Abstract
Hypermucoviscosity phenotypic Klebsiella pneumoniae (HV-Kp) serotype K1 is the predominant pathogen of a pyogenic liver abscess, an emerging infectious disease that often complicates septic metastatic syndrome in diabetic patients with poor sugar control. HV-Kpisolates were more resistant to neutrophil phagocytosis than non-HV-Kpisolates because of different pathogen-associated molecular patterns. The protein expression of HV-Kp after interaction with neutrophils is unclear. We studied KP-M1 (HV phenotype; serotype K1), DT-X (an acapsularmutant strain of KP-M1), and E. coli (ATCC 25922) with the model of Kp-infected neutrophils, using a comparative proteomic approach. One the identified protein, namely fructose-1, 6-bisphosphate aldolase (FBA), was found to be distributed in the KP-M1 after infecting neutrophils. Cell fractionation experiments showed that FBA is localized both to the cytoplasm and the outer membrane. Flow cytometry demonstrated that outer membrane-localized FBA was surface-accessible to FBA-specific antibody. The fba gene expression was enhanced in high glucose concentrations, which leads to increasing bacterial resistance to neutrophils phagocytosis and killing. The KP-M1 after FBA inhibitors and FBA-specific antibody treatment showed a significant reduction in bacterial resistance to neutrophils phagocytosis and killing, respectively, compared to KP-M1 without treatment. FBA is a highly conserved surface-exposed protein that is required for optimal interaction of HV-Kp to neutrophils.
Highlights
In the past 30 years, disseminated Klebsiella pneumoniae (KP) invasive syndrome has usually been observed in diabetic patients, especially in those with poor glycemic control [1]
The fba gene expression was enhanced in high glucose concentrations, which leads to increasing bacterial resistance to neutrophils phagocytosis and killing
Our previous data suggest that KP serotype K1 can prolong the lifespan of infected neutrophils
Summary
In the past 30 years, disseminated Klebsiella pneumoniae (KP) invasive syndrome has usually been observed in diabetic patients, especially in those with poor glycemic control [1]. In addition to causing primary liver abscesses with bacteremia, disseminated KP invasive syndrome causes metastatic endophthalmitis or meningitis [1]. This invasive syndrome has emerged in many countries, such as the US, Denmark and Taiwan [2,3,4]. The mechanism of invasive syndrome caused by KP in diabetics is still unclear, it is speculated that it may be related to vulnerable host and virulent strains. The capsule of KP has anti-phagocytic function against host phagocytes [5]. Invitro studies revealed that the KP serotype K1 increased gene expression increased synthesis of Pathogens 2020, 9, 1009; doi:10.3390/pathogens9121009 www.mdpi.com/journal/pathogens
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