Different to other glycolytic enzymes [22,23], FBA has important functions other than its principal role as cytoplasmic enzyme in glycolysis. causes metastatic endophthalmitis or meningitis [1]. This invasive syndrome has emerged in many countries, such as the US, Denmark and Taiwan [2,3,4]. Even though mechanism of invasive syndrome caused by KP in diabetics is A-582941 still unclear, it is speculated that it may be related to vulnerable host and virulent strains. Diabetes itself can inhibit the chemotaxis of phagocytes, phagocytosis and bactericidal function [5], meaning that bacteria could infect diabetics. The capsule of KP has anti-phagocytic function against host phagocytes [5]. Furthermore, invitro studies revealed that this KP serotype K1 increased gene expression then increased synthesis of the capsular polysaccharide (CPS) in high glucose media, which is an important virulence factor for KP [6]. It was observed that phagocytosis of KP serotypes K1 and K2 by neutrophils was impaired in type 2 diabetic patients with poor glycemic control, and this was associated with an increased risk of metastatic complications [5,6]. However, 25% of patients with KP liver abscess do not have diabetes [2]; this reflects that the host factor may be one ofimportant factors rather than a decisive factor in the pathogenicity of disseminated KP invasive syndrome. Previous studies on the pathogenic factors of A-582941 KP strain have mostly focused on the study of genes related to capsule serotype and A-582941 its control of capsule synthesis [7]. The main function of these genes and capsule is resistance to phagocytosis of phagocytes [8], which likely acts as a warriors shield rather than an attacking sword. The pathogenic factors might be closely related to bacterial surface proteins, but there has been no in-depth study yet. The research into protein expression level will thus be warranted. In the innate immunity system, neutrophils play an important role in the fight against microbial infections. The neutrophils could migrate to the place where the pathogenic bacteria cause inflammation and execute phagocytosis of pathogens [9,10]. Our previous GU/RH-II study revealedthat KP serotype K1 could extend the lifespan of neutrophils, making them suitable host cells for bacterial survival and multiplication after infection occurs [11]. The pathogens might be carried by neutrophils all over the body and form sporadic infections if the neutrophils cannot eliminate KP. Neutrophils may be used as Trojan horses for subsequent infection of other cells. The effect may contribute to the development of a distinctive invasive syndrome [11]. Although neutrophil immune responses are involved in disseminated KP infection, many questions remain unanswered. The investigation of the KPCneutrophils crosstalk can provide a comprehensive understanding of the pathogenesis of disseminated KP infection. Despite scattered efforts in this field, a systematic identification A-582941 of interactions between host and bacterial proteins remains unavailable. The KPCneutrophils infection model was used to find out the special protein under the two-dimensional electrophoresis analysis of proteomics study. The aim of this study was to characterize the special protein on KP, its sub-cellular localization and its putative role in the pathogenesis of disseminated KP infection. 2. Materials and Methods 2.1. Ethics Statement The Institutional Review Board of Chang Gung Memorial Hospital approved the protocol (permit No. 103-6901B). All subjects provided their written informed consent to participate in the study in accordance with the Declaration of Helsinki. 2.2. Bacterial Strains A KP-M1 (ST23; serotype K1) strain, ahypermucoviscosity phenotypicisolate that was isolated from a patient with a liver abscess, an acapsularmutant of DT-X, a non-hypermucoviscosity phenotype strainwas isolated by subculture of strain DT-S (biotype (ATCC 25922) were used as the representative strains in the following experiments. The lack of a capsule in DT-X was confirmed by staining with India ink [10]. Bacteria were routinely cultured at 37C in LuriaCBertani (LB) medium. The hypermucoviscosity phenotype of the test isolates was determined using.