A single-cell atlas of mouse central nervous system immune cells reveals unique infection-stage immune signatures during the progression of meningitis caused by Streptococcus suis.

Meningitis caused by Streptococcus suis serotype 2 (SS2) in humans and pigs is an acute nervous disorder associated with serious sequelae. Bacterial meningitis is tightly associated with immune cell responses and the local immune microenvironment. However, the dynamic changes of the immune system during the disease progression in the brain remains unclear.

Establishment of an ELISA for the detection of antibodies against Stenotrophomonas maltophilia.

Background: Stenotrophomonas maltophilia (S. maltophilia) is a conditionally pathogenic bacterium around the world. In humans, it mainly harms patients with immunodeficient or chronic diseases, leading to high mortality rate of patients with pneumonia and bacteremia.

Carbon dot-based treatment for bacterial pneumonia by promoting a PI3K-mediated M1 polarization of macrophages.

As the incessant emergence of drug-resistant bacterial strains, bacterial pneumonia poses a serious threat to the public health worldwide. There is an urgent need to explore unconventional therapeutic strategies. Carbon dots are usually designed to directly kill bacteria, however, carbon dots that enhance the anti-infection function of immune cells are rarely reported.

Identification and characterization of ugpE associated with the full virulence of Streptococcus suis.

Streptococcus suis (S. suis) is an emerging zoonotic pathogen that threatens both animal and human health worldwide. UgpE is a protein subunit of the Ugp (uptake of glycerol phosphate) transporter system that is involved in glycerophospholipid synthesis in bacterial membranes.

Mass cytometry analysis reveals a cross-tissue immune landscape in -induced pneumonia.

Unlabelled: Porcine contagious pleuropneumonia caused by (APP) is a fatal respiratory disease that threatens the worldwide farming industry's health. The immune responses of extrapulmonary tissues play an important role in developing porcine contagious pleuropneumonia; however, the immune responses of extrapulmonary tissues induced by APP are rarely uncovered. Here, we used high-dimensional mass cytometry to investigate the immune cell response in the spleen and peripheral blood during APP infection in mice.

Metabolic signaling of ceramides through the FPR2 receptor inhibits adipocyte thermogenesis.

Ceramides play a central role in human health and disease, yet their role as systemic signaling molecules remain poorly understood. In this work, we identify formyl peptide receptor 2 (FPR2) as a membrane receptor that specifically binds long-chain ceramides (C14 to C20). In brown and beige adipocytes, C16:0 ceramide binding to FPR2 inhibits thermogenesis through G cyclic adenosine monophosphate signaling pathways, an effect that is reversed in the absence of FPR2.

Sodium Butyrate Alleviates Heat Stress-Induced Oxidative Stress and Skeletal Muscle Homeostasis Disruption by Promoting Autophagy in Mice.

Background: The gradual rise in global temperatures can affect skeletal muscle development and intestinal microorganisms. However, the influence of microbial metabolites on skeletal muscle homeostasis under heat stress (HS) remains unclear.

Methods: C57BL/6J mice were exposed to normal temperature or 40 °C conditions for 3 d, 7 d, or 14 d.

Brain Immune Cell Infiltration and Serum Metabolomic Characteristics Reveal that Lauric Acid Promotes Immune Cell Infiltration in Brain and Streptococcus suis Meningitis in Mice.

Although naturally Streptococcus suis serotype 2 (SS2) causes meningitis resulting in death or sequela of neurological symptoms in pigs and humans, severely threatening public health in the world, it has been difficult to build up and confirm experimental meningitis mouse models with obvious neurological syndrome for about two decades, which strongly hampers the in-depth study on the control measures and mechanisms of SS2-induced meningitis. In this study, a typical meningitis mouse model of SS2 was successfully established, as confirmed by the behavioral indicators of balance beam test, suspension test, and gait analysis. With bacteria gathering in the brain, distinguishable unique features including meningeal thickening, vacuolization of the Nissl body, brain barrier damage, glial cell activation, and more infiltration of T cells, macrophages, and DCs are observed in SS2 meningitis mice with typical neurological signs.

Identification and application of an endophytic fungus from against crop fungal disease.

Endophytic fungi are important microbial resources for developing novel antibacterial and antifungal drugs to prevent and control crop diseases. has been used as a Chinese medicinal herb for a long time, as it has various bioactivities. However, information on endophytic fungi isolated from is rare.

