Exfoliative toxin E, a new Staphylococcus aureus virulence factor with host-specific activity

Exfoliative toxin E, a new [i]Staphylococcus aureus[/i] virulence factor with host-specific activity. Microbes, 15e Congrès National de la SF

Inflammation, DNA damage and Staphylococcus aureus infection

Inflammation, DNA damage and Staphylococcus aureus infection. Meeting du LIA Bact-Infla

Invasion of the Host Epithelium by the Microorganisms: Good or Bad News for the Host?

The host epithelium has permanent contact with the environment and a multitude of diverse microorganisms, resulting in a network of the host's defense mechanisms. Pathogens use various strategies to invade epithelial barriers, to hijack eukaryotic host function to their own benefit and use the epithelium as a reservoir for dissemination throughout the host. Alteration of the host cell apoptosis, promotion of cell proliferation or conversely, inhibition of cell growth and modulation of the cell differentiation by blocking of cell cycle progression are some of them. The mechanisms all of the stratagems employed by the pathogens are not fully elucidated, but they can contribute to the virulence of those microorganisms. However, the latest investigation of the interaction between host epithelium and microorganisms suggest that the epithelium is not a simple mechanical barrier: epithelial cells recognize microorganisms and initiate appropriate signaling which contribute to the endocytosis of microorganisms. It appears that capture of microorganisms by the epithelial cells is selective and that the different endocytic mechanisms may be enhanced by proinflammatory cytokines. The specificity of the recognition is illustrated by the various studies, showing that the epithelial cells distinguish the different morphotypes of the microorganisms. Using the model of the infection of respiratory epithelium by opportunistic pathogen Aspergillus fumigatus, we have shown that the airway epithelial cells identify the most invasive fungal form that may be beneficial for the host defense. Moreover, host epithelium exposed to the microorganisms, express various cytokines and different protective substances, such as antimicrobial peptides, with direct microbicidal or chemotactic activities, which might contribute to the regulation of host adaptive immunity against microbial invasion. Autocrine mechanismes of antimicrobial peptides expression was shown with the epithelial cells exposed to Aspergillus fumigatus. Further study of the regulation of antimicrobial peptides expression might provide the new approaches that may enhance its expression for potential therapeutic use.Nevertheless, despite permanent exposure to a considerable amount of the microorganisms present in the environment, epithelium possesses the enormous capacity to keep its integrity, suggesting that some microbial strategies link to the mechanisms, which control the structural integrity of the tissue. Recent evidence supports the role of microbial factors in the maintenance of the integrity of the epithelial tissue: it was shown that Staphylococcus aureus as well as other microbial products induce epithelