A high profile review article from MIMS group leader Barbara S. Sixt on host cell death modulation by the bacterial pathogen Chlamydia
A significant number of bacterial pathogens has the capacity to invade human cells and to exploit the interior of the host cell as growth niche. The bacteria reprogram host cellular functions to promote their growth and to suppress the intrinsic defense systems of the host cell. Pathogens have evolved to protect or compromise the viability of the host cell as their survival and life cycle within the cell depends on it. This interplay between host and microbe can be very complex. For instance, after a phase of growth, intracellular bacteria may actively induce cell death to promote their release and spread. While in other cases, the host cell may activate molecular suicide programs as defense response to restrict pathogen growth by removing the growth niche.
In a new review article published in FEMS Microbiology Reviews, MIMS group leader Barbara S. Sixt discusses the significance of this complex interplay and outstanding questions in the context of Chlamydia, a group of important pathogens causing for instance blinding eye infections, respiratory infections, and sexually transmitted diseases.
For his innovative research project on the infection biology of microsporidia, Jonas Barandun has been awarded a prestigious Starting Grant by the European Research Council (ERC), funded with 1.5 million euros over five years. Dr. Barandun joined Umeå University from The Rockefeller, University, New York, in January 2019 to start a research group at the Laboratory for Molecular Infection Medicine Sweden.
Scientists have created the first cell atlas of mosquito immune cells, to understand how mosquitoes fight malaria and other infections. Researchers from the Wellcome Sanger Institute, Umeå University, Sweden and the National Institutes of Health (NIH), USA, discovered new types of mosquito immune cells, including a rare cell type that could be involved in limiting malaria infection. They also identified molecular pathways implicated in controlling the malaria parasite.
Antibiotics bind to and corrupt the functioning of crucial elements of bacterial cells, such as the ribosome that synthesises proteins or RNA polymerase that reads genes to generate mRNA. To counter the action of antibiotics, bacteria have evolved numerous dedicated mechanisms of resistance. Commonly, these resistance mechanisms act by either destroying the antibiotic, pumping it out of the cell or permanently modifying the molecular target so it becomes immune to the antibiotic, e.g. by post-translational modification such as methylation.
