Helicobacter pylori and gut microbiota in multiple sclerosis versus Alzheimer's disease: 10 pitfalls of microbiome studies

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Abstract

Alteration of microbiota has been associated with intestinal, inflammatory and neurological diseases. An abundance of “good bacteria,” such as Bifidobacterium, or their products has been generally believed to be beneficial for any diseases, whereas “bad bacteria,” such as pathogenic Helicobacter pylori, are assumed to be always detrimental for hosts. However, this is not the case when we compare and contrast the association of the gut microbiota with two neurological diseases, multiple sclerosis and Alzheimer's disease. After H. pylori infection, pro-inflammatory T helper (Th)1 and Th17 immune responses are initially induced to eradicate bacteria. However, H. pylori evades the host immune response by inducing Th2 cells and regulatory T cells that produce anti-inflammatory interleukin-10. Suppression of anti-bacterial Th1/Th17 cells by regulatory T cells might enhance gastric H. pylori propagation, followed by a cascade reaction involving vitamin B12 and folic acid malabsorption, plasma homocysteine elevation, and reactive oxygen species induction. This can damage the blood-brain barrier, leading to accumulation of amyloid-β in the brain, a hallmark of Alzheimer's disease. In contrast, this suppression of pro-inflammatory Th1/Th17 responses to H. pylori has protective effects on the hosts, as it prevents uncontrolled gastritis as well as suppresses the induction of encephalitogenic Th1/Th17 cells, which can mediate neuroinflammation in multiple sclerosis. The above scenario might explain why chronic H. pylori infection is positively associated with Alzheimer's disease, whereas it is negatively associated with multiple sclerosis. Finally, we list “10 pitfalls of microbiota studies,” which will be useful for evaluating and designing clinical and experimental microbiota studies.

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