Burkholderia cepacia complex (Bcc) is an opportunistic pathogen in cystic
fibrosis patients which is inherently resistant to antimicrobial agents. The mechanisms of
attachment and pathogenesis of Bcc, a group of 17 species, are poorly understood. The most
commonly identified Bcc species in newly colonised patients, Burkholderia multivorans,
continues to be acquired from the environment. Development of therapies which can
prevent or reduce the risk of colonization on exposure to Bcc in the environment would be
a better alternative to antimicrobial agents. Previously, it has been shown that Bcc strains
bound to many glycolipid receptors on lung epithelia. Using a real-time PCR method to
quantify the levels of binding of B. multivorans to the lung epithelial cells, we have
examined glycoconjugate derivatives for their potential to inhibit host cell attachment.
Bivalent lactosides previously shown to inhibit galectin binding significantly reduced the
attachment of B. multivorans to CF lung epithelial cells at micromolar concentrations. This
was in contrast to monosaccharides and lactose, which were only effective in the
millimolar range. Development of glycoconjugate therapies such as these, which inhibit
attachment to lung epithelial cells, represent an alternative means of preventing infection
with inherently antimicrobially resistant pathogens such as B. multivorans
