The lung microbiome changes during cystic fibrosis flare-ups

Cystic fibrosis is a genetically inherited disease characterized in part by thick mucus secretion that can obstruct the lungs and aid in the harboring of bacteria in airways. A leading cause of death within persons with cystic fibrosis (CF) is infection of the lungs and inflammation that leads to respiratory failure. In a study performed by members of the Department of Pediatrics and Communicable Diseases at the University of Michigan Medical School, and published by Microbiome, sputum (mucus) samples were taken from four CF patients over a period of a days leading up to pulmonary exacerbation, a period of worsening lung infection. The hope was to identify possible bacterial changes that lead to exacerbation.

 The samples collected from individuals with cystic fibrosis – referred to as subjects A, B, C, and D – were sequenced to identify bacterial and viral content during the period leading up to and including exacerbation. At baseline, the most abundant bacteria in subject A was Staphlyococcus, in subject C Streptococcus, and in subjects B and D Burkholeria. Subject A showed to most change in bacterial communities during the week prior to exacerbation symptoms, subject B showed bacterial community change just after onset of exacerbation, and subjects C and D remained relatively stable with the onset of exacerbation. After the changes that occurred in subject A’s bacterial community it never bounced back to its pre-exacerbation population, and stabilized to one with reduced Staphylococcus and increased Pseudomonas and Prevotella. Different from subject A, subject B’s bacterial community shifted one week after the onset of exacerbation from one dominated by Burkholderia  to Pseudomonas.

 While there were many differences among the four subjects sampled in the study, there was one similarity in that the dominant taxa of subjects A, B, and C all decreased in relative abundance around the period of exacerbation. The study’s findings also suggest that rather than changes in total bacterial density, it is more likely that shifts in relative abundance of a member of a bacterial community is associated with changes in CF symptoms. Additionally, none of the respiratory viruses tested for were found present during time of exacerbation, which was surprising to the researchers.

 The results of this study do not give us any solid rules for the characteristics of bacterial communities in the lungs during time of exacerbation in cystic fibrosis patients; however it is a step in the right direction toward identifying such characteristics. Perhaps with a larger sample size we can better understand the changes in community composition that lead to changes in CF symptoms.  

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