Due to persistent bacterial infections, long-chain fatty acids (LCFA) are linked to continued inflammation in cystic fibrosis (CF) patients — and may contribute to pulmonary exacerbations in children with CF, according to a recent study.
The scientists said further studies are needed to examine how bacterial functions following antibiotic treatments could be used to predict an individual’s risk of pulmonary exacerbations, or episodes of symptom worsening with an acute decrease in lung function.
The role that bacterial LCFA production plays in the occurrence of such exacerbations also needs to be investigated, they said.
The study, “Inflammation in children with cystic fibrosis: contribution of bacterial production of long-chain fatty acids,” was published in the journal Pediatric Research.
Bacterial lung infections often accompany CF and can lead to pulmonary exacerbations — the disorder’s main cause of lower quality of life and mortality.
While genetic studies have shed light on the bacterial species infecting CF patients’ airways, less is known regarding their antibiotic resistance mechanisms and how bacterial metabolic changes associate with different CF stages.
Now, a team of researchers from the Children’s National Research Institute and George Washington University, both in Washington, D.C., studied these changes in children with CF. The researchers examined bacterial metabolic changes in relation to the children’s clinical status and intravenous (IV, or into-the-vein) antibiotic treatment.
A total of 27 hospitalized children — not older than 18 and with a mean age of 10 — were followed from the onset of pulmonary exacerbations, and through antibiotic treatment, to their next pulmonary clinic visit. Most participants (63%) were not taking any antibiotic or anti-inflammatory medications at the beginning of the study.
The most common signs of pulmonary exacerbations included changes in the physical exam of the patients’ chests, which occurred in 41% of participants, and X-ray imaging consistent with infection, found in 37%. A decrease of at least 10% in forced expiratory volume in one second, known as FEV1 — a standard measure of pulmonary function that records how much air a person can exhale during a forced breath — also occurred in 37% of the children.
Results showed a change in bacterial metabolic pathways related to LCFAs. Notably, LCFAs serve various biological functions, including the regulation of gene activity. They also are part of cellular membranes.
Pathways involved in LCFAs production and elongation were more highly activated in follow-up samples than in those collected at the end of treatment.
LCFAs can bind to receptors on cell surfaces, which past research has linked to certain metabolic — and possibly inflammatory — diseases. For instance, LCFAs have been associated with increased lung inflammation in asthma.
Although the proportions of various bacterial species found in the patients’ lungs and airways changed from the onset of pulmonary exacerbations through treatment, most of these changes occurred among the “normal” bacteria that are always present.
There were, however, two exceptions: Achromobacter xylosoxidans and an unclassified Escherichia species were significantly more prevalent in follow-up compared with pulmonary exacerbations samples.
That the investigators did not find as much Pseudomonas aeruginosa — commonly seen in CF-related lung infections — in this study as in others could be due to the way in which samples are grown in the lab, which prioritizes other species. It also could be due to the participants’ young ages, as P. aeruginosa is more common in adolescents and adults. Finally, the scientists said it could be due to antibiotic resistance, as both A. xylosoxidans and Escherichia have been associated with persistent infection despite treatment.
This is the first report of LCFAs in the airway of people with CF, to the researchers’ knowledge.
“Our study findings,” the scientists concluded, “suggest that following an IV antibiotic treatment course, LCFAs may be associated with continued inflammation due to opportunistic and persistent pathogens.”
“Future studies should evaluate LCFAs as predictors of future” pulmonary exacerbations, they added.
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