Injury of Macrophages Induced by Type C Exotoxins.

is a kind of anaerobic Gram-positive bacterium that widely exists in the intestinal tissue of humans and animals. And the main virulence factor in is its exotoxins. type C is the main strain of livestock disease, its exotoxins can induce necrotizing enteritis and enterotoxemia, which lead to the reduction in feed conversion, and a serious impact on breeding production performance.

Dual-specificity phosphatase 5-mediated fatty acid oxidation promotes Mycobacterium bovis BCG -induced inflammatory responses.

Mycobacterium tuberculosis (Mtb) reprograms FAs metabolism of macrophages during infection and affects inflammatory reaction eventually, however, the mechanism remains poorly understood. Here we show that Mycobacterium bovis (BCG) induces DUSP5 expression through TLR2-MAPKs signaling pathway and promotes fatty acid oxidation (FAO). Silencing DUSP5 by adeno-associated virus vector (AAV) ameliorates lung injury and DUSP5 knockdown reduces the expression of IL-1β, IL-6 and inactivated NF-κB signaling in BCG-infected macrophages.

Pyroptosis of Macrophages Induced by Beta-1 Toxin.

beta-1 toxin (CPB1) is responsible for necrotizing enteritis and enterotoxemia. However, whether the release of host inflammatory factors caused by CPB1 is related to pyroptosis, an inflammatory form of programmed cell death, has not been reported. A construct expressing recombinant beta-1 toxin (rCPB1) was created, and the cytotoxic activity of the purified rCPB1 toxin was assessed via CCK-8 assay.

Vitamin C inhibits apoptosis in THP‑1 cells in response to incubation with Mycobacterium tuberculosis.

Tuberculosis (TB) is a chronic and fatal zoonotic infectious disease caused by () infection. The THP-1 cell line is a cell model for studying the function, mechanism and signaling pathways of macrophages; macrophages are the primary host cells of . Macrophages are important for the progression of tuberculosis, as they affect the release of various inflammatory cytokines, including IL-1β, IL-6 and TNF-α.

polysaccharide attenuates pyocyanin-induced cellular injury in mice airway epithelial cells.

Background: berries have been utilized in Asia for many years. However, the mechanisms of its lung-defensive properties are indeterminate.

Objective: We investigate whether polysaccharide (LBP) could weaken infection-induced lung injury.

Vitamin D3 promotes autophagy in THP-1 cells infected with .

Tuberculosis (TB) is a major disease that causes mortality worldwide. The lethality of this disease is a result of the contagious bacteria . Infection can inhibit phagosomal maturation, with mainly attacking macrophages and inhibiting autophagy and apoptosis.

Transcriptomic analyses reveal dynamic changes of defense response in Glycyrrhiza uralensis leaves under enhanced ultraviolet-B radiation.

The amount of solar ultraviolet-B (UV-B) radiation reaching the Earth's surface is increasing due to stratospheric ozone dynamics and global climate change. Increased UV-B radiation poses a major threat to ecosystems. Although many studies have focused on the potential effects of enhanced UV-B radiation on plants, the dynamic changes of defense response in plants under continuous UV-B radiation remains enigmatic.

DUSP5 (dual-specificity protein phosphatase 5) suppresses BCG-induced autophagy via ERK 1/2 signaling pathway.

Autophagy is considered as an effective strategy for host cells to eliminate intracellular Mycobacterium tuberculosis (Mtb). Dual-specificity phosphatase 5 (DUSP5) is an endogenous phosphatase of ERK1/2, and plays an important role in host innate immune responses, its function in autophagy regulation however remains unexplored. In the present study, the function of DUSP5 in autophagy in Mycobacterium bovis Bacillus Calmette-Guerin (BCG)-infected RAW264.

Modulation of Wnt/β-catenin signaling in IL-17A-mediated macrophage polarization of RAW264.7 cells.

Macrophages play pivotal roles in host defense and immune homeostasis, which have two major functional polarization states, the classically activated M1 and the alternatively activated M2. Interleukin (IL)-17A is an immune modulator able to shape macrophage phenotypes. Wnt/β-catenin is a developmental signaling pathway that plays crucial roles in morphogenesis and tissue homeostasis, which has also been recently demonstrated playing roles in immune regulation.

N-acetylcysteine (NAC) Attenuating Apoptosis and Autophagy in RAW264.7 Cells in Response to Incubation with Mycolic Acid from Bovine Complex.

Bovine tuberculosis is an airborne infectious disease caused by organisms of the (MTB) complex. Mycolic acid (MA) is the main lipid component of the cell membrane of MTB. It is non-enzymatically reduced by NAD(P)H and further produces reactive oxygen species (ROS), which can cause oxidative stress in human cells.

Capsular Polysaccharide is a Main Component of in the Pathogen-Induced Toll-Like Receptor-Mediated Inflammatory Responses in Sheep Airway Epithelial Cells.

() is characterized as an etiological agent of primary atypical pneumonia that specifically infects sheep and goat. In an attempt to better understand the pathogen-host interaction between the invading and airway epithelial cells, we investigated the host inflammatory responses against capsular polysaccharide (designated as CPS) of using sheep bronchial epithelial cells cultured in an air-liquid interface (ALI) model. Results showed that CPS derived from could activate toll-like receptor- (TLR-) mediated inflammatory responses, along with an elevated expression of nuclear factor kappa B (NF-B), activator protein-1 (AP-1), and interferon regulatory factor 3 (IRF3) as well as various inflammatory-associated mediators, representatively including proinflammatory cytokines, such as IL1, TNF, and IL8, and anti-inflammatory cytokines such as IL10 and TGF of TLR signaling cascade.

Capsular Polysaccharide of Induces Sheep Airway Epithelial Cell Apoptosis ROS-Dependent JNK/P38 MAPK Pathways.

In an attempt to better understand the pathogen-host interaction between invading () and sheep airway epithelial cells, biological effects and possible molecular mechanism of capsular polysaccharide of (CPS) in the induction of cell apoptosis were explored using sheep bronchial epithelial cells cultured in air-liquid interface (ALI). The CPS of was first isolated and purified. Results showed that CPS had a cytotoxic effect by disrupting the integrity of mitochondrial membrane, accompanied with an increase of reactive oxygen species and decrease of mitochondrial membrane potential (ΔΨ).

The Generation and Characterization of Recombinant Protein and Antibodies of Beta2 Toxin.

() beta2 toxin (CPB2) is an important virulent factor of necrotic enteritis in both animals and humans. However, studies of its pathogenic roles and functional mechanisms have been hampered due to the difficulty of purification and lack of specific antibodies against this toxin. A recombinant His-tagged beta2 (rCPB2) toxin and monoclonal antibodies (McAbs) against CPB2 were generated and characterized by assays of cytotoxicity, immunoblotting, ELISA, neutralization, and immunofluorescence.