Our laboratory is the study of peptidoglycan (PGN) metabolism to better understand how bacteria collect mature and substantially PGN, which adds rigidity and shape of cells, despite the high dynamics accompanying growth and cell division. We use
Helicobacter pylor I as a bacterial model of genome analysis shows a minimal set of genes involved in metabolism of PGN and installation of believing that it can be a simple model to study PGN metabolism. This seems confirmed by our recent work on the PGN hydrolase of H. pylori

. Long-term goal of this part of my research to better understand how bacteria coordinate PGN synthesis, and thus identify new therapeutic targets, but also better understand the mechanisms of resistance to antibiotics and related expenses fitness. Investigation of fitness costs of resistance to antibiotics is an addition to the discovery of new therapeutic targets, as this may lead to more effective management of existing antibiotics and expand their storage lives. In the second part of our research aimed at studying the role of PGN in host-microbial interactions cheap strattera. Using several bacterial model, the goal is to understand how pathogens can undermine / modulate the host response by modifying their PGN, the basic molecular pattern recognized by the host immune system. Other models include
H.pylori,
Neisseria meningitidis,
Yersinia sp. ,
Lister and others. For example, it is intriguing that extracellular pathogens such as H. pylori
acquired virulence factors, such as four of secretion to deliver PGN fragments in the host cell allows its detection owner. Thus, part of the project aimed at studying various bacterial virulence strategy for studying the biological activity of PGN. The second goal is to understand the dynamics of PGN sensing in the host cell during infection: which PGN structures are different pathogens, as the owner finds them, react to them and eventually cleans them. These studies aimed at better understanding the role of PGN in the pathogenesis, in determining what may distinguish the pathogen from synanthropic organism, normal development of the gastrointestinal tract and in the etiology of several chronic inflammatory diseases of the gastrointestinal tract (stomach cancer or Crohn's disease). .
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