• Skip to primary navigation
  • Skip to main content
  • Skip to primary sidebar
MRC Laboratory of Molecular Biology

MRC Laboratory of Molecular Biology

One of the world's leading research institutes, our scientists are working to advance understanding of biological processes at the molecular level - providing the knowledge needed to solve key problems in human health.

  • Home
  • About LMB
  • Research
  • Research Groups
  • Students
  • Recruitment
  • Life at the LMB
  • Achievements
  • News & Events
Home > Insight on Research > The sweet way of detecting bacterial invasion in cells

The sweet way of detecting bacterial invasion in cells

Published on 16 January, 2012

Sweet Way Of Detecting BacteriaFelix Randow’s group in the LMB’s PNAC Division has identified Galectin-8 as a novel danger receptor and factor of the cellular machinery that protects human cells against bacterial invasion. Galectin 8, a sugar-binding protein in the cytosol, was discovered to be a key component in limiting the growth of Salmonella and to participate in the early line of defence against infection.

Galectin-8 limits the ability of pathogenic bacteria such as Salmonella to grow in the cytosol of human cells. Whilst other receptors of the innate immune system detect pathogen-derived molecules, Galectin-8 senses damage to cell-derived organelles, i.e. bacteria-containing vacuoles. Vacuoles are an essential stepping-stone for bacteria invading the cytosol of cells. Damage caused by bacteria to vesicles releases glycans, complex sugar-containing molecules, into the glycan-free environment of the cytosol. Here their detection by Galectin-8 triggers anti-bacterial effector mechanisms such as autophagy. Since Galectin-8 monitors the integrity of cellular vesicles, it only indirectly detects the entry of pathogens into the cytosol. However, since many pathogens in addition to Salmonella cause vesicle damage, the function of Galectin-8 as a danger receptor enables the detection of even evolutionary distant pathogens.

Defects in the delicate network of autophagy-inducing defence pathways are likely to cause susceptibility to infections and promote inflammation, for example in Crohn’s disease.

Further references:

Article in Nature
Randow Group webpage

Primary Sidebar

Search

  • Privacy & Cookies
  • Contact Directory
  • Freedom of Information
  • Site Map
Find Us
©2023 MRC Laboratory of Molecular Biology,
Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. 01223 267000

The MRC is part of UK Research and Innovation

Contact Us