The secret of cholesterol inside the tick may stop the spread of Lyme disease
Washington State University researchers have discovered how bacteria caused the disease of non -inflammation in Lyme and Lyme cellular kidnappings in ticks to ensure their survival and spread to new hosts, including humans.
At the Faculty of Veterinary Medicine, the team found that bacteria can manipulate a protein known as ATF6, which helps cells to discover and respond to infection, to support their growth and survival inside the tick. The results published in the magazine The facts of the National Academy of SciencesIt can serve as a launch point for developing ways to get rid of bacteria in ticks before moving to humans and other animals.
“Most of the research looked at how these bacteria interacted with humans and animals, not how they survive and spread in ticks,” said Kylie Vospegi, a PhD student and a major author of the study. “What we found can open the door to target these pathogens in ticks, before they pose a threat to people.”
Fossibijian and her advisor, Dana Shaw, the author corresponding to the study and a professor in the Department of Veterinary Biology and Pathology, focused their research on Ixodes SCAPULARISAlso known as the Blacklegged brand, responsible for publishing both anaplasma phagocytophilum and Borillia BurgdorphiCausing factors and Lym disease. Both disease are increasingly common and can cause a serious disease in humans and animals.
The team discovered that when ATF6 is activated in tick cells, it leads to the production of stomatin, a protein that helps transmit cholesterol across cells as part of normal cellular processes. Bacteria use this process against tick hosts, using cholesterol – which need to grow and build their cell membranes but they cannot produce themselves – to support their survival and success.
“Stomatin plays a variety of roles in the cell, but one of its main functions is to help the shuttle cholesterol on different regions,” said Fossibijian. “Bacteria benefit from this, and stealing cholesterol basically they need to survive.”
When the researchers prevented the production of floors, which restricts cholesterol availability, bacteria growth significantly. The researchers believe that this indicates that targeting the ATF6-Stomatin path can lead to new ways to boycott the disease cycle in the tick before the transmission occurs.
As part of the study, Vosbigian has also developed a new research tool called Arthroquest, which is a free web platform hosted by WSU, which allows scientists to search in tick genes, mosquitoes, lice, sandy flies, fleas, and other arthropods of binding sites for copying factors such as genetic activities that control gene activity.
“There are not many tools to study genetics regulation in arthropods,” said Fossibijian. “Most of them are designed for humans or stereotypes such as fruit flies, which are completely genetically different from ticks.”
Using arthroquest, the team found that the control of ATF6 on the cylinders look prevalent in the blood feeding arthropods. Since the kidnapping of cholesterol and other fats is common among the pathogens that are transmitted by arthropods, researchers suspect that many may also take advantage of ATF6.
“We know many pathogens that are transmitted by vectors, such as Borillia Burgdorphi And the causal child PlasmodiumShu said: “It depends on cholesterol and other fats of their hosts. Therefore, the fact that the ATF6-Stomatin track is present in other arthropods can be related to a wide range of pathogens,” said Shu said.
The research was partially supported by the National Health Institutes Scholarships and the College of Veterinary Medicine Scholarship within veterinary medicine.
(Tagstotranslate) Lyme disease; Diseases and conditions; Infectious diseases; malaria; New types; Biotechnology and Biomatic Engineering; Insects (including butterflies); Animals
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