RESUMEN
BACKGROUND: Elevated levels of particulate matter PM2.5 and rhinovirus infection have been known to exacerbate asthma. However, the combined effect of rhinovirus infection and high PM2.5 has not been investigated. PURPOSE: To investigate the effect of PM2.5 and concomitant rhinovirus infection on airway function in asthma in an area with high PM2.5 concentration. METHODS: Asthmatics and their matched controls were monitored for lung function, exhaled nitric oxide (eNO) and respiratory symptoms on days with varying levels of PM2.5. As the study was a repeated measure design, repeated clinical findings, and laboratory data were used in the mixed model analysis. RESULTS: Wheezing and dyspnea in asthmatics were worsened with increasing ambient PM2.5. Increasing PM2.5 decreased FEV1% predicted (-0.51, -0.79 to -0.23) and FEF25-75% predicted (-0.66, -1.07 to -0.24) in subjects with asthma (all P < .01). Rhino viral infection reduced FEF25-75% predicted in subjects with asthma (-11.7, -20 to -2.9). The reductions in FEV25-75 and FEV1 per 10 µg/m(3) increase in ambient PM2.5 were 6% and 5% respectively. A significant interaction was observed between presence of rhinovirus infection and elevated PM2.5 in asthmatics causing a 4-fold decrease in FEF25-75 (P = .01) and a 2-fold decrease in FEV1% predicted values (P = .01) compared with asthmatics with no rhino viral infection. CONCLUSIONS: Increasing ambient PM2.5 and low temperature independently worsened airway function in asthma. The interaction between rhinovirus and PM2.5 significantly impairs airway function in asthma. A larger sample size study is suggested to investigate these observations.
Asunto(s)
Asma/etiología , Asma/fisiopatología , Material Particulado/efectos adversos , Infecciones por Picornaviridae/complicaciones , Rhinovirus , Adulto , California , Estudios de Casos y Controles , Exposición a Riesgos Ambientales/efectos adversos , Femenino , Volumen Espiratorio Forzado , Humanos , Flujo Espiratorio Medio Máximo , Proyectos PilotoRESUMEN
The first step during bacillithiol (BSH) biosynthesis involves the formation of N-acetylglucosaminylmalate from UDP-N-acetylglucosamine and l-malate and is catalyzed by a GT4 class glycosyltransferase enzyme (BshA). Recombinant Staphylococcus aureus and Bacillus subtilis BshA were highly specific and active with l-malate but the former showed low activity with d-glyceric acid and the latter with d-malate. We show that BshA is inhibited by BSH and similarly that MshA (first enzyme of mycothiol biosynthesis) is inhibited by the final product MSH.