■尽管机制尚不清楚,铜绿假单胞菌(PA)感染直接影响支气管扩张患者急性加重的频率。本文的目的是分析PA中algUmucABD操纵子的遗传突变特征,从住院的支气管扩张患者中分离出来,探讨支气管扩张频繁急性加重的独立危险因素。
■根据过去一年发生的急性加重次数,这些支气管扩张患者分为频繁急性加重患者(A组)和非频繁急性加重患者(B组).我们确定了PA中粘液表型(MPs)和藻酸盐形态型(AMs)的分布,并根据其不同的AM将其分为I-IV类;否则,检测了algUmucABD操纵子的基因突变类型(GMT).随后,GMT之间的关系,MP,和AM以及支气管扩张患者频繁急性加重的独立危险因素。
■共有93名患者和75种PA菌株,从2019年1月至2023年8月,纳入本研究。PA的MP和AM分布如下:粘液样64株(85.33%)(AM为I型38株,3株II型,和23株IV型)和11株非粘液(AM仅为III型)。粘液PA与algU,muka,mucB,mucD突变占19.61%,74.51%,31.37%,50.98%,分别。GMT分为以下几种:仅mucA突变,与其他基因突变结合的mucA,其他没有mucA突变的基因突变,没有基因突变.在91.7%的PA与I型AM中,只有mucA突变发生,在单独的MP和AM中,GMT差异有统计学意义。最后,有支气管扩张的肺叶数量和仅有mucA突变的PA数量是频繁急性加重的独立危险因素.
■mucA突变主要负责PA中MP的粘液样和I型AM,它也是支气管扩张频繁加重的独立危险因素。
UNASSIGNED: Although the mechanism is unclear, Pseudomonas aeruginosa (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 algUmucABD operon in PA, isolated from hospitalized patients with bronchiectasis, and to explore independent risk factors for frequent acute exacerbations of bronchiectasis.
UNASSIGNED: 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 algUmucABD 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.
UNASSIGNED: 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 algU, mucA, mucB, and mucD mutations accounted for 19.61%, 74.51%, 31.37%, and 50.98%, respectively. GMT was divided into the following: mucA mutations only, mucA combined with other gene mutations, other gene mutations without mucA mutations, and without gene mutations. In 91.7% of PA with type I of AM, only mucA 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 mucA mutations only were the independent risk factors for frequent acute exacerbations.
UNASSIGNED: The mucA 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.