Prevalence and Molecular Characterization of Fluoroquinolone Resistance in<i>Escherichia coli</i>Isolates from Dairy Cattle with Endometritis in China

Zhao, Hongxia; Zhao, Junli; Shen, Jianzhong; Fan, Hong-Liang; Guan, Hong; An, Xiaoping; Li, Peifeng

doi:10.1089/mdr.2013.0073

Cited by 27 publications

(21 citation statements)

References 41 publications

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“…Nowadays, antibiotics have become the first choice of the treatment for liver inflammation. However, many reports have shown that the prevalence of multi-antibiotic Escherichia coli increased markedly in animals (Zhao et al, 2014 ). Therefore, we need to put out new prophylactic and therapeutic approaches to treat liver inflammation.…”

Section: Introductionmentioning

confidence: 99%

Baicalin Alleviates Lipopolysaccharide-Induced Liver Inflammation in Chicken by Suppressing TLR4-Mediated NF-κB Pathway

et al. 2017

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As a kind of potent stimulus, lipopolysaccharide (LPS) has the ability to cause cell damage by activating toll-like receptor(TLR)4, then nuclear factor kappa B (NF-κB) translocates into the nucleus and changes the expression of related inflammatory genes. Baicalin is extracted from Radix Scutellariae, which possesses anti-inflammation, antioxidant and antibacterial properties. However, the effects of it on LPS-induced liver inflammation have not been fully elucidated. This study aims to investigate the anti-inflammatory effects of Baicalin on the LPS-induced liver inflammation and its underlying molecular mechanisms in chicken. The results of histopathological changes, serum biochemical analysis, NO levels and myeloperoxidase activity showed that Baicalin pretreatment ameliorated LPS-induced liver inflammation. ELISA and qPCR assays showed that Baicalin dose-dependently suppressed the production of IL-1β, IL-6, and TNF-α. Furthermore, the mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were significantly decreased by Baicalin. TLR4 is an important sensor in LPS infection. Molecular studies showed that the expression of TLR4 was inhibited by Baicalin pretreatment. In addition, Baicalin pretreatment inhibited NF-kB signaling pathway activation. All results demonstrated the protective effects of Baicalin pretreatment against LPS-induced liver inflammation in chicken via negative regulation of inflammatory mediators through the down-regulation of TLR4 expression and the inhibition of NF-kB activation.

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Section: Introductionmentioning

confidence: 99%

Baicalin Alleviates Lipopolysaccharide-Induced Liver Inflammation in Chicken by Suppressing TLR4-Mediated NF-κB Pathway

et al. 2017

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“…Therefore, methods are needed to eradicate the causative bacteria earlier and control inflammation. Although antibiotics have been effective, increasing drug resistance and concerns about food safety limit their use (Malinowski et al, 2011;Zhao et al, 2014;Mackeen et al, 2015;Ward and Duff, 2016).…”

Section: Introductionmentioning

confidence: 99%

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Lyu

Chen

Wang

et al. 2017

J. Zhejiang Univ. Sci. B

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Abstract:Objective: Bovine endometritis is one of the most common reproductive disorders in cattle. The aim of this study was to investigate the anti-inflammation potential of punicalagin in lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and to uncover the underlying mechanisms. Methods: bEECs were stimulated with different concentrations (1, 10, 30, 50, and 100 μg/ml) of LPS for 3, 6, 9, 12, and 18 h. MTT assay was used to assess cell viability and to identify the conditions for inflammatory injury and effective concentrations of punicalagin. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess gene expression of pro-inflammatory cytokines. Western blotting was used to assess levels of inflammation-related proteins. Results: Treatment of bEECs with 30 µg/ml LPS for 12 h induced cell injury and reduced cell viability. Punicalagin (5, 10, or 20 µg/ml) pretreatment significantly decreased LPS-induced productions of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) in bEECs. Molecular research showed that punicalagin inhibited the activation of the upstream mediator nuclear factor-κB (NF-κB) by suppressing the production of inhibitor κBα (IκBα) and phosphorylation of p65. Results also indicated that punicalagin can suppress the phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Conclusions: Punicalagin may attenuate LPS-induced inflammatory injury and provide a potential option for the treatment of dairy cows with Escherichia coli endometritis.

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“…One isolates (CM4) with a single mutation in gyrA did not exhibit any mutation in parC . This is because according to the currently accepted alternating-target model, high-level fluoroquinolone resistance in E. coli develops by stepwise acquisition of target mutations, in which DNA gyrase is the primary target and topoisomerase IV is the secondary target for fluoroquinolones in E. coli [ 21 - 23 ]. Most common mutation noticed were at S83⟶L and D87⟶N of gyrA and S80⟶I of ParC in our study ( Table-3 ).…”

Section: Resultsmentioning

confidence: 99%

Genetic characterization of fluoroquinolone-resistant Escherichia coli associated with bovine mastitis in India

Balakrishnan¹,

Antony²,

Mukhopadhyay³

et al. 2016

Vet World

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Aim:The present study was undertaken to characterize the mutation in gyrA (DNA gyrase) and parC (topoisomerase IV) genes responsible for fluoroquinolone resistance in Escherichia coli isolates associated with the bovine mastitis.Materials and Methods:A total of 92 milk samples from bovine mastitis cases were sampled in and around Puducherry (Southern India). Among these samples, 30 isolates were bacteriologically characterized as E. coli. Minimum inhibitory concentrations (MIC) of fluoroquinolones of these 30 E. coli isolates were evaluated by resazurin microtiter assay. Then, the quinolone resistance determining region (QRDR) (gyrA and parC genes) of these E. coli isolates was genetically analyzed for determining the chromosomal mutation causing fluoroquinolone resistance.Results:E. coli isolates showed a resistance rate of 63.33%, 23.33% and 30.03% to nalidixic acid, ciprofloxacin and enrofloxacin, respectively. Mutations were found at 83rd and 87th amino acid position of gyrA gene, and at 80th and 108th amino acid position of parC gene in our study isolates. Among these five isolates, one had a single mutation at 83 amino acid position of gyrA with reduced susceptibility (0.5 µg/ml) to ciprofloxacin. Then, in remaining four isolates, three isolates showed triple mutation (at gyrA: S83⟶L and D87⟶N; at parC: S80⟶I) and the fifth isolate showed an additional mutation at codon 108 of parC (A108⟶T) with the increased ciprofloxacin MIC of 16-128 µg/ml. The most common mutation noticed were at S83⟶L and D87⟶N of gyrA and S80⟶I of ParC.Conclusion:The study confirms the presence of mutation/s responsible for fluoroquinolone resistance in QRDR of gyrA and parC genes of E. coli isolates of animal origin, and there is increased rate of fluoroquinolone resistance with high-level of MIC. The mutations observed in this study were similar to that of human isolates.

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Prevalence and Molecular Characterization of Fluoroquinolone Resistance inEscherichia coliIsolates from Dairy Cattle with Endometritis in China

Cited by 27 publications

References 41 publications

Baicalin Alleviates Lipopolysaccharide-Induced Liver Inflammation in Chicken by Suppressing TLR4-Mediated NF-κB Pathway

Baicalin Alleviates Lipopolysaccharide-Induced Liver Inflammation in Chicken by Suppressing TLR4-Mediated NF-κB Pathway

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Genetic characterization of fluoroquinolone-resistant Escherichia coli associated with bovine mastitis in India

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