Please use this identifier to cite or link to this item: https://doi.org/10.3389/fcimb.2017.00401
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dc.titleComparison of diabetic and non-diabetic human leukocytic responses to different capsule types of Klebsiella pneumoniae responsible for causing pyogenic liver abscess
dc.contributor.authorLee, I.R
dc.contributor.authorSng, E
dc.contributor.authorLee, K.-O
dc.contributor.authorMolton, J.S
dc.contributor.authorChan, M
dc.contributor.authorKalimuddin, S
dc.contributor.authorIzharuddin, E
dc.contributor.authorLye, D.C
dc.contributor.authorArchuleta, S
dc.contributor.authorGan, Y.-H
dc.date.accessioned2020-09-14T08:01:29Z
dc.date.available2020-09-14T08:01:29Z
dc.date.issued2017
dc.identifier.citationLee, I.R, Sng, E, Lee, K.-O, Molton, J.S, Chan, M, Kalimuddin, S, Izharuddin, E, Lye, D.C, Archuleta, S, Gan, Y.-H (2017). Comparison of diabetic and non-diabetic human leukocytic responses to different capsule types of Klebsiella pneumoniae responsible for causing pyogenic liver abscess. Frontiers in Cellular and Infection Microbiology 7 (SEP) : 401. ScholarBank@NUS Repository. https://doi.org/10.3389/fcimb.2017.00401
dc.identifier.issn2235-2988
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/176080
dc.description.abstractThe major risk factor for Klebsiella liver abscess (KLA) is type 2 diabetes mellitus (DM), but the immunological mechanisms involved in the increased susceptibility are poorly defined. We investigated the responses of neutrophils and peripheral blood mononuclear cells (PBMCs) to hypervirulent Klebsiella pneumoniae (hvKP), the causative agent of KLA. DNA and myeloperoxidase levels were elevated in the plasma of KLA patients compared to uninfected individuals indicating neutrophil activation, but diabetic status had no effect on these neutrophil extracellular trap (NET) biomarkers in both subject groups. Clinical hvKP isolates universally stimulated KLA patient neutrophils to produce NETs ex vivo, regardless of host diabetic status. Ability of representative capsule types (K1, K2, and non-K1/K2 strains) to survive intra- and extra-cellular killing by type 2 DM and healthy neutrophils was subsequently examined. Key findings were: (1) type 2 DM and healthy neutrophils exhibited comparable total, phagocytic, and NETs killing against hvKP, (2) phagocytic and NETs killing were equally effective against hvKP, and (3) hypermucoviscous K1 and K2 strains were more resistant to total, phagocytic, and NETs killing compared to the non-mucoviscous, non-K1/K2 strain. The cytokine response and intracellular killing ability of type 2 DM as well as healthy PBMCs upon encounter with the different capsule types was also examined. Notably, the IL-12-IFNγ axis and its downstream chemokines MIG, IP-10, and RANTES were produced at slightly lower levels by type 2 DM PBMCs than healthy PBMCs in response to representative K1 and non-K1/K2 strains. Furthermore, type 2 DM PBMCs have a mild defect in its ability to control hvKP replication relative to healthy PBMCs. In summary, our work demonstrates that type 2 DM does not overtly impact neutrophil intra- and extra-cellular killing of hvKP, but may influence cytokine/chemokine production and intracellular killing by PBMCs. © 2017 Lee, Sng, Lee, Molton, Chan, Kalimuddin, Izharuddin, Lye, Archuleta and Gan.
dc.sourceUnpaywall 20200831
dc.subjectantibiotic agent
dc.subjectgamma interferon
dc.subjectglucose
dc.subjecthemoglobin A1c
dc.subjectinterleukin 10
dc.subjectinterleukin 12
dc.subjectinterleukin 17
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectbacterial antigen
dc.subjectbacterial DNA
dc.subjectbacterial polysaccharide
dc.subjectcapsular polysaccharide K1
dc.subjectchemokine
dc.subjectcytokine
dc.subjectgamma interferon
dc.subjectinterleukin 12
dc.subjectperoxidase
dc.subjecttumor necrosis factor receptor 1
dc.subjecttumor necrosis factor receptor 2
dc.subjectvirulence factor
dc.subjectArticle
dc.subjectbacterial infection
dc.subjectbactericidal activity
dc.subjectcontrolled study
dc.subjectcytokine production
dc.subjectcytokine response
dc.subjectenzyme linked immunosorbent assay
dc.subjectextracellular trap
dc.subjectflow cytometry
dc.subjectglycemic control
dc.subjecthuman
dc.subjecthuman experiment
dc.subjectimmunofluorescence microscopy
dc.subjectinnate immunity
dc.subjectKlebsiella pneumoniae
dc.subjectleukocyte activation
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectnonhuman
dc.subjectperipheral blood mononuclear cell
dc.subjectphagocytosis
dc.subjectpyogenic liver abscess
dc.subjectadult
dc.subjectaged
dc.subjectbacterial capsule
dc.subjectblood
dc.subjectcomplication
dc.subjectimmunology
dc.subjectKlebsiella infection
dc.subjectKlebsiella pneumoniae
dc.subjectmetabolism
dc.subjectmicrobiology
dc.subjectmiddle aged
dc.subjectmononuclear cell
dc.subjectneutrophil
dc.subjectnon insulin dependent diabetes mellitus
dc.subjectpathogenicity
dc.subjectpyogenic liver abscess
dc.subjectserum bactericidal activity
dc.subjectAdult
dc.subjectAged
dc.subjectAntigens, Bacterial
dc.subjectBacterial Capsules
dc.subjectBlood Bactericidal Activity
dc.subjectChemokines
dc.subjectCytokines
dc.subjectDiabetes Mellitus, Type 2
dc.subjectDNA, Bacterial
dc.subjectExtracellular Traps
dc.subjectHumans
dc.subjectInterferon-gamma
dc.subjectInterleukin-12
dc.subjectKlebsiella Infections
dc.subjectKlebsiella pneumoniae
dc.subjectLeukocytes, Mononuclear
dc.subjectLiver Abscess, Pyogenic
dc.subjectMiddle Aged
dc.subjectNeutrophils
dc.subjectPeroxidase
dc.subjectPhagocytosis
dc.subjectPolysaccharides, Bacterial
dc.subjectReceptors, Tumor Necrosis Factor, Type I
dc.subjectReceptors, Tumor Necrosis Factor, Type II
dc.subjectVirulence Factors
dc.typeArticle
dc.contributor.departmentDEPT OF BIOCHEMISTRY
dc.contributor.departmentDEPT OF MEDICINE
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.3389/fcimb.2017.00401
dc.description.sourcetitleFrontiers in Cellular and Infection Microbiology
dc.description.volume7
dc.description.issueSEP
dc.description.page401
dc.published.statePublished
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