| Autor: |
Ferreira JA; California Institute for Medical Research, San Jose, California, United States of America; Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University, Stanford, California, United States of America., Penner JC; California Institute for Medical Research, San Jose, California, United States of America., Moss RB; Division of Pulmonology, Department of Pediatrics, Stanford University, Stanford, California, United States of America., Haagensen JA; Department of Civil and Environmental Engineering, Stanford University, Stanford, California, United States of America., Clemons KV; California Institute for Medical Research, San Jose, California, United States of America; Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University, Stanford, California, United States of America., Spormann AM; Department of Civil and Environmental Engineering, Stanford University, Stanford, California, United States of America., Nazik H; California Institute for Medical Research, San Jose, California, United States of America; Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University, Stanford, California, United States of America; Department of Medical Microbiology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey., Cohen K; California Institute for Medical Research, San Jose, California, United States of America., Banaei N; Department of Pathology, Stanford University, Stanford, California, United States of America., Carolino E; Escola Superior de Tecnologia da Saúde de Lisboa (Lisbon School of Health Technology), Lisbon, Portugal., Stevens DA; California Institute for Medical Research, San Jose, California, United States of America; Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University, Stanford, California, United States of America. |
| Abstrakt: |
Aspergillus fumigatus (Af) and Pseudomonas aeruginosa (Pa) are leading fungal and bacterial pathogens, respectively, in many clinical situations. Relevant to this, their interface and co-existence has been studied. In some experiments in vitro, Pa products have been defined that are inhibitory to Af. In some clinical situations, both can be biofilm producers, and biofilm could alter their physiology and affect their interaction. That may be most relevant to airways in cystic fibrosis (CF), where both are often prominent residents. We have studied clinical Pa isolates from several sources for their effects on Af, including testing involving their biofilms. We show that the described inhibition of Af is related to the source and phenotype of the Pa isolate. Pa cells inhibited the growth and formation of Af biofilm from conidia, with CF isolates more inhibitory than non-CF isolates, and non-mucoid CF isolates most inhibitory. Inhibition did not require live Pa contact, as culture filtrates were also inhibitory, and again non-mucoid>mucoid CF>non-CF. Preformed Af biofilm was more resistant to Pa, and inhibition that occurred could be reproduced with filtrates. Inhibition of Af biofilm appears also dependent on bacterial growth conditions; filtrates from Pa grown as biofilm were more inhibitory than from Pa grown planktonically. The differences in Pa shown from these different sources are consistent with the extensive evolutionary Pa changes that have been described in association with chronic residence in CF airways, and may reflect adaptive changes to life in a polymicrobial environment. |
