Brucella abortus transcriptional regulator ArsR6 inhibits host pyroptosis via BAB_RS28760 by triggering the endoplasmic reticulum stress pathway.

Pyroptosis, which is accompanied by inflammatory responses, is critical for pathogen clearance. However, the mechanism through which Brucella evades host pyroptosis remains unclear. The transcriptional regulator ArsR6 maintains bacterial intracellular homeostasis and possibly influences host cell death.

A Case Report of Meningitis Caused by Biovar 3.

Background: Brucellosis, a major endemic disease in northern China, is contracted by zoonosis of . We report a case of meningitis caused by biovar 3.

Case Presentation: A 46-year-old man was hospitalized at a local medical facility due to symptoms of fever, soreness, and weakness on April 16, 2021.

secretory protein VceA promotes FOXO1 entry into the nucleus to shift host cell metabolism toward glycolysis.

Increased glycolytic metabolism is a key step in the reproduction of and the induction of brucellosis, however, little is known about how this process is regulated during infection. Forkhead box protein O1 (FOXO1) is a transcription factor that regulates energy metabolism. In this study, we employ the yeast two-hybrid system (Y2H) and immunoprecipitation (Co-IP) to reverse screen for the FOXO1 for the first time and identify interactions between FOXO1 and the secretory protein VceA.

Brucella induced upregulation of NO promote macrophages glycolysis through the NF-κB/G6PD pathway.

Increased glycolytic metabolism recently emerged as an essential process driving host defense against Brucella, but little is known about how this process is regulated during infection. We have identified a critical role for nuclear factor kappa B (NF-κB) transcription factor regulation in glycolytic switching during Brucella infection for the first time. Chromatin immunoprecipitation with next-generation sequencing for NF-κB and DNA Pull-Down revealed two novel NF-κB-binding sites in the enhancer region of the Nitric oxide (NO)production-response regulator gene glucose-6-phosphate dehydrogenase (G6PD), which is important for the switch to glycolysis during a Brucella infection.

Systemic Pharmacology Reveals the Potential Targets and Signaling Mechanisms in the Adjuvant Treatment of Brucellosis with Traditional Chinese Medicine.

Human brucellosis is one of the world's most common zoonoses, caused by infection and characterized by induced inflammation, which in severe cases can lead to abortion and sterility in humans and animals. There is growing evidence that traditional Chinese medicine (TCM) is beneficial as an adjunct to the treatment of brucellosis. However, its specific targets of action and molecular mechanisms remain unclear.

modulates macrophage polarization and inflammatory response by targeting glutaminases through the NF-κB signaling pathway.

Objectives: The mechanism of Brucella infection regulating macrophage phenotype has not been completely elucidated until now. This study aimed to determine the mechanism of in the modulation of macrophage phenotype using RAW264.7 cells as a model.

The Flagellar Transcriptional Regulator FtcR Controls 16M Biofilm Formation via a -Mediated Pathway in Response to Hyperosmotic Stress.

The expression of flagellar proteins in species likely evolved through genetic transference from other microorganisms, and contributed to virulence, adaptability, and biofilm formation. Despite significant progress in defining the molecular mechanisms behind flagellar gene expression, the genetic program controlling biofilm formation remains unclear. The flagellar transcriptional factor (FtcR) is a master regulator of the flagellar system's expression, and is critical for 16M's flagellar biogenesis and virulence.

Survival characteristics and transcriptome profiling reveal the adaptive response of the 16M biofilm to osmotic stress.

can inhabit hostile environments, including osmotic stress. How responds collectively to osmotic stress is largely unexplored, particularly in spatially structured communities such as a biofilm. To gain insight into this growth mode, we set out to characterize the 16M biofilm, describe its phenotype, and carry out a comparative transcriptomic analysis between biofilms under osmotic stress and control conditions.

Molecular Detection of Zoonotic and Veterinary Pathogenic Bacteria in Pet Dogs and Their Parasitizing Ticks in Junggar Basin, North-Western China.

Despite the recognized epidemiological importance of ticks as vectors for pathogens that cause numerous zoonotic and veterinary diseases, data regarding the pathogens of pet dogs and their parasitic ticks in the Junggar Basin are scarce. In this study, a total of 178 blood samples and 436 parasitic ticks were collected from pet dogs in Junggar Basin, Xinjiang Uygur Autonomous Region (XUAR), north-western China. All ticks were identified as sensu stricto (s.

Corrigendum: -Induced Downregulation of lncRNA Gm28309 Triggers Macrophages Inflammatory Response Through the miR-3068-5p/NF-κB Pathway.

[This corrects the article DOI: 10.3389/fimmu.2020.

-Induced Downregulation of lncRNA Gm28309 Triggers Macrophages Inflammatory Response Through the miR-3068-5p/NF-κB Pathway.

Objectives: The underlying mechanism of the inflammatory response against Brucellosis caused by remains poorly understood. This study aimed to determine the role of long non-coding RNAs (lncRNAs) in regulating of inflammatory and anti- responses.

Materials And Methods: Microarray analysis was performed to detect differentially expressed lncRNAs in THP-1 cells infected with an S2308 strain.

Functional analysis of Bucella reveals transcriptional regulation of MarR.

Brucellosis is a zoonotic infectious disease caused by Brucella infection. MarR-family transcription factors are closely related to diverse physiological functions necessary for many pathogens adaptation to environmental changes. However, whether the MarR-family transcription factors are involved in virulence, mediated inflammatory responses and regulated virulence gene expression in the intracellular pathogen Brucella are still unknown.