Project description:The aim of this study was to explore whether, and if so, how Bacillus subtilis KC1 can enhance the growth performance of broilers that have been adversely affected by Mycoplasma gallisepticum (MG) infection. A total of 96 1-day-old male broilers were randomly divided into 4 groups: the control group (basal diet), the MG group (basal diet + MG challenge), the Bacillus subtilis KC1 group (basal diet + Bacillus subtilis KC1 supplementation), the Bacillus subtilis KC1 + MG group (basal diet + Bacillus subtilis KC1 supplementation + MG challenge). The trial lasted 42 days, and the results showed that the MG group had significantly reduced body weight and average daily gain, as well as increased feed conversion ratio of broilers, compared to the control group. Dietary supplementation with Bacillus subtilis KC1 significantly improved the growth performance of MG-infected broilers. In addition, dietary supplementation with Bacillus subtilis KC1 significantly improved oxidative stress and inflammatory response markers, characterized by increased superoxide dismutase levels and reduced levels of malondialdehyde, interleukin-1β, and tumor necrosis factor-α. Furthermore, both metabolomics and transcriptomics analyses indicated that MG infection markedly disrupted amino acid metabolism in broilers, whereas Bacillus subtilis KC1 supplementation alleviated the abnormal amino acid metabolism caused by MG infection. These results suggested that Bacillus subtilis KC1 may alleviate the poor growth performance caused by MG infection in broilers by improving amino acid metabolism.
Project description:Azole resistance was induced in vitro by growth of a susceptible C. parapsilosis isolate in the presence of voriconazole. Whole genome microarrays were used to compare the transcriptional response of the voriconizole-resistant and susceptible isolates.
Project description:Azole resistance was induced in vitro by growth of a susceptible C. parapsilosis isolate in the presence of posaconazole. Whole genome microarrays were used to compare the transcriptional response of the posaconazole-resistant and susceptible isolates.
Project description:Azole resistance was induced in vitro by growth of a susceptible C. parapsilosis isolate in the presence of fluconazole. Whole genome microarrays were used to compare the transcriptional response of the fluconazole-resistant and susceptible isolates.
Project description:The present study describes a novel mechanism of antifungal resistance affecting the susceptibility of both the azole and echinocandin antifungals in an azole-resistant isolate from a matched pair of C. parapsilosis isolates obtained from a patient with prosthetic valve endocarditis. Transcriptome analysis indicated differential expression of several genes in the resistant isolate including upregulation of ERG1, ERG2, ERG5, ERG6, ERG11, ERG24, ERG25, ERG27, DAP1 and UPC2, of the ergosterol biosynthesis pathway. Whole genome sequencing revealed a mutation in the ERG3 gene leading to a G111R amino acid substitution in the resistant isolate. Subsequent introduction of this allele in the native ERG3 locus in the susceptible isolate resulted in a fluconazole MIC of >64 mg/ml and a caspofungin MIC of 8 mg/ml. Corresponding allelic replacement of the wildtype allele for the mutant allele in the resistant isolate resulted in a drop in MIC to 1 mg/ml for both fluconazole and caspofungin. Sterol profiles indicated a loss of sterol demethylase activity as a result of this mutation. This work demonstrate that this G111R mutation is wholly responsible for the resistant phenotype in the C. parapsilosis resistant isolate and is the first report of this multidrug resistance mechanism.
Project description:We performed RNA-sequencing of Bgh-infected barley leaves at two different time-points after infection to examine gene expression in the barley powdery mildew isolate DH14 during plant pathogenesis.