Abstract
Mitochondria are essential organelles that are not only responsible for energy production but are also involved in cell metabolism, calcium homeostasis, and apoptosis. Targeting mitochondria is a key strategy for bacteria to subvert host cells’ physiology and promote infection. Helicobacter (H.) pylori targets mitochondria directly. However, mitochondrial genome (mtDNA) polymorphism (haplogroup) is not yet considered an important factor for H. pylori infection. Here, we clarified the association of mitochondrial haplogroups with H. pylori prevalence and the ability to perform damage. Seven mtDNA haplogroups were identified among 28 H. pylori-positive subjects. Haplogroup B was present at a higher frequency and haplotype D at a lower one in the H. pylori population than in that of the H. pylori-negative one. The fibroblasts carrying high-frequency haplogroup displayed a higher apoptotic rate and diminished mitochondrial respiration following H. pylori infection. mtDNA mutations were accumulated more in the H. pylori-positive population than in that of the H. pylori-negative one in old age. Among the mutations, 57% were located in RNA genes or nonsynonymous protein-coding regions in the H. pylori-positive population, while 35% were in the H. pylori-negative one. We concluded that gastric disease caused by Helicobacter virulence could be associated with haplogroups and mtDNA mutations.
Highlights
Helicobacter pylori is a gram-negative, microaerophilic bacterium that colonizes the gastric mucosa of at least half of all humans worldwide [1]
We demonstrated that the frequency of haplogroup B was higher in the H. pylori-positive population, suggesting that this haplogroup could be associated with a greater risk of H. pylori infection
This study demonstrated that the mtDNA haplogroup was associated with cellular damage upon H. pylori infection (Figure 7)
Summary
Helicobacter pylori is a gram-negative, microaerophilic bacterium that colonizes the gastric mucosa of at least half of all humans worldwide [1]. The integrity of the gastric mucosa is maintained by a balance between cell proliferation and death. H. pylori can induce their imbalance, resulting in gastric diseases, such as chronic gastritis, peptic ulceration, gastric carcinoma, and lymphoma [2,3]. The prevalence of H. pylori in the global population was steadily decreasing, it was recently estimated to be approximately 50% [4,5,6]. Mitochondria play essential roles in normal cellular function in eukaryotes, such as energy production, calcium homeostasis, apoptotic activation, and cell death [7,8]. Several studies showed that H. pylori induces the instability of mtDNA in stomach tissue [9,10]
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