a bcam0223 mutant of burkholderia cenocepacia is deficient in hemagglutination, serum resistance, adhesion to epithelial cells and virulencebcam0223突变的洋葱cenocepacia缺乏红细胞凝集,血清抵抗,上皮细胞粘附和毒性.pdf

A BCAM0223 Mutant of Burkholderia cenocepacia Is Deficient in Hemagglutination, Serum Resistance, Adhesion to Epithelial Cells and Virulence 1 1,2 Dalila Mil-Homens , Arsenio M. Fialho * ´ 1 IBB-Institute for Biotechnology and Bioengineering, Center for Biological and Chemical Engineering, Instituto Superior Tecnico, Lisbon, Portugal, 2 Department of ´ Bioengineering, Instituto Superior Tecnico, Technical University of Lisbon, Lisbon, Portugal Abstract Burkholderia cepacia complex (Bcc) bacteria are a problematic group of microorganisms causing severe infections in patients with Cystic Fibrosis. In early stages of infection, Bcc bacteria must be able to adhere to and colonize the respiratory epithelium. Although this is not fully understood, this primary stage of infection is believed to be in part mediated by a specific type of adhesins, named trimeric autotransporter adhesins (TAAs). These homotrimeric proteins exist on the surface of many Gram negative pathogens and often mediate a number of critical functions, including biofilm formation, serum resistance and adherence to an invasion of host cells. We have previously identified in the genome of the epidemic clinical isolate B. cenocepacia J2315, a novel cluster of genes putatively encoding three TAAs (BCAM0219, BCAM0223 and BCAM0224). In this study, the genomic organization of the TAA cluster has been determined. To further address the direct role of the putative TAA BCAM0223 in B. cenocepacia pathogenicity, an isogenic mutant was constructed via insertional inactivation. The BCAM0223::Tp mutant is deficient in he