Goblet cell hyperplasia (GCH) is induced by active smoke exposure and does not necessarily correlate with the clinical symptoms of chronic bronchitis (CB), according to study results published in Scientific Reports.
While chronic obstructive pulmonary disease (COPD), CB, and active smoking have all been associated with GCH in small studies, only active smoking is strongly associated with CB. There appears to be a disconnect between CB clinical symptoms and pathology, and chronic cough and sputum production poorly correlate with the presence of GCH or COPD.
Therefore, researchers hypothesized that the primary determinant of GCH in ever smokers with or without airflow obstruction is active smoking. They measured goblet cell density (GCD) in 71 current or former smokers (32 individuals without COPD and 39 individuals with COPD). Log10GCD was greater in current smokers compared with former smokers and that those with classically defined CB or Saint George’s Respiratory Questionnaire (SGRQ)-defined CB had a greater log10GCD compared with those without CB. Current smoking was independently associated with tertile 3 (high log10GCD) whereas CB was not in multivariable regression when adjusting for lung function and demographics. Thus, these results suggest that GCH is induced by active smoke exposure and does not necessarily correlate with the clinical symptoms of CB.
“[W]e have shown that goblet cell hyperplasia is related more so to current smoking as opposed to the presence or absence of chronic bronchitis, no matter how it is defined,” concluded the authors. “These findings need to be validated in other studies and their clinical relevance need[s] to be better defined.”
Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.
Kim V, Jeong S, Zhao H, et al. Current smoking with or without chronic bronchitis is independently associated with goblet cell hyperplasia in healthy smokers and COPD subjects. Sci Rep. 2020;10(1):20133. doi:10.1038/s41598-020-77229-1