Abstract
BackgroundKlebsiella pneumoniae (KP) expressing hypermucoviscosity phenotype (HV-KP) has abundant capsular polysaccharide (CPS) and is capable of causing invasive syndrome. Sodium salicylate (SAL) reduces the production of CPS. The study was aimed to investigate the relationship between aspirin usage and KP-mediated invasive syndrome and the effect of SAL on HV-KP.MethodsPatients with community-acquired KP bacteraemia were prospectively enrolled. KP-M1, a serotype-K1 HV-KP clinical isolate, was used in the following experiments: CPS production, HV-KP phenotype, and the effect of SAL on neutrophils phagocytosis. The effect of oral aspirin intake on the leukocyte bactericidal activity was evaluated.ResultsPatients infected by HV-KP and diabetic patients with poor glycemic control were at an increased risk for invasive syndrome (p < 0.01); those who had recent use of aspirin (p = 0.02) were at a lower risk. CPS production was significantly reduced in the presence of SAL. The HV-KP phenotype and resistance to neutrophil phagocytosis were both significantly reduced in the KP-M1 after incubation with SAL (p < 0.01). Aspirin treatment significantly enhanced the killing of KP-M1 by leukocytes (p < 0.01).ConclusionTreatment with SAL significantly reduces CPS production in HV-KP, thereby contributing to leukocyte phagocytosis and bactericidal activity against this pathogen.
Highlights
Klebsiella pneumoniae (KP) expressing hypermucoviscosity phenotype (HV-KP) has abundant capsular polysaccharide (CPS) and is capable of causing invasive syndrome
The proportion of KP infection-related invasive syndrome was significantly higher among these diabetic mellitus (DM) patients (p = 0.04), especially those with poor glycemic control (HbA1c ≥ 9%; p < 0.01)
Aspirin therapy received during the month prior to the diagnosis of the KP infection was found in 58 (14.2%) patients, and they were less likely to develop invasive syndrome (p < 0.01; Table 1)
Summary
Klebsiella pneumoniae (KP) expressing hypermucoviscosity phenotype (HV-KP) has abundant capsular polysaccharide (CPS) and is capable of causing invasive syndrome. The study was aimed to investigate the relationship between aspirin usage and KP-mediated invasive syndrome and the effect of SAL on HV-KP. The capsular polysaccharide (CPS) contributes to the mucoid phenotype, and Chemotherapeutic agents that reduce CPS production may be effective as an adjunct therapy for HV-KP infection. Safe concentrations of sodium salicylate (SAL), the major metabolite of aspirin, can reduce CPS production by up to 70% [9,10]. We tried to examine this hypothesis by investigating the effect of SAL on bacterial survival, hypermucoviscosity, CPS production, leukocyte phagocytosis, and bactericidal activity against HV-KP. We conducted a prospective study to evaluate the relationship between aspirin usage and KP-mediated invasive syndrome
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