A Decade of Burkholderia cenocepacia Virulence Determinant Research

Abstract

The Burkholderia cepacia complex (Bcc) is a group of genetically related environmental bacteria that can cause chronic opportunistic infections in patients with cystic fibrosis (CF) and other underlying diseases. These infections are difficult to treat due to the inherent resistance of the bacteria to antibiotics. Bacteria can spread between CF patients through social contact and sometimes cause cepacia syndrome, a fatal pneumonia accompanied by septicemia. Burkholderia cenocepacia has been the focus of attention because initially it was the most common Bcc species isolated from patients with CF in North America and Europe. Today, B. cenocepacia, along with Burkholderia multivorans, is the most prevalent Bcc species in patients with CF. Given the progress that has been made in our understanding of B. cenocepacia over the past decade, we thought that it was an appropriate time to review our knowledge of the pathogenesis of B. cenocepacia, paying particular attention to the characterization of virulence determinants and the new tools that have been developed to study them. A common theme emerging from these studies is that B. cenocepacia establishes chronic infections in immunocompromised patients, which depend more on determinants mediating host niche adaptation than those involved directly in host cells and tissue damage.

The suhB gene of Burkholderia cenocepacia is required for protein secretion, biofilm formation, motility and polymyxin B resistance

“…Bcc members have emerged as serious respiratory multidrug-resistant pathogens in patients with cystic fibrosis (CF) (Isles et al, 1984) and chronic granulomatous disease (Guide et al, 2003). B. cenocepacia can infect and survive in amoebae, human respiratory epithelial cells and macrophages (Loutet & Valvano, 2010;Saldías & Valvano, 2009). In macrophages, the maturation of the B. cenocepacia-containing vacuole (BcCV) is altered, as revealed by decreased acidification and delayed fusion with lysosomes (Lamothe et al, 2007) and Rab7 inactivation (Huynh et al, 2010).…”

Depletion of the Ubiquitin-binding Adaptor Molecule SQSTM1/p62 from Macrophages Harboring cftr ΔF508 Mutation Improves the Delivery of Burkholderia cenocepacia to the Autophagic Machinery

“…Unfortunately, B. cepacia is resistant to most known antibiotics and, thus, is nearly impossible to treat. B. cepacia adopts an extracellular or intracellular lifestyle (23,24). This bacterium can survive within a variety of eukaryotic cells such as amoebae, epithelial cells, and macrophages (25)(26)(27)(28).…”

RND-4 efflux transporter gene deletion in Burkholderia cenocepacia J2315: a proteomic analysis

“…The RND-4 gene deletion affects the cell metabolism leading to a variation in some proteins associated with the well-established intracellular virulence determinants (amino acid metabolism, lipid biosynthesis, protection from oxidative stress) [44]. This could be the consequence of a stress condition connected to the loss of the RND-4 protein or it could be linked to the physiological role of this protein efflux pump.…”