Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Weil's Disease - from Gut Dysbiosis to Immunopathogenesis and Multiple Organ Failure

Version 1 : Received: 17 November 2022 / Approved: 21 November 2022 / Online: 21 November 2022 (03:26:33 CET)

A peer-reviewed article of this Preprint also exists.

Petakh, P.; Isevych, V.; Kamyshnyi, A.; Oksenych, V. Weil’s Disease—Immunopathogenesis, Multiple Organ Failure, and Potential Role of Gut Microbiota. Biomolecules 2022, 12, 1830. Petakh, P.; Isevych, V.; Kamyshnyi, A.; Oksenych, V. Weil’s Disease—Immunopathogenesis, Multiple Organ Failure, and Potential Role of Gut Microbiota. Biomolecules 2022, 12, 1830.

Abstract

Leptospirosis is an important zoonotic disease, causing about 60,000 deaths annually. One of the reasons for the severe course of leptospirosis is a cytokine storm, which develops as a result of an excessive immune response. The gut microbiota that resides in the gastrointestinal tract provides essential health benefits to its host, particularly by regulating immune homeostasis and a bidirectional relationship with many internal organs. A change in the gut microbiota can be caused not only by antibiotics, but also by infectious agents such as the coronavirus or the flu virus. It is known that L. interrogans can change the microbiota of mice. Thus, gut dysbiosis in leptospirosis can affect the clinical course of the disease, through the gut–organ axis. Modulation of intestinal microbiota by probiotics and/or fecal microbiota transplantation in leptospirosis may become an important area of scientific research.

Keywords

leptospirosis; dysbiosis; Weil's disease

Subject

Medicine and Pharmacology, Gastroenterology and Hepatology

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