By Naomi Balaban, Dacheng Ren, Michael Givskov (auth.), Naomi Balaban (eds.)
The clinical miracle of antibiotics is being eroded through the emergence and unfold of bacterial drug resistance. this is often compounded by means of the truth that bacterial biofilms are believed to be a typical reason for power infections, while simply because becoming in biofilms, micro organism are protected against the host’s immune reaction and from antibiotics. moreover, biofilms might spawn systemic infections by way of sloughing of planktonic micro organism, resulting in dissemination, bacteremia, sepsis, and loss of life. The variety of sufferers stricken by and demise from what could be regarded as a "biofilm disorder" is greater than middle affliction and melanoma mixed, making clinical biofilms the most important unmarried illness that the healthcare procedure is dealing with today.
This booklet describes the molecular mechanisms of cell-to-cell communique between bacterial cells in a biofilm, the improvement of antibiofilm inhibitors, like quorum-sensing inhibitors, and using biofilm inhibitors to avoid and deal with bacterial infections in people and different animals.
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Extra resources for Control of Biofilm Infections by Signal Manipulation, 1st Edition
RNAIII levels are evident from the midexponential phase of growth and reach a maximum in late logarithmic- and stationary-phase cultures. As mentioned above, RNAIII also encodes the small peptide δ -hemolysin in its 5 -end. Intriguingly, translation of the RNAIII transcript into δ -hemolysin is delayed 1 h after the appearance of RNAIII in the midexponential phase. This inhibitory mechanism seems to involve the 3 -end of RNAIII, possibly by blocking access of the ribosome to the ribosomebinding region (Balaban and Novick 1995a).
Complementation analysis suggests that the 3 -end of RNAIII is important for repression of the spa-gene that encodes the well-known IgG-binding protein, protein A (Novick et al. 1993). In this case, RNAIII is believed to function either directly or indirectly at the transcriptional level, although it is possible that RNAIII affects the stability of the spa transcript. RNAIII levels are evident from the midexponential phase of growth and reach a maximum in late logarithmic- and stationary-phase cultures.
The AI-2 (Fig. 2c,d) and its synthase LuxS have been identified in a few bacterial species (Chen et al. 2002; Miller et al. 2004, Schauder et al. 2001; Xavier and Bassler 2005). However, the presence of luxS analogs in more than 55 species indicates that it is widely used in cell-to-cell signaling (Vendeville et al. 2005) to regulate genes specifying diverse functions, such as those encoding virulence factors in Actinobacillus actinomycetemcomitans, enterohemorrhagic E. coli (EHEC) O157:H7, P. gingivalis, Streptococcus pyogenes, Vibreio cholerae, and V.