RND efflux pumps of Gram-negative bacteria bestow an MDR phenotype. Because deletion of the AcrAB-TolC main efflux pump of E. coli promotes the over-expression of the AcrEF-TolC as well as 8 others redundant efflux pumps (Viveiros M, Dupont M, Rodrigues L, Couto I, Davin-Regli A, Martins M, Pagès JM, Amaral L. Antibiotic stress, genetic response and altered permeability of E.

coli. PLoS One. 2007 Apr 11;2(4):e365. PubMed PMID: 17426813; PubMed Central

PMCID: PMC1838523: Viveiros M, Jesus A, Brito M, Leandro C, Martins M, Ordway D, Molnar AM,

Molnar J, Amaral L. Inducement and reversal of tetracycline resistance in Escherichia coli K-12 and expression of proton gradient-dependent multidrug efflux pump genes. Antimicrob Agents Chemother. 2005 Aug;49(8):3578-82. PubMed PMID: 16048990; PubMed Central PMCID: PMC1196278.) the chance to inhibit an efflux pump and render the MDR bacterium susceptible to antibiotics may not be readily possible. However, the RND efflux pumps of a given Gram negative bacterium all share a common TolC protein. If the exposed portion of the TolC channel on the surface of the bacterium contains antigenic determinants, and if nano antibodies can be made against these antigenic determinants, then it may be possible to block the TolC channel and thus inhibit the activity of the efflux pump. Are there any RG members interested in this problem?