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Bacterial Cell Surfaces and Pathogenesis

Several lines of research are being followed. See below a brief description of them.



 The macromolecule of peptidoglycan (or its small components) seems to be able to induce an inflammatory response in different hosts. We believe that in order to understand how this macromolecule is sensed by the infected host we will need  to learn how this molecule is synthesized, organized, modified and degraded during the bacterial cell cycle.

There are four essential questions that represent the different research lines being followed in the Bacterial Cell Surfaces and Pathogenesis laboratory:

  • Does the composition of the peptidoglycan interfere with its recognition by the host?
  • Does the metabolism of the peptidoglycan, as the bacteria divides into two daughter cells, interfere with its recognition by the host?
  • Are polysaccharides, linked to the bacterial surface, capable of interfering with peptidoglycan recognition?
  • Are there other bacterial strategies to hide the inflammatory peptidoglycan macromolecule?

We use Staphylococcus aureus and Streptococcus pneumoniae, Gram-positive bacterial pathogens, as model organisms to study how the metabolism of the bacteria cell surface, mainly cell wall synthesis and turnover,  can modulate a response of the innate immune system of the infected host.
 Possible outcomes when a protein (yellow pacman) from the host encounters peptidoglycan in live bacteria: A) recognition is impaired by bacterial surface proteins or other polysaccharides; B) recognition occurs only when degradation of bacterial cell wall allows the release of peptidoglycan fragments that are recognized by the protein; C) recognition of peptidoglycan occurs only at specific sites of the bacterial surface or D) recognition is only possible with "naked" peptidoglycan, when no proteins or other polysaccharides are attached. 



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