Enolase of Streptococcus suis serotype 2 promotes biomolecular condensation of ribosomal protein SA for HBMECs apoptosis.

Background: Ribosomal protein SA (RPSA) of human brain microvascular endothelial cells (HBMECs) can transfer from the cytosol to the cell surface and act as a receptor for some pathogens, including Streptococcus suis serotype 2 (SS2), a zoonotic pathogen causing meningitis in pigs and humans. We previously reported that SS2 virulence factor enolase (ENO) binds to RPSA on the cell surface of HBMECs and induces apoptosis. However, the mechanism that activates RPSA translocation to the cell surface and induces ENO-mediated HBMEC apoptosis is unclear.

Development and application of an indirect ELISA and nested PCR for the epidemiological analysis of among pigs in China.

Introduction: () is an important opportunistic and zoonotic pathogen which is associated with many diseases in humans and animals. However, the pathogenicity of has been neglected and the prevalence of is poorly studied due to the lack of rapid and sensitive diagnosis techniques.

Methods: In this study, we infected mice and pigs with strain from a human patient.

O-acetyl-homoserine sulfhydrylase deficient Streptococcus suis serotype 2 strain SC19 becomes an avirulent strain and provides immune protection against homotype infection in mice.

O-acetyl-homoserine sulfhydrylase (OAHS) is a pyridoxal 5'-phosphate-dependent enzyme involved in microbial methionine biosynthesis, which catalyzes the conversion of o-acetyl-homoserine (OAH) to homocysteine. In our previous study, we found that OAHS of Streptococcus suis serotype 2 (SS2) can interact with the porcine blood-brain barrier (BBB) model, but whether OAHS regulates the penetration of BBB during SS2 infection is still unclear. To explore the role of OAHS in SS2 infection, OAHS-deficient SS2 mutant strain (SC19-ΔOAHS) and gene complemental strain (SC19-cΔOAHS) were constructed.

Tracheal epithelial cell-exosome-derived MiR-21-5p inhibits alveolar macrophage pyroptosis to resist pulmonary bacterial infection through PIK3CD-autophagy pathway.

Aims: Structural cells play an important role in regulating immune cells during infection. Our aim was to determine whether structural porcine tracheal epithelial cells (PTECs) can regulate alveolar macrophages (AMs) to prevent bacterial pneumonia, explore the underlying mechanism(s) and therapeutic target.

Materials And Methods: Actinobacillus pleuropneumoniae (APP) was used as the model strain for infection studies.

High-dimensional analysis reveals an immune atlas and novel neutrophil clusters in the lungs of model animals with Actinobacillus pleuropneumoniae-induced pneumonia.

Due to the increase in bacterial resistance, improving the anti-infectious immunity of the host is rapidly becoming a new strategy for the prevention and treatment of bacterial pneumonia. However, the specific lung immune responses and key immune cell subsets involved in bacterial infection are obscure. Actinobacillus pleuropneumoniae (APP) can cause porcine pleuropneumonia, a highly contagious respiratory disease that has caused severe economic losses in the swine industry.

Characterisation of Variants of Cyclic di-GMP Turnover Proteins Associated with Semi-Constitutive rdar Morphotype Expression in Commensal and Uropathogenic Strains.

Expression of rdar (red, dry, and rough) colony morphology-based biofilm formation in is highly variable. To investigate the molecular mechanisms of semi-constitutive rdar morphotype formation, we compared their cyclic di-GMP turnover protein content and variability to the highly regulated, temperature-dependent morphotype of the historical and modern ST10 isolates MG1655 and Fec10, respectively. Subsequently, we assessed the effects of cyclic di-GMP turnover protein variants of the EAL phosphodiesterases YcgG and YjcC and the horizontally transferred diguanylate cyclase DgcX on biofilm formation and motility.

An In-Situ Tester for Extracting Piezoresistive Coefficients.

In this study, an electrostatic force-driven on-chip tester consisting of a mass with four guided cantilever beams was employed to extract the process-related bending stiffness and piezoresistive coefficient in-situ for the first time. The tester was manufactured using the standard bulk silicon piezoresistance process of Peking University, and was tested on-chip without additional handling. In order to reduce the deviation from process effects, the process-related bending stiffness was first extracted as an intermediate value, namely, 3590.

