Muellerklausen6642

n 0.01) in the expression of all tested efflux pump genes in treated E. coli, K. pneumoniae and P. aeruginosa isolates with EDTA compared to untreated isolates was observed. In conclusion, these results suggest that the combination of antibiotic especially gentamicin with EDTA may be fruitful for management of resistant gram negative infections.Streptococcus mutans is the most important acid-producing pathogen that causes dental caries, while Candida albicans is an opportunistic fungal pathogen that is frequently detected in conjunction with heavy infection by S. mutans. Their interactions in dental plaque biofilms remain unclear. Extracellular DNA (eDNA) is found in oral biofilms, but its effects have not been thoroughly defined. In this study, the role of eDNA in dual-species biofilms formed by S. mutans and C. albicans was investigated. With eDNA removal, the growth of both strains was not affected, but the formation of dual-species biofilms obviously decreased. In addition, the removal of eDNA spatially disrupted the structure of the dual-species biofilm. It was also shown that eDNA mainly affected the initial attachment and development stages of the dual-species biofilms but not the well-developed biofilms. A similar phenomenon was also observed in the cell viability of dual-species biofilms after DNase I treatment. To further exploration, we analyzed the expression of genes associated with biofilm formation in both S. mutans and C. albicans. We determined that the co-cultivation of S. mutans and C. albicans promotes the expression of genes related to extracellular polysaccharide production (e.g., gtfC), adhesion (e.g., spaP, epa1), mycelial transformation (e.g., hwp1), and drug resistance (e.g., cdr2). However, these genes were significantly downregulated when the eDNA of the dual-species biofilm was removed by adding DNase I compared to those untreated groups. Altogether, eDNA removal, such as that by DNase I treatment, could be considered a promising strategy to control oral biofilms and biofilm-associated oral diseases.Although the study of immune priming in insects is a growing area of research, its occurrence in various biological models has not been evaluated, and its mechanisms are poorly understood. Whether entomopathogenic nematodes (EPNs) can induce immune priming and what role their virulence might play in it has not been assessed. Here, we tested for the first time 1) whether a nematode is capable of eliciting immune priming, and 2) whether nematode virulence affects immune priming. Host larvae of Tenebrio molitor were first exposed to one of two EPN strains (low or high virulence). They were then exposed again to a challenge (high) dose of their respective strain, and their survival was recorded. Based on current literature, we expected that host larvae primed with a low-virulence strain would not show immune priming but that those exposed to a high-virulence strain would. Instead, we found that host larvae primed with either strain did not exhibit immune priming. Further, the survival of the hosts primed with the highly virulent strain was significantly reduced relative to the control group, and no measurable immune priming was found, as also indicated by resting metabolic rate (production of CO2). read more Future research is needed to determine whether virulence-associated bacteria underlie this lowered survival and/or whether another factor, such as immune evasion strategies, is related to these results.Staphylococcus aureus (S. aureus) is a frequent and major cause of bovine mastitis; it poses a tremendous economic burden to dairy industries of numerous countries. Early-secretion antigen-6 secretion system (ESS) has been viewed as an essential virulence and pathogenic factor of S. aureus. EsxA and EsxB are small acidic proteins secreted by ESS and identified as potential T-cell antigens of S. aureus. Unlike those of Mycobacterium tuberculosis (M. tuberculosis), the EsxA and EsxB of S. aureus do not form a dimer. Instead, EsxA dimerizes with itself or EsaC. Therefore, the interaction of EsxA and EsxB remains incompletely understood. In this study, to explore their interactions, EsxA and EsxB were expressed and used for immunization, alone or in combination, of murine infection models. Both components can interact with each other. Through the analysis of the immune response by immunological method, EsxB could significantly enhance the EsxA-specific IgG2a antibody level and increase the proliferation proportion of CD8+ T cells. These results indicate that when vaccinated with EsxA, EsxB can play a critical role in stimulating T helper 1 immunity by activating IgG2a and CD8+ T cells. We further show that vaccination with the combination of EsxA and EsxB resulted in enhanced stimulation of TLR-4 and improved protection against S. aureus. The findings may help us better understand the role of EsxB in the virulence and pathogenesis of S. aureus.Hypervirulent Klebsiella pneumoniae (hvKP), an increasing important pathotype, was initially recognized as a cause of severe liver abscesses and subsequently as a cause of other complications posing a clinical threat. Outer membrane vesicles (OMVs) secreted from abundant gram-negative bacteria are considered an important vehicle for delivery of effector molecules to target cells. However, the products and role in bacterial pathogenesis of OMVs secreted from hvKP, have not yet been determined. In order to examine the production of OMVs from hvKP and to determine their effects on the stimulation of the host innate immune response, we used ultracentrifugation to obtain homogeneous OMVs from hvKP ATCC 1706 cultured in vitro. Proteomic analysis was performed and hvKP OMVs were found to contain diverse proteins. Furthermore, hvKP OMVs exhibited discrepant cytotoxic effects on different cell types, in vitro. The vesicles induced the expression of proinflammatory cytokines including interleukin (IL)-6 and IL-8 in host cells. In addition, transtracheal injection of hvKP OMVs in wild-type mice led to an inflammatory response manifested by elevated levels of pro-inflammatory mediators including IL-6, IL-8 and TNF-α in bronchoalveolar lavage fluid (BAL), in accord with in vitro experiments. However, hvKP OMVs were insufficient to kill mice. In summary, OMVs originating from hvKP may serve to provoke the inflammatory response.