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Researchers at the Francis Crick Institute have discovered that the Cryptosporidium parasite releases a protein into infected intestinal cells, which modifies the gut environment and aids in the parasite’s survival and multiplication.
Cryptosporidium is a significant intestinal parasite, recognized for causing acute diarrhea, particularly in young children. It invades epithelial cells in the intestines and induces the growth of microvilli—tiny projections that play a critical role in nutrient absorption.
In a study published in Cell Host & Microbe, the researchers identified a set of proteins that Cryptosporidium injects into intestinal cells upon infection, which subsequently accumulate within the microvilli of the host.
The research focused on a key protein from this family, identified as microvilli protein 1 (MVP1). It was found to engage with human proteins essential for maintaining cellular structure and regulating projections such as microvilli.
Following the removal of MVP1 from a Cryptosporidium strain through CRISPR-based genetic editing, researchers noted a complete halt in the elongation of microvilli within the infected cells. This modified strain, lacking MVP1, was also unable to establish a typical infection in laboratory mice.
One significant interaction of MVP1 is with a protein known as EBP50, which is crucial for stabilizing cell surface pumps responsible for salt transport. Disruption of these pumps is associated with diarrhea, leading the researchers to propose that MVP1 could be a key player in the symptoms associated with Cryptosporidium infections.
Adam Sateriale, Group Leader of the Cryptosporidiosis Laboratory at the Crick, commented, “The disease caused by Cryptosporidium poses a serious risk to children and can result in chronic malnutrition. Our understanding of how this parasite influences cellular structures is an important step towards addressing the severe diarrhea it causes. These insights into the underlying mechanisms could be vital for preventing long-term health consequences.”
Convergent Evolution: Shared Mechanisms Among Pathogens
Cryptosporidium is not alone in promoting the elongation of microvilli in the intestine. Certain strains of E. coli are known to infect the intestine and contribute to diarrhea through a similar mechanism, using a protein called Map to manipulate structural proteins in intestinal epithelial cells.
Interestingly, the research team found that MVP1 from Cryptosporidium interacts with the same structural proteins as Map from E. coli, specifically EBP50 and CDC42. This represents a striking case of convergent evolution, suggesting that disease-causing proteins in both bacteria and parasites have independently developed similar functions.
Elena Rodrigues, a former Ph.D. student in the Cryptosporidiosis Laboratory, stated, “The parallels in effector proteins between E. coli and Cryptosporidium are an intriguing example of convergent evolution, revealing how pathogens from different biological domains have evolved similar strategies to impact their host. Although further research is necessary to clarify how Cryptosporidium induces diarrhea through these mechanisms, our findings provide a strong starting point.”
More information: Elena Rodrigues et al, Cryptosporidium modifies intestinal microvilli through an exported virulence factor, Cell Host & Microbe (2025). DOI: 10.1016/j.chom.2025.04.001
Citation: Researchers uncover how intestinal parasite Cryptosporidium alters host cells (2025, April 28) retrieved 28 April 2025 from https://phys.org/news/2025-04-uncover-intestinal-parasite-cryptosporidium-host.html
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