Anti-bacterial activity of baicalin against APEC through inhibition of quorum sensing and inflammatory responses

Lu-Yuan Peng,Qiang An,Zong-Mei Wu,Jia-Lin Yu,Meng Yuan,Ben-Dong Fu,Chun-Lei Zhang,Hai-Qing Shen,Ke Song,Peng-Fei Yi,Fang Xia

doi:10.1038/s41598-019-40684-6

Abstract

Avian pathogenic Escherichia coli (APEC), collectively known as causative agent of extraintestinal infections, is an important cause of morbidity and mortality in poultry. Currently, quorum sensing (QS), biofilm formation and virulence factors are considered as novel prospective targets for antimicrobial therapy to control APEC invasion. In addition, inflammatory responses are also served as the major pathological features of APEC invasion. This study was aimed to explore the effect of baicalin on APEC and APEC-induced inflammatory responses. After treatment with baicalin, we mainly examined the AI-2 secretion, biofilm formation, expression of virulence genes of APEC, and the levels of inflammatory cytokines, as well as the expression of NF-κB pathway. Our results showed that baicalin significantly inhibited the QS via decreasing the AI-2 secretion, biofilm formation, and the expression of virulence genes of APEC such as LsrB, LsrK, LuxS, pfs, H-NS, fimA, fimB, fyuA, csgA, csgB, and rpoS. Moreover, baicalin significantly attenuated the release of lactate dehydrogenase (LDH), and the adhesion of APEC to chicken type II pneumocytes to reduce cell damage. Furthermore, baicalin also inhibited the expression of pro-inflammatory cytokines and NF-κB activation. Thus, our data revealed that baicalin could interfere with the quorum sensing, biofilm formation and virulence genes expression to relieve the APEC pathogenicity. Additionally, baicalin decreased the inflammatory responses of chicken type II pneumocytes induced by APEC. Taken together, these data provide a novel potential pharmaco-therapeutic approach to chicken colibacillosis.

Highlights

Chicken colibacillosis, as one of the principal causes of morbidity and mortality in poultry worldwide, is characterized by multiple organ lesions such as air sacculitispericarditis, peritonitis, salpingitis, synovitis, osteomyelitis or yolk sac infection, and caused by a group of pathogens designated avian pathogenic Escherichia coli (APEC)[1,2]
In order to handle with bacterical infections, the effect of baicalin on quorum sensing (QS) of Avian pathogenic Escherichia coli (APEC)-O78 and inflammatory response induced by APEC-O78 were tested in the present study
We have demonstrated that baicalin is able to inhibit QS, biofilm formation and the expression of virulence genes

Summary

Introduction

As one of the principal causes of morbidity and mortality in poultry worldwide, is characterized by multiple organ lesions such as air sacculitispericarditis, peritonitis, salpingitis, synovitis, osteomyelitis or yolk sac infection, and caused by a group of pathogens designated avian pathogenic Escherichia coli (APEC)[1,2]. The pathogenicity of APEC is regulated by QS systems, and AI-2 regulates the expression of genes involved in various processes, including secretion of virulence factors, biofilm formation, motility, genetic competence, sporulation, and antibiotic production[5,6]. The pathogenic stimulation will lead to the production of a large number of pro-inflammatory cytokines, including TNF-α, IL-1β, and so on. These up-regulated cytokines cause edema, cellular metabolic stress, and tissue necrosis[12]. We investigated the effects of baicalin on QS, biofilm formation, virulence genes expression of APEC and inflammatory responses induced by APEC, aiming to find one new treatment to suppress the chicken colibacillosis

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