RESUMEN
To investigate the effects of subminimum inhibitory concentrations of cephalosporins on bacterial biofilm formation, the biofilm production of 52 Escherichia (E.) coli strains was examined following treatment with cephalosporin compounds at 1/4 minimum inhibitory concentrations (MICs). Ceftazidime (CAZ) inhibited biofilm formation in seven isolates, while cefoperazone (CFP) enhanced biofilm formation in 18 isolates. Biofilm formation of E. coli E42 was inhibited by CAZ and induced by CFP. Therefore, using reverse transcriptionpolymerase chain reaction, the expression of the biofilmmodulating genes of this isolate was investigated. To monitor the production of the autoinducer of quorum sensing in E. coli, autoinducer2 (AI2) production was detected by measuring the bioluminescence response of Vibrio harveyi BB170. Antisense oligonucleotides (ASODNs) targeting Sribosylhomocysteine lyase (luxS) inhibited the expression of the luxS gene in E. coli. CAZ at 1/4 MIC reduced luxS mRNA levels and the production of AI2, whereas CFP at 1/4 MIC had the opposite effect. ASODNs targeting luxS significantly decreased the aforementioned inhibitory effects of CAZ and the induction effects of CFP on E. coli biofilm formation. Therefore, biofilm formation by the E. coli clinical isolate E42 was evoked by CFP but attenuated by CAZ at subMICs, via a luxS/AI2based quorum sensing system.
Asunto(s)
Antibacterianos/farmacología , Proteínas Bacterianas/metabolismo , Biopelículas/efectos de los fármacos , Liasas de Carbono-Azufre/metabolismo , Cefoperazona/farmacología , Ceftazidima/farmacología , Proteínas de Escherichia coli/metabolismo , Escherichia coli/fisiología , Proteínas Bacterianas/genética , Liasas de Carbono-Azufre/genética , Escherichia coli/efectos de los fármacos , Escherichia coli/aislamiento & purificación , Infecciones por Escherichia coli/microbiología , Proteínas de Escherichia coli/genética , Expresión Génica/efectos de los fármacos , Regulación Bacteriana de la Expresión Génica/efectos de los fármacos , Genes Bacterianos , Humanos , Pruebas de Sensibilidad Microbiana , Percepción de Quorum/efectos de los fármacos , ARN Mensajero/genética , ARN Mensajero/metabolismoRESUMEN
Plasmodium yoelii 17XL was used to investigate the mechanism of Plasmodium falciparum-caused cerebral malaria, although its histological effect on other mouse organs is still unclear. Here, histological examination was performed on mice infected with P. yoelii 17XL; the effect of P. yoelii 17XL infection on anemia and body weight loss, as well as its lesions in the brain, liver, kidney, lung, and spleen, also was investigated. Plasmodium yoelii 17XL-infected red blood cells were sequestered in the microcirculation of the brain and in the kidney. Compared with the nonlethal P. yoelii 17XNL strain, infection by P. yoelii 17XL caused substantial pulmonary edema, severe anemia, and significant body weight loss. Although P. yoelii 17XNL and 17XL produced a similar focal necrosis in the mouse liver, infection of P. yoelii 17XL induced coalescing of red and white pulp. Mortality caused by P. yoelii 17XL may be due to cerebral malaria, as well as respiratory distress syndrome and severe anemia. Plasmodium yoelii 17XL-infected rodent malaria seems to be a useful model for investigating severe malaria caused by P. falciparum.
