aureus [13]. In STEC, our results demonstrated that in presence of sugars or low oxygen there was an increase in biofilms respect to basal conditions, and this could have been related to the low production of ROS and NO observed in the present investigation. either The role of the periplasmic antioxidant enzymes of the Shiga toxin-producing E. coli O157:H7 in the formation of biofilms was studied by proteomic analyses, and significantly higher expression levels of zinc superoxide dismutase and thiol peroxidase were found in STEC cells grown under biofilm conditions than these under planktonic conditions [28]. We found in STEC, that SOD and CAT levels are low under favorable conditions, because the levels of ROS are also low in these biofilm cells.Mai-Prochnow et al.
[26] have suggested that H2O2 allows to (directly or indirectly) kill a subpopulation of cells and increase in DNA damage and mutation frequency of the remaining live cells and shown that high CAT activity can prevent penetration of hydrogen peroxide into biofilms of Pseudomonas aeruginosa at a concentration of 50mM. In our work, it was observed that biofilm development is influenced by the production of oxidants metabolites and the levels of antioxidant defenses, which can be variable in different environmental conditions. We found that SOD and CAT levels are low under favorable conditions, because the levels of ROS are also low in these biofilm cells. We suggest that when this balance was altered by unfavorable conditions, an increase in the ROS production induces an overproduction of cellular stress, resulting in higher levels of SOD and CAT being able to successfully detoxify the ROS generated by H2O2.
Our results show that there was release of toxin from biofilms, with this being the first report in STEC. This release was influenced by different culture conditions and a link was found between this release and the stress present in sessile cells. In conclusion, in the present study, we have observed that biofilm development was influenced by the production of oxidants (ROS and RNI) and the levels of antioxidant defenses (SOD and CAT), which may have been affected by environmental conditions and this has an effect on the release of Stx. This oxidative imbalance produced by the alteration of biofilm environment may have an important role in the pathogenesis of infections caused by E.
coli strains that produce this toxin. In future, an improved understanding of the mechanisms involved in the Anacetrapib release of toxins during biofilm formation would contribute to a better understanding of the pathogenesis of STEC.AcknowledgmentsMaria Paraje, Maria Becerra and Anal��a Etcheverr��a are Members of the Research Career of CONICET. Anal��a Etcheverr��a and Nora Padola are Members of the Scientific Research Commission, Prov. Buenos Aires (CIC-PBA).