Galectin-3 in blood may predict lung outcomes in children with CF
Researchers explored relationship between protein, disease's characteristics
Elevated levels of the pro-inflammatory signaling protein galectin-3 in the bloodstream of children with clinically stable cystic fibrosis (CF) significantly correlated with worse lung function, according to a study.
The findings suggest galectin-3 may serve as a noninvasive biomarker to predict lung disease outcomes in children with CF, the researchers said in “Galectin-3 levels in children with cystic fibrosis,” which was published in the European Journal of Pediatrics.
In CF, the buildup of thick mucus in the lungs provides a breeding ground for chronic infections. The ongoing inflammatory response to infections can worsen the development and progression of lung disease.
Galectin-3 regulates chronic inflammation in the lungs, liver, and kidneys. Emerging evidence suggests it’s increased in several diseases marked by inflammation and scar formation, called fibrosis, so it may serve as a biomarker for inflammation and lung function outcomes, leading researchers in Turkey to collect blood and sputum samples from 143 children with clinically stable CF to investigate a possible relationship between galectin-3 levels in the bloodstream and the disease’s clinical characteristics. The children (69 girls, 74 boys) were a median age of 11.5 and most (97.2%) had a chronic bacterial infection with at least one microorganism. Thirty healthy children served as controls.
Exploring role of galectin-3 protein in CF
Galectin-3 levels were measured alongside other established pro-inflammatory proteins, including interleukin-17A (IL-17A), interleukin-8 (IL-8), and neutrophil elastase (NE).
The analysis found galectin-3 and NE levels were higher in the serum, that is, the cell-free, liquid portion of blood, of patients than in the control group. No differences were noted between the groups’ levels of IL-17A and IL-8.
“The results suggest that Galectin-3, like NE, may be related to the inflammation process of CF,” the researchers wrote.
Galectin-3 levels were higher in females than in male patients and among those older than 10. Generally, elevated galectin-3 correlated with older age and higher body mass index (BMI), that is, body fat content.
No relationships were detected between galectin-3 and airway chronic bacterial colonization or indicators of body-wide inflammation, namely erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Also, no correlations were found between blood NE, IL-8, IL-17A, and patients’ demographics and clinical characteristics.
Elevated galectin-3 did correlate with worse lung function, as assessed by the forced expiratory volume (FEV1) and forced vital capacity (FVC), however. FEV1 is the amount of air that can be forced out of the lungs in a second, while FVC represents the total amount of air exhaled after a maximal inhalation.
In sputum, there was no correlation between galectin-3 and age, sex, BMI, ESR, CRP, and chronic airway bacterial colonization. No correlation was seen between galectin-3 in blood and sputum samples, and between patients with one and more than one infection in terms of blood and sputum markers.
“The study shows that serum Galectin-3 levels increased in clinically stable CF patients, and serum Galectin-3 response may depend on the age, gender, and BMI of the CF patients,” the researchers said. “The sputum Galectin-3 was found to be negatively correlated with patients’ lung functions.”
More research is needed before Galectin-3 could be considered a biomarker in CF and other chronic lung diseases, they said.
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