Abstract
Reversible switching between opaque and translucent colony formation is a novel feature of Acinetobacter baumannii that has been associated with variations in the cell morphology, surface motility, biofilm formation, antibiotic resistance and virulence. Here, we assessed a number of phenotypic alterations related to colony switching in A. baumannii clinical isolates belonging to different multi-locus sequence types. Our findings demonstrated that these phenotypic alterations were mostly strain-specific. In general, the translucent subpopulations of A. baumannii produced more dense biofilms, were more piliated, and released larger amounts of outer membrane vesicles (OMVs). In addition, the translucent subpopulations caused reduced fertility of Caenorhabditis elegans. When assessed for effects on the immune response in RAW 264.7 macrophages, the OMVs isolated from opaque subpopulations of A. baumannii appeared to be more immunogenic than the OMVs from the translucent form. However, also the OMVs from the translucent subpopulations had the potential to evoke an immune response. Therefore, we suggest that OMVs may be considered for development of new immunotherapeutic treatments against A. baumannii infections.
Highlights
Acinetobacter baumannii has emerged as one of the most common causative agents of a wide range of nosocomial infections, such as ventilator-associated pneumonia, septicaemia, skin and soft tissue infections, and catheter-associated urinary tract infections [1,2,3]
Colony phase variation in Acinetobacter baumannii types, six isolates were selected for further assays (Table 1), including three strains from the Pakistanis collection, Ab-Pak-Pesh-22 belonging to sequence type 23 (ST23), Ab-Pak-Pesh-37 (ST1106), and Ab-Pak-Lah-14 (ST1), two strains from our Swedish collection of A. baumannii, A095 (ST2) and A100 (ST1) [19], and the hyper virulent A. baumannii reference strain AB5075 (ST1) [12]
The panel of isolates subjected to more detailed analysis of phase switching consists of A. baumannii Ab-Pak-Pesh-22 (ST23), Ab-Pak-Pesh-37 (ST1106), Ab-Pak-Lah-141(ST1), two isolates from our Swedish collection of A. baumannii, A095(ST2) and A100 (ST1) [19] and the hyper virulent A. baumannii reference strain AB5075 (ST1)
Summary
Acinetobacter baumannii has emerged as one of the most common causative agents of a wide range of nosocomial infections, such as ventilator-associated pneumonia, septicaemia, skin and soft tissue infections, and catheter-associated urinary tract infections [1,2,3]. Communityacquired A. baumannii infections have been reported, mainly in patients with underlying comorbidities, including pulmonary disorders, diabetes mellitus, alcohol use disorder and cancer [4]. A. baumannii acquired the status of “key human pathogen” in the late 20th century because of the frequent isolation from patients all over the world. The capacity of producing discernible toxins with virulence potential, as found in many other bacterial pathogens, has not been reported in A. baumannii. Our current understanding of A. baumannii virulence and pathogenesis suggests that a ‘persist and resist’ strategy is a major virulence feature [5]. Like many other Gram negative bacteria, A. baumannii secretes outer membrane vesicles (OMVs). OMVs from A. baumannii are equipped with phospholipases and exhibit haemolytic and leucocytic potential [6]. Surface proteins of A. baumannii OMVs were shown to elicit pro-
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