Medicine
Bacteria Finds Way to Thrive in Oxygen-Rich Gut Environment
Scientists have discovered that a pathogenic bacterium uses a toxin to create an "oxidative niche" that supports its growth in the inflamed gut.
Illustration: Blue Dot News
2 min read
In the densely populated large intestine, where oxygen levels are scarce, enteric pathogens must navigate complex microbial landscapes to establish a foothold on their host. To colonize and cause disease, these pathogens deploy virulence factors to create distinct nutrient niches, allowing them to outcompete other microorganisms and thrive in this challenging environment. One such pathogen is Enterotoxigenic Bacteroides fragilis (ETBF), a classically anaerobic bacterium implicated in inflammation-associated diseases, including colitis and colorectal cancer.
To understand how ETBF constructs its nutrient niche, researchers Spiga L et al. investigated the role of its virulence factor, Bacteroides fragilis toxin (BFT). They found that BFT manipulates colonic epithelial signaling and the bile acid recycling pathway, inducing a metabolic shift in the epithelium from oxidative phosphorylation to glycolysis. This shift increases local concentrations of lactate and oxygen, nutrients that support oxidative metabolism in ETBF. By adapting the host's metabolic pathways to its own needs, ETBF creates an oxidative niche that supports its growth and colonization.
This unexpected strategy by which a classically anaerobic pathogen leverages host metabolic remodeling raises important questions about the evolution of virulence factors and the adaptations that allow pathogens to thrive in diverse environments. It also highlights the complex interplay between microbial communities and their hosts, where the manipulation of host metabolism can have far-reaching consequences for both the microbe and the host. By studying this phenomenon, researchers can gain insights into the mechanisms underlying disease progression and develop new strategies for preventing or treating inflammation-associated diseases.
As we reflect on the ways in which ETBF has rewired its host's metabolism to fuel oxidative growth, we are reminded of the profound interconnectedness of life in the universe. The intricate web of relationships between microorganisms, hosts, and environments is a testament to the awe-inspiring complexity of biological systems. By exploring the intricacies of this relationship, we can gain a deeper appreciation for the delicate balance that sustains us all – and for the ways in which even the most seemingly disparate organisms are linked in a vast, cosmic dance.
1 min read
In the darkest recesses of our own bodies, a tiny enemy lurks, manipulating our metabolism to fuel its own sinister growth. Enteric pathogens like Bacteroides fragilis have long been masters of deception, using their virulence factors to carve out distinct nutrient niches within our gut. But how do they manage to thrive in the densely populated large intestine, where oxygen is scarce and resources are plentiful? We've only recently begun to scratch the surface of this complex puzzle.
Meet Bacteroides fragilis toxin (BFT), a potent virulence factor produced by one particularly insidious strain of B. fragilis. Research has shown that BFT is capable of reprogramming the colonic epithelial cells' metabolic pathways, inducing a shift from oxidative phosphorylation to glycolysis. This metabolic makeover creates an unexpected oasis of oxygen and lactate within the gut, providing the perfect conditions for ETBF to grow and thrive.
But what's truly remarkable about this discovery is how it challenges our understanding of these enteric pathogens. For years, we've viewed B. fragilis as a strictly anaerobic organism, unable to survive in the presence of oxygen. Yet, here we find an unexpected strategy by which this pathogen has co-opted host metabolic remodeling to create its own oxidative niche. This finding not only sheds new light on the biology of enteric pathogens but also underscores the intricate and dynamic relationship between our bodies and the tiny creatures that call us home.
This research matters because it highlights the complex, often counterintuitive ways in which our bodies can be manipulated by external factors. It also underscores the importance of continued scientific inquiry into the mysteries of our own biology, and the potential consequences for human health and disease prevention.
1 min read
In the darkest corners of our bodies, where oxygen barely reaches, a tiny invader can thrive. The bacteria that cause colitis, a painful inflammation of the intestines, have always seemed like an enemy to be vanquished. But now scientists have discovered how they actually survive and even grow in these hostile environments.
It turns out that these enteric pathogens use a clever trick to create a tiny bubble of oxygen around themselves, where they can multiply and cause more harm. They do this by manipulating the way our intestines process nutrients, turning off the normal system that uses oxygen for energy and switching on one that produces lactic acid instead. This creates a localized "oxygen oasis" that supports their own metabolism, allowing them to fuel their growth and spread disease in the inflamed gut.
The people behind the work
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Spiga L et al.
Author
Published in Cell
Source: Cell
Sources & Verification
Every statement in this story is drawn from the facts below. Each is linked to a primary or reputable source — follow any citation to check it for yourself.
- To colonize their host and cause disease, enteric pathogens must deploy their virulence factors to establish distinct nutrient niches. Cell
- How anaerobic pathogens construct nutrient niches in the densely populated large intestine remains poorly understood. Cell
- Enterotoxigenic Bacteroides fragilis (ETBF) is a classically anaerobic bacterium implicated in inflammation-associated diseases, including colitis and colorectal cancer. Cell
- Here, we show that ETBF uses its virulence factor, Bacteroides fragilis toxin (BFT), to generate and adapt to a localized oxidative niche that supports gut colonization. Cell
- BFT manipulates colonic epithelial signaling and the bile acid recycling pathway, inducing a metabolic shift in the epithelium from oxidative phosphorylation to glycolysis. Cell
- This shift increases local concentrations of lactate and oxygen, nutrients that support oxidative metabolism in ETBF. Cell
- These findings reveal an unexpected strategy by which a classically anaerobic pathogen leverages host metabolic remodeling to generate and exploit an oxidative niche in the inflamed gut. Cell
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