Similar to what was observed for P. aeruginosa, ahpC and ahpF were highly upregulated, while

katB was only modestly upregulated (upregulations of 41.3-, 15.5- and 1.8-fold, respectively, after 30 min of treatment with H2O2) (Peeters et al., 2010). However, biofilms formed by a B. cenocepacia katB mutant (which still contains a functional ahpCF) were nevertheless highly susceptible to H2O2, and there is already substantial expression of katB in untreated biofilms. This clearly indicates that, unlike in P. aeruginosa, this catalase is crucial for the protection of sessile cells against exogenous H2O2, although Cisplatin nmr its expression is not increased following exposure to reactive oxygen species. Treatments with H2O2 or NaOCl also resulted in the increased transcription of several organic hydroperoxide resistance (ohr) genes, including BCAS0085. Interestingly, in addition to the upregulation of BCAS0085 (49.3-fold), a marked increase in the expression of BCAS0086 (encoding an exported lipase) was also observed (96.6-fold), probably due to the cotranscription of both genes. As a result of the marked overexpression of BCAS0086, an increased extracellular lipase activity was observed in treated biofilms. BCAS0085

and BCAS0086 orthologues in other Burkholderia genomes are organized in a similar operon-like manner, and increased lipase activity EPZ6438 was also observed in the supernatant of H2O2-treated biofilms of B. cenocepacia C5424, HI2424 and AU1054, Burkholderia multivorans LMG 17588, Burkholderia ambifaria LMG 19182 and Burkholderia dolosa AU0158 (Peeters et al., 2010). It remains to be determined whether this increased lipase activity has a protective effect or is merely the consequence of the cotranscription of a lipase-encoding gene. The molecular mechanisms of antifungal resistance in C. albicans have been studied extensively and changes in the expression of genes have been reported frequently

Celecoxib in resistant clinical isolates (White, 1997; White et al., 1998; Sanglard, 2002). Azole antifungal drugs (including fluconazole, miconazole and itraconazole) target the P450 mono-oxygenase encoded by the ERG11 gene. This enzyme is involved in the conversion of lanosterol into ergosterol by mediating 14-α-demethylation, a key step in ergosterol biosynthesis (White et al., 1998). Resistance to fluconazole, the most commonly used antifungal agent, is associated with overexpression of ERG11, but changes in the expression of other ERG genes (including ERG3 and ERG25) have also been associated with azole resistance (Franz et al., 1998; Lopez-Ribot et al., 1998; Henry et al., 2000). In addition, in fluconazole-resistant isolates, genes encoding efflux pumps (including MDR1, CDR1 and CDR2) are often upregulated, resulting in increased efflux (Lopez-Ribot et al., 1998; White et al., 2002; Rogers & Barker, 2003).