Gastroenterology

Gut Microbiota #11

Tuberculosis

By Prof. Markku Voutilainen
Turku University Faculty of Medicine; Turku University Hospital, Department of Gastroenterology, Turku, Finland

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Coloured scanning electron micrograph (SEM) of Mycobacterium tuberculosis.

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Created 24 August 2021
Updated 12 August 2024

TUBERCULOSIS AND GUT MICROBIOTA

Eribo OA, du Plessis N, Ozturk M, et al. The gut microbiome in tuberculosis susceptibility and treatment response: guilty or not guilty? Cell Mol Life Sci 2020 ; 77 : 1497-509.

5-10% of persons infected worldwide with Mycobacterium tuberculosis (MT) will progress to active TB. Recent research highlighted that gut dysbiosis induced by treatment could be involved in the disease development by compromising immune protection against MT. This review summarizes how the gut microbiota, lung immunity could be linked during the disease; and how the gut microbiota dysbiosis induced by the protracted anti-TB antibiotics treatment is involved to an increased susceptibility to MT re-infection or TB recrudescence after successful treatment cure. The authors also indicate that the gut microbiota biosignature might help recognizing healthy from active TB patients.

KETOGENIC DIET, GUT MICROBIOTA AND IMMUNE RESPONSES

Ang QY, Alexander M, Newman JC, et al. Ketogenic diets alter the gut microbiome resulting in decreased intestinal Th17 cells. Cell 2020 ; 181 : 1263-75.

Very low-carbohydrate, high-fat ketogenic diet (KD) is used in refractory pediatric epilepsy, and some evidence supports KD use in diabetes and obesity but their metabolic and immune consequences remain unclear. The authors examined the impact of KD on human and mice gut microbiota via metagenomics and metabolomics and compared with high-fat diets impact: several bifidobacterial species were reduced, and an increase of Firmicutes/Bacteroidetes ratio induced by high-fat diet reversed. Increased plasma β-hydroxybutyrate levels inhibit bifidobacterial growth. KD reduced proinflammatory Th17 cell accumulation in mice adipose tissue and inhibited induction of intestinal Th17 cells.

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