Contribution of mammary epithelial cells to the immune response during early stages of a bacterial infection to Staphylococcus aureus

f During infectious processes, antimicrobial proteins are produced by both epithelial cells and innate immune cells. Some of these antimicrobial molecules function by targeting transition metals and sequestering these metals in a process referred to as "nutritional immunity." This chelation strategy ultimately starves invading pathogens, limiting their growth within the vertebrate host. Recent evidence suggests that these metal-binding antimicrobial molecules have the capacity to affect bacterial virulence, including toxin secretion systems. Our previous work showed that the S100A8/S100A9 heterodimer (calprotectin, or calgranulin A/B) binds zinc and represses the elaboration of the H. pylori cag type IV secretion system (T4SS). However, there are several other S100 proteins that are produced in response to infection. We hypothesized that the zinc-binding protein S100A12 (calgranulin C) is induced in response to H. pylori infection and also plays a role in controlling H. pylori growth and virulence. To test this, we analyzed gastric biopsy specimens from H. pylori-positive and -negative patients for S100A12 expression. These assays showed that S100A12 is induced in response to H. pylori infection and inhibits bacterial growth and viability in vitro by binding nutrient zinc. Furthermore, the data establish that the zinc-binding activity of the S100A12 protein represses the activity of the cag T4SS, as evidenced by the gastric cell "hummingbird" phenotype, interleukin 8 (IL-8) secretion, and CagA translocation assays. In addition, high-resolution field emission gun scanning electron microscopy (FEG-SEM) was used to demonstrate that S100A12 represses biogenesis of the cag T4SS. Together with our previous work, these data reveal that multiple S100 proteins can repress the elaboration of an oncogenic bacterial surface organelle. Helicobacter pylori is a Gram-negative member of the Epsilonproteobacteria commonly found in the human stomach (1). More than 50% of the world's population is chronically infected with H. pylori, despite a robust immune response to this bacterium (2, 3). The vast majority of infected persons exhibit no symptoms of disease; however, the presence of this pathogen can increase the risk of negative outcomes, including duodenal ulcer, dysplasia, mucosa-associated lymphoid tissue (MALT) lymphoma, and invasive gastric cancer (4). Negative outcomes of H. pylori infection are associated with multiple factors, including host genetics, environmental contributions such as diet and smoking, and bacterial virulence properties.One major virulence factor that contributes to H. pylori-associated disease outcomes is the cag pathogenicity island-encoded type IV secretion system (cag T4SS) (5). The cag T4SS is a macromolecular nanomachine responsible for translocating substrates, including peptidoglycan and the oncogenic effector molecule CagA, into host epithelial cells (6). The translocation activity of the cag T4SS leads to multiple consequences in host cell biology, including cytoskeletal rearrangements, indu...

Objective. The objective of this study was to evaluate the effect of subclinical infection by agents of tick fever in dairy cattle on milk parameters, such as production, composition, and quality. Materials and methods. The study was conducted in a private farm with 75 free-stall-housed dairy cows, from which 37 were evaluated. Monthly, individual milk samples were collected for compositional (fat, lactose, protein, and total solids) and quality (somatic cell counts (SCC)) analyses. In addition, blood samples were collected in order to identify cows that were tick fever-negative and positive by PCR for one or more of the following etiological agents: Babesia bovis, Babesia bigemina and Anaplasma marginale. Results. The results showed increased SCC in positive animals for at least one of the agents when compared to non-infected cows (p<0.05). Milk production was significantly lower in A. marginale positive animals (p<0.05). An increase of about 40% in milk solids content was found in B. bovis positive cows. Also, an increment of approximately 23% in lactose was found on cows positives for B. bigemina. Conclusions. We may conclude that the presence of at least one of these parasites in dairy cattle affects composition or quality of their milk.Keywords: Infectious agents, SCC, lactose, total solids (Source: CAB, MeSH). RESUMENObjetivo. El objetivo de este estudio fue evaluar el efecto de la infección subclínica por agentes de la fiebre por garrapatas en el ganado lechero en producción de leche, la composición y calidad. Materiales y métodos. El estudio se realizó en una finca privada con 75 vacas lecheras alojadas-libre puesto, y de estas se evaluaron 37. Se recogieron muestras de leche individuales mensuales para determinar la composición (grasa, lactosa, proteína y sólidos totales) y la calidad (recuento de células somáticas (SCC)). Además, se recogieron muestras de sangre para identificar vacas que fueron negativas a fiebre de garrapatas y positivos por PCR para uno o más de los siguientes agentes etiológicos: Babesia Influence of subclinical infection by agents of tick fever in milking dairy cows

Bovine mastitis is the most common disease in dairy cattle. Bacterial infections are the main cause of mastitis. Lipopolysaccharide (LPS), a major structural component of the cell wall of Escherichia coli, is a good inducer used to replicate inflammation models. 8‐Methoxypsoralen (8‐MOP), a formerly considered photosensitizing agent, has been used in immunotherapy. This study investigated the protective effects of 8‐MOP on LPS‐induced inflammatory injury in bovine mammary epithelial cells (BMECs). LPS treatment (50 μg/mL for 12 hr) caused a decrease in cell viability, morphological damage, and cell apoptosis. Pretreatment with 8‐MOP at concentrations of 25 and 50 μg/ml significantly attenuated LPS‐induced inflammation in BMECs. qRT‐PCR analysis revealed that the messenger RNA expression of inflammatory cytokines and chemokine (interleukin‐1β [IL‐1β], IL‐6, tumor necrosis factor‐α, and IL‐8) was suppressed by 8‐MOP in LPS‐stimulated BMECs. Western blot analysis showed that 8‐MOP could also reduce the protein levels of cyclooxygenase‐2 and promote the translocation of high‐mobility group box 1 from the nucleus to cytoplasm. Furthermore, the anti‐inflammatory property of 8‐MOP was mediated by inhibiting nuclear factor kappa‐light‐chain‐enhancer of activated B cells activation and STAT1 phosphorylation. Taken together, 8‐MOP could protect cells from inflammatory injury induced by LPS, and may be a potential agent against bovine mastitis.