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. furthermore, biofilms may perhaps spawn systemic infections via sloughing of planktonic micro organism, resulting in dissemination, bacteremia, sepsis, and demise. The variety of sufferers tormented by and loss of life from what might be regarded as a "biofilm affliction" is larger than center disorder and melanoma mixed, making clinical biofilms the most important unmarried sickness that the healthcare procedure is dealing with today.
This e-book describes the molecular mechanisms of cell-to-cell verbal exchange between bacterial cells in a biofilm, the advance 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 info for Control of Biofilm Infections by Signal Manipulation
Indeed, 3-oxo-C12 HSL was found to inhibit lymphocyte proliferation and tumor necrosis factor alpha (TNF-α ) production by macrophages. In addition, IgE production, which is stimulated by interleukin-4, was found to be upregulated by 3-oxo-C12 HSL. Furthermore, the presence of the AHL signal molecule downregulated production of interleukin 12 (a Th-1 response promoting signal). As a consequence, a Th-2 response is encouraged (Telford et al. 1998). In contrast, other researchers found that 3-oxo-C12 HSL activates T-cells to produce interferon-γ , an inflammatory cytokine that promotes a Th-1 environment (Smith et al.
J Bacteriol 186: 4665–4684 Benito Y, Kolb FA, Romby P, Lina G, Etienne J, Vandenesch F (2000) Probing the structure of RNAIII, the Staphylococcus aureus agr regulatory RNA, and identification of the RNA domain involved in repression of protein A expression. RNA 6:668–679 Bjarnsholt T, Jensen PO, Burmolle M, Hentzer M, Haagensen JA, Hougen HP, Calum H, Madsen KG, Moser C, Molin S, Hoiby N, Givskov M (2005a) Pseudomonas aeruginosa tolerance to tobramycin, hydrogen peroxide and polymorphonuclear leukocytes is quorum-sensing dependent.
2002b; Ledgham et al. 2003). 5 bp upstream of the luxI start codon. The dimer overlaps the −35 region and acts as an ambidextrous activator of transcription (Egland and Greenberg 1999). Located at this position, the LuxR dimer interacts with the alpha-subunit C-terminal domain of RNA polymerase, where two residues of the subunit interact directly with the C-terminal part of LuxR (Finney et al. 2002; Johnson et al. 2003). Alanine mutation scanning of the N-termini of LuxR has provided evidence for a direct correlation between the binding of LuxR to the lux box and activation of QS-controlled target genes (Trott and Stevens 2001; Egland and Greenberg 2001).
Control of Biofilm Infections by Signal Manipulation by Naomi Balaban, Dacheng Ren, Michael Givskov (auth.), Naomi Balaban (eds.)