Adh Promotes Survival in Porcine Alveolar Macrophages by Inhibiting CHAC2-Mediated Respiratory Burst and Inflammatory Cytokine Expression.

() causes porcine pleuropneumonia that seriously endangers pig's health. Adh, located in the head region of trimeric autotransporter adhesion of , affects bacterial adhesion and pathogenicity. However, how Adh mediates immune invasion is still unclear.

Untargeted metabolomics reveals alternations in metabolism of bovine mammary epithelial cells upon IFN-γ treatment.

Background: IFN-γ is a pleiotropic cytokine that has been shown to affect multiple cellular functions of bovine mammary epithelial cells (BMECs) including impaired milk fat synthesis and induction of malignant transformation via depletion of arginine, one of host conditionally essential amino acids. But the molecular mechanisms of these IFN-γ induced phenotypes are still unknown.

Methods: BMECs were treated with IFN-γ for 6 h, 12 h, and 24 h.

Metagenomics analysis reveals potential pathways and drivers of piglet gut phage-mediated transfer of ARGs.

The growing prevalence of antibiotic-resistant pathogens has led to a better understanding of the underlying processes that lead to this expansion. Intensive pig farms are considered one of the hotspots for antibiotic resistance gene (ARG) transmission. Phages, as important mobile carriers of ARGs, are widespread in the animal intestine.

Recent advances on the regulation of bacterial biofilm formation by herbal medicines.

Biofilm formation is a fundamental part of life cycles of bacteria which affects various aspects of bacterial-host interactions including the development of drug resistance and chronic infections. In clinical settings, biofilm-related infections are becoming increasingly difficult to treat due to tolerance to antibiotics. Bacterial biofilm formation is regulated by different external and internal factors, among which quorum sensing (QS) signals and nucleotide-based second messengers play important roles.

Therapeutic effects of JLX001 on neuronal necroptosis after cerebral ischemia-reperfusion in rats.

In recent years, more attention has been given to novel patterns of cell death observed during ischemia/reperfusion (I/R). Necroptosis is a regulable secondary cell death pathway; necroptosis is different from traditional forms of cell death, and it is regulated by the RIPK1-RIPK3-MLKL signaling pathway. JLX001 is the double hydrochloride of the natural compound cyclovirobuxine D (CVB-D).

LAP3 contributes to IFN-γ-induced arginine depletion and malignant transformation of bovine mammary epithelial cells.

Background: IFN-γ has been traditionally recognized as an inflammatory cytokine that involves in inflammation and autoimmune diseases. Previously we have shown that sustained IFN-γ induced malignant transformation of bovine mammary epithelial cells (BMECs) via arginine depletion. However, the molecular mechanism underlying this is still unknown.

Carnosine Synthase 1 Contributes to Interferon Gamma-Induced Arginine Depletion via Mitogen-activated Protein Kinase 11 Signaling in Bovine Mammary Epithelial Cells.

Arginine is one of the host semiessential amino acids with diverse biological activities, and arginine depletion is associated with the incidence of many diseases. Arginine depletion induced by diet-derived interferon gamma (IFN-γ) leads to malignant transformation and impaired milk quality in healthy lactating bovine mammary epithelial cells (BMECs). However, the molecular mechanism of IFN-γ-induced arginine depletion is unclear.

Novel strategies to promote resolution of inflammation to treat lower extremity artery disease.

Lower extremity artery disease (LEAD) is a chronic inflammatory disease that occurs when atherosclerotic plaques form in the lower extremities, which may lead to amputation if not manged properly. Given clinical standardcare (pharmacological and surgical) have limited efficacy in LEAD, developing novel strategies to manage LEAD remains an unmet clinical need. Given that active resolution of inflammation is essential to facilitate tissue healing and repair, failure to resolve inflammation may lead to chronic inflammation, dysregulated cellular homeostasis and adverse tissue remodeling.

Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is clinically characterized by a progressive increase in pulmonary artery pressure, followed by right ventricular hypertrophy and subsequently right heart failure. The underlying mechanism of PAH includes endothelial dysfunction and intimal smooth muscle proliferation. Numerous studies have shown that oxidative stress is critical in the pathophysiology of PAH and involves changes in reactive oxygen species (ROS), reactive nitrogen (RNS), and nitric oxide (NO) signaling pathways.