Influence of LncRNA NKILA on Bloodstream Infection of Hypervirulent Klebsiella pneumoniae and Its Ability to Induce Delayed Neutrophil Apoptosis.

Yang Li,Suzhen Ma,Juan Wang,Weijia Wang,Kang Chen

doi:10.1155/2021/6101078

Abstract

Objective Pneumonia due to hypervirulent Klebsiella pneumoniae (hvKP) is a high-risk subtype of pneumonia with high mortality and disability rates. An in-depth understanding of hvKP's pathogenic process and mechanism of action is the focus of achieving early disease diagnosis and early symptomatic treatment. This study conducted a preliminary analysis on the influence of lncRNA NKILA (NKILA) on hvKP, aiming at providing a new approach to the diagnosis and treatment of hvKP and laying a reliable foundation for subsequent NKILA-related studies. Methods Selected from our hospital from October 2016 to February 2018, 67 patients who were examined for the pathogenic microorganisms of alveolar lavage fluid were selected as the research subjects. Among them, 29 were diagnosed as hvKP (research group), and the other 38 had no pathogenic bacteria (control group). Serum and bronchoalveolar lavage fluid (BALF) NKILA and inflammatory factors were detected, and the clinical significance of NKILA was analyzed. In addition, neutrophils from research group were extracted and NKILA expression was increased to observe the alterations in cell apoptosis, respiratory burst intensity, and NF-kappa B inhibitor alpha (NF-κB) p65 protein. Results Serum and BALF levels of NKILA and inflammatory factors were higher in research group than in control group, and NKILA decreased in both cohorts after treatment (P < 0.05). NKILA had an excellent predictive effect on the occurrence of hvKP (P < 0.001) and was positively correlated with inflammatory factors (P < 0.05). Prognostic follow-up revealed that NKILA also had a good predictive value for death in hvKP patients (P < 0.05), and increased posttreatment levels predicted an increased risk of death (P < 0.05). In vitro, increased NKILA hindered the delayed apoptosis rate, decreased respiratory burst intensity of hvKP neutrophils, and activated NF-κB p65 protein (P < 0.05). Conclusion With an elevated expression profile in hvKP, NKILA can induce the delayed apoptosis of neutrophils, enhance the ability of releasing inflammatory mediators, and promote the progression of hvKP via activating NF-κB p65.

Highlights

Pneumonia is the most common pulmonary infectious disease derived from infections of pathogens such as bacteria and viruses, presenting clinical symptoms such as fever and cough [1]
Referring to the relevant research, we found that some special genes on virulence plasmids are considered to be the best markers for identifying Hypervirulent Klebsiella pneumoniae (hvKP) at present [10]
NF-κB p65 protein was higher in pcDNA-NKILA group at 12, 24, and 48 h compared with pcDNA-NC group (P < 0.05), and its protein expression elevated with transfection time (P < 0.05). Both hvKP and Klebsiella pneumoniae (KP) belong to the high-risk subtype of pneumonia [14], and their differences mainly lie in the bacterial phenotypic characteristics [15]. hvKP pathogen shows high viscosity and carries many virulence genes such as mag A, rmp A, and aerogenin, which possesses stronger survival ability and has more obvious invasiveness to other organs and tissues [16]

Summary

Objective

Pneumonia due to hypervirulent Klebsiella pneumoniae (hvKP) is a high-risk subtype of pneumonia with high mortality and disability rates. Serum and bronchoalveolar lavage fluid (BALF) NKILA and inflammatory factors were detected, and the clinical significance of NKILA was analyzed. Neutrophils from research group were extracted and NKILA expression was increased to observe the alterations in cell apoptosis, respiratory burst intensity, and NF-kappa B inhibitor alpha (NF-κB) p65 protein. Serum and BALF levels of NKILA and inflammatory factors were higher in research group than in control group, and NKILA decreased in both cohorts after treatment (P < 0.05). In vitro, increased NKILA hindered the delayed apoptosis rate, decreased respiratory burst intensity of hvKP neutrophils, and activated NF-κB p65 protein (P < 0.05). With an elevated expression profile in hvKP, NKILA can induce the delayed apoptosis of neutrophils, enhance the ability of releasing inflammatory mediators, and promote the progression of hvKP via activating NF-κB p65

Introduction

Materials and Methods

Results

Discussion