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References
Baldelli V et al. (2021). The role of Enterobacteriaceae in gut microbiota dysbiosis in inflammatory bowel diseases. Microorganisms 9, 697.
Glenn SJ et al. (2024). Bacterial vampirism mediated through taxis to serum. eLife 12, RP93178.
Zhou B et al. (2022). Bacterial chemotaxis in human diseases. Trends Microbiol 31, 453–467.
Bacterial Vampirism Causes Bloodlust in Pathogens


Vampires are menacing creatures with a deadly thirst for human blood, lurking in the dark of the night and stalking their victims for their next meal. But while they may be the stuff of nightmares, the lore tells us we can ward these monsters off with crucifixes and garlic, and even the light of the sun can protect us from their threat.
So, what if there was a version of a vampire that could invade the body without invitation and without your knowledge? This Halloween, gather around and we’ll tell you a scary story about a phenomenon known as bacterial vampirism.
High Stakes
First, let’s take a step back and set the scene: the tortured gut.
Inflammatory bowel disease (IBD) describes a group of conditions in which persistent, chronic inflammation affects the gastrointestinal (GI) tract. While the cause of IBD is largely unknown, several factors have been implicated in its pathogenesis. One such factor is the disruption of the normal gut microbiota — the community of typically harmless (and often beneficial) microorganisms that inhabit the human body. The loss of favorable microbes in the microbiota allows space for potentially harmful species to take their place and flourish, in a state known as microbiota dysbiosis. Many studies have demonstrated an increase in the amount of bacteria of the Enterobacteriaceae family in particular in IBD patients (Baldelli et al. 2021).
The leading cause of death for patients with IBD is sepsis, which describes a situation where bacteria enters the blood and triggers an extreme immune response by the body that can ultimately cause tissue damage, organ failure, and potentially death. The bacterial species of the Enterobacteriaceae family that haunt the inflamed gut of IBD patients are commonly associated with GI bleeding, and this breach of the GI barrier gives them free access to the bloodstream. But why these bacteria, in particular, have such a taste for blood has been a bit of a mystery.
In a recent paper, Glenn et al. (2024) investigate the biting truth behind bacteria's bloodthirsty behavior.
On the Prowl
How do bacteria typically choose their lair within the human body?
A process known as chemotaxis allows bacteria to sense the stimuli in their environment and respond appropriately. In the gut, where the peristaltic flow of fluid leads to a dynamic local environment, the chemosensing of stimuli enables rapid changes in the bacterial structure, allowing movement towards (or away from depending on the signal) the source of stimuli in a matter of seconds (Zhou et al. 2022).
When it comes to sepsis in IBD patients, we know that GI bleeding provides an entry point for bacteria, but why exactly do they leave the gut behind and prowl the circulatory system instead? Well, serum, the liquid component of the blood, contains an abundance of nutrients such as sugars and amino acids that provide a potential source of energy for bacteria (Glenn et al 2024). So, what specific component of the serum is so alluring to these bacterial vampires?
Blood Cravings
Glenn et al. used a microfluidics device, which they spiked with human serum to simulate GI bleeding, to investigate the chemoattraction mechanism of cultured non-typhoidal Salmonella enterica. Remarkably, S. enterica showed immense sensitivity to human serum, rapidly responding to mere femtoliter quantities in the environment.
Based on the chemoreceptors present on the bacteria that had corresponding chemoattractant ligands present in the serum, the team proposed a handful of potential mediators of the chemotaxis. One of the most abundant of these potential perpetrators in the serum is L-serine, which is recognized by the taxis to serine and repellents (Tsr) receptor. Therefore, to test whether this receptor is crucial for the attraction to blood of S. enterica, a strain was generated with a specific deletion in the tsr gene. The microfluidics setup was then used again to compare the blood-loving behavior of this mutant compared to the wildtype (WT) bacteria. The WT was able to efficiently outcompete the mutant with a 3:1 ratio of WT to tsr-negative bacteria next to the serum source at 5 minutes posttreatment. However, some degree of serum attraction was still detected in the mutant, albeit to a much lesser extent, indicating that multiple factors could be at play for optimal chemotaxis.
To drive home the significance of L-serine and hammer the final stake in the coffin, purified L-serine was added to the microfluidics setup as opposed to complete serum, and, as expected, a strong chemoattractant response of the bacteria was observed. Interestingly, other ligands of the Tsr receptor, norepinephrine (NE) and 3,4-dihydroxymandelic acid (DHMA), did not provoke chemotaxis. Additionally, the scientists noted that, while the presence of serum boosted the growth of bacteria, this was not mediated by L-serine, suggesting that L-serine entices the bacteria towards the blood, but other nutrients in the serum bestow the major growth benefits.
This research provides scientists with some extra knowledge that they can sink their teeth into when attempting to develop novel therapeutic options to prevent sepsis. Knowing what tempts these bloodsuckers into the serum and the receptors they use to chase their target allows a future where vampire hunters can develop drugs to block these pathways, preventing their deadly ways.
Interested in Studying the Creatures that Plague the Gut?
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References
Baldelli V et al. (2021). The role of Enterobacteriaceae in gut microbiota dysbiosis in inflammatory bowel diseases. Microorganisms 9, 697.
Glenn SJ et al. (2024). Bacterial vampirism mediated through taxis to serum. eLife 12, RP93178.
Zhou B et al. (2022). Bacterial chemotaxis in human diseases. Trends Microbiol 31, 453–467.
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