Источник
  • dimensions