Now that I no longer have access to academic papers at whim, I am starting to understand the frustration of those advocating for open access. But I still have my ways, and came across an exciting new story on the gut microbiota in Cell Host Microbe.
If you haven't heard, the gut microbiota (ie the bacteria that naturally live in our gut) is one of the most exciting topics in biology at the moment. In the past decade, it has become clear that we are in fact a 'superorganism', as it is both our genes and the genes of the bacteria that live within us that shape who we are. We are slowly uncovering the numerous roles the gut microbiota has, from regulating the responses of our immune system to controlling the development of our blood vessels, our metabolism and even our behaviour. If you are interested and have access, here is an excellent review and a viewpoint article on the topic (ahem, commissioned by me during my Nature Reviews Microbiology days).
And now a study has shown that the gut microbiota doesn't just shape our immune responses, it actually regulates the production of the immune cells that fight pathogens.
When the authors looked at differences in haemopoiesis (ie the production of blood cells) between germ-free mice (which lack any bacteria) and mice that lack a defined set of bacteria (known as specific-pathogen free (SPF) mice), they found that the germ-free mice had fewer progenitor cells in the bone marrow (where blood cells are born). Specifically, the germ-free mice had fewer granulocyte and monocyte progenitors, the cells that eventually give rise to innate immune cells, the first-line of defense against pathogens.
Importantly, the germ-free mice were more susceptible to infection with the bacterium Listeria monocytogenes than the SPF mice, which the authors attribute to the defective production and development of progenitors caused by the lack of a gut microbiota.
How exactly the gut microbiota regulates haemopoiesis is still not entirely clear. However, the authors did conclude from their work that a complex molecular signal is likely necessary, as treating the germ-free mice with one type of signal (known as MAMPs, or microbial-associated molecular patterns) was not sufficient to restore their defect in defending against Listeria monocytogenes infection. By contrast, recolonising them with the gut microbiota of SPF mice restored their resistance to the bacterium..
This story adds to the growing list of beneficial roles for the gut microbiota. But there is also another dimension, as it suggests that treatment with broad-spectrum antibiotics, which deplete the natural gut flora, may in fact make us more susceptible to infection with opportunistic pathogens.
If you haven't heard, the gut microbiota (ie the bacteria that naturally live in our gut) is one of the most exciting topics in biology at the moment. In the past decade, it has become clear that we are in fact a 'superorganism', as it is both our genes and the genes of the bacteria that live within us that shape who we are. We are slowly uncovering the numerous roles the gut microbiota has, from regulating the responses of our immune system to controlling the development of our blood vessels, our metabolism and even our behaviour. If you are interested and have access, here is an excellent review and a viewpoint article on the topic (ahem, commissioned by me during my Nature Reviews Microbiology days).
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| 3D model of intestinal cells colonised with gut bacteria. Image from the Pacific Northwest National Laboratory obtained on Flickr (https://www.flickr.com/photos/pnnl/8146322408) |
And now a study has shown that the gut microbiota doesn't just shape our immune responses, it actually regulates the production of the immune cells that fight pathogens.
When the authors looked at differences in haemopoiesis (ie the production of blood cells) between germ-free mice (which lack any bacteria) and mice that lack a defined set of bacteria (known as specific-pathogen free (SPF) mice), they found that the germ-free mice had fewer progenitor cells in the bone marrow (where blood cells are born). Specifically, the germ-free mice had fewer granulocyte and monocyte progenitors, the cells that eventually give rise to innate immune cells, the first-line of defense against pathogens.
Importantly, the germ-free mice were more susceptible to infection with the bacterium Listeria monocytogenes than the SPF mice, which the authors attribute to the defective production and development of progenitors caused by the lack of a gut microbiota.
How exactly the gut microbiota regulates haemopoiesis is still not entirely clear. However, the authors did conclude from their work that a complex molecular signal is likely necessary, as treating the germ-free mice with one type of signal (known as MAMPs, or microbial-associated molecular patterns) was not sufficient to restore their defect in defending against Listeria monocytogenes infection. By contrast, recolonising them with the gut microbiota of SPF mice restored their resistance to the bacterium..
This story adds to the growing list of beneficial roles for the gut microbiota. But there is also another dimension, as it suggests that treatment with broad-spectrum antibiotics, which deplete the natural gut flora, may in fact make us more susceptible to infection with opportunistic pathogens.
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