AUTHOR=Tan Yuxue , Dai Zhongshang 

TITLE=Pseudomonas aeruginosa mucinous phenotypes and algUmucABD operon mutant characteristics obtained from inpatients with bronchiectasis and their correlation with acute aggravation

JOURNAL=Frontiers in Cellular and Infection Microbiology

VOLUME=14

YEAR=2024

URL=https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2024.1402348

DOI=10.3389/fcimb.2024.1402348

ISSN=2235-2988

ABSTRACT=<sec><title>Objective</title><p>Although the mechanism is unclear, <italic>Pseudomonas aeruginosa</italic> (PA) infection directly affects the frequency of acute exacerbations in patients with bronchiectasis. The aims of this article are to analyze the genetic mutation characteristics of the <italic>algUmucABD</italic> operon in PA, isolated from hospitalized patients with bronchiectasis, and to explore independent risk factors for frequent acute exacerbations of bronchiectasis.</p></sec><sec><title>Methods</title><p>Based on the number of acute exacerbations that occurred in the past year, these patients with bronchiectasis were divided into those with frequent acute exacerbations (Group A) and those with non-frequent acute exacerbations (Group B). We identified the distribution of mucoid phenotypes (MPs) and alginate morphotypes (AMs) in PA, and classified them into I–IV categories based on their different AMs; otherwise, the gene mutation types (GMTs) of the <italic>algUmucABD</italic> operon were tested. Subsequently, the relationship between GMT, MP, and AM and the independent risk factors for frequent acute exacerbations in patients with bronchiectasis were explored.</p></sec><sec><title>Results</title><p>A total of 93 patients and 75 PA strains, from January 2019 to August 2023, were included in this study. The MP and AM distributions of PA were as follows: 64 strains (85.33%) of mucoid (the AMs were 38 strains of type I, 3 strains of type II, and 23 strains of type IV) and 11 strains of non-mucoid (the AM was type III only). Mucoid PA with <italic>algU</italic>, <italic>mucA</italic>, <italic>mucB</italic>, and <italic>mucD</italic> mutations accounted for 19.61%, 74.51%, 31.37%, and 50.98%, respectively. GMT was divided into the following: <italic>mucA</italic> mutations only, <italic>mucA</italic> combined with other gene mutations, other gene mutations without <italic>mucA</italic> mutations, and without gene mutations. In 91.7% of PA with type I of AM, only <italic>mucA</italic> mutations occurred, and in both separate MP and AM, the GMT differences were statistically significant. Lastly, the number of lung lobes with bronchiectasis and the number of PA with <italic>mucA</italic> mutations only were the independent risk factors for frequent acute exacerbations.</p></sec><sec><title>Conclusion</title><p>The <italic>mucA</italic> mutation was primarily responsible for the mucoid of MP and type I of AM in PA, and it was also an independent risk factor for frequent exacerbations of bronchiectasis.</p></sec>