Abstract
Blastocystis is the most common eukaryotic microbe in the human gut. It is linked to irritable bowel syndrome (IBS), but its role in disease has been contested considering its widespread nature. This organism is well-adapted to its anoxic niche and lacks typical eukaryotic features, such as a cytochrome-driven mitochondrial electron transport. Although generally considered a strict or obligate anaerobe, its genome encodes an alternative oxidase. Alternative oxidases are energetically wasteful enzymes as they are non-protonmotive and energy is liberated in heat, but they are considered to be involved in oxidative stress protective mechanisms. Our results demonstrate that the Blastocystis cells themselves respire oxygen via this alternative oxidase thereby casting doubt on its strict anaerobic nature. Inhibition experiments using alternative oxidase and Complex II specific inhibitors clearly demonstrate their role in cellular respiration. We postulate that the alternative oxidase in Blastocystis is used to buffer transient oxygen fluctuations in the gut and that it likely is a common colonizer of the human gut and not causally involved in IBS. Additionally the alternative oxidase could act as a protective mechanism in a dysbiotic gut and thereby explain the absence of Blastocystis in established IBS environments.
Highlights
A healthy human gut is characterized by the presence of obligate anaerobic bacteria from the Firmicutes and Bacteroides phyla who are considered to play a protective role in maintaining the gut ecosystem (Donaldson et al, 2016)
Cells were grown under anoxic conditions and all culturing work performed in an anaerobic chamber (Ruskinn SCI-tive with HEPA Hypoxia station)
LYSGM is a modification of TYSGM-9 in which the trypticase and yeast extract of the latter are replaced with 0.25% yeast extract (Sigma) and 0.05% neutralized liver digest (Oxoid)
Summary
A healthy human gut is characterized by the presence of obligate anaerobic bacteria from the Firmicutes and Bacteroides phyla who are considered to play a protective role in maintaining the gut ecosystem (Donaldson et al, 2016) The establishment of this protective microbial ecosystem in the gut has its origin within the first few days/weeks after birth and even the mode of birth (cesarean or natural) can result in effects in later life (Sommer et al, 2017). A mechanistic coupling between gut microbes and the presence of molecular oxygen was described by Byndloss et al Activation of a colonocyte peroxisome proliferator-activated receptor-γ (PPARγ) results in reduction of the nitrate and oxygen concentrations in the gut thereby controlling the proliferation of facultative anaerobes (Byndloss et al, 2017) This clearly demonstrates a link between oxygen in the human intestine and dysbiosis as previously hypothesized by Rigottier-Gois (2013)
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