The association of air pollutants (CO2, MTBE) on Candida albicans and Candida glabrata drug resistance

Introduction Therapeutic methods are very important in the prevalence of opportunistic fungal infections, which are an important cause of human diseases. In this study, air pollution agents that are in direct contact with microorganisms, and the effects of carbon sources using CO2 and MTBE on growth of fungi, and particularly the evaluation of changes in the expression of interfering genes in susceptibility and drug resistance in these fungi, were investigated. Materials and Methods Collecting samples and isolating Candida glabrata and Candida albicans with phenotypic methods were accomplished. We then evaluated the minimum inhibitory concentration (MIC) with the M27A4 protocol of CLSI. We adjusted 20 strains of C. albicans and 10 strains of C. glabrata whose sensitivity was evaluated in the MIC test with 5% CO2 and 5mg/ml methyl tert-butyl ether (MTBE) considered as air pollutants, and followed by re-evaluating MIC testing to separate azole-resistant strains. Interfering agents were also considered. Results Upregulation of some genes on the two mentioned yeasts had led to drug resistance in them; they were previously sensitive to both drugs. Correspondingly, 41% of C. glabrata samples in sputum showed sensitivity to these drugs. Upregulation of ERG11 (71%) and EPA1 (90%) were observed in resistant strains. Upregulation of genes associated with aspartate proteins and downregulation of SAP3 genes were recognized in C. glabrata in sputum and a 15% downregulation of bronchoalveolar lavage (BAL) isolate and 50% upregulation of SAP1 gene in C. albicans sensitive samples were observed and compared to fluconazole and itraconazole with the oral and joint sources. Remarkably, decreased SAP2 expression in oral sources and a 60% increase in resistant strains in C. albicans were observed. The downregulation of SAP3 expression showed in the joint samples. An increase in HWP1 expression (30%) was noted in isolated and drug-sensitive samples at the sputum and BAL source. CDR1 expression was increased in MTBE-affected species; however, it decreased in the vicinity of CT. Conclusions Air pollutants such as CO2 and MTBE eventually caused drug resistance in Candida, which can be one of the causes of drug resistance in candidiasis infections.

Automated summary

This study investigated the effects of air pollutants on the growth and drug resistance of fungi, and found that exposure to CO2 and MTBE led to drug resistance in Candida. This has important implications for understanding and addressing treatment methods for candidiasis infections.