echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Biochemistry News > Biotechnology News > Bacterial self-sacrifice: Dying cells absorb large amounts of antibiotics to keep neighboring cells alive and continue to grow.

    Bacterial self-sacrifice: Dying cells absorb large amounts of antibiotics to keep neighboring cells alive and continue to grow.

    • Last Update: 2020-08-05
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    Bacteria have a number of strategies to survive in antibiotics: genetic resistance to drugs, delayed growth or hidden in protective biofilms.
    new work by researchers at Princeton University and California State University Northridge (CSUN) reveals another approach: self-sacrifice.
    researchers found that in the E. coli community treated with specific antimicrobial molecules, some dying cells absorbed large amounts of antibiotics, allowing their neighbors to survive and continue to grow.
    researchers have created a green fluorescent marker target antibiotic.
    this is a peptide molecule called LL37, which is naturally produced by human skin, airways and other organs that are often exposed to outside bacteria.
    , as shown in the image above, is found to accumulate antibiotics in a group of bacteria in a group of dying cells.
    Andrej Ko?mrlj, an associate professor in the Department of Mechanical and Aerospace Engineering at Princeton University, worked with the CSUN team to develop a mathematical model to explain the phenomenon more fully and to help with further research.
    the model describes the dynamic changes of bacterial communities under different concentrations of antimicrobial agents, shows how dead cells isolate dangerous molecules, and predicts the delayed growth of living cells.
    results confirm the experiment at the Sattar Taheri-Araghi Laboratory, an associate professor of physics at CSUN and co-author of the study by Ko?mrlj. "The model provides a physical explanation of how it actually works, " says
    Ko?mrlj.
    we were surprised to find that the critical inhibition concentration of antimicrobial peptides depended on the number of bacteria, and our model could explain why this happened. "Despite this new understanding, there are still questions about what happens at the molecular level," said
    Taheri-Araghi.
    this study opens the door to many questions that have never been raised before.
    our findings will have a profound impact on the evolution of bacteria that have existed for billions of years, as well as for the design and management of new antibiotic drugs.
    " Source: DeepTech Deep Tech.
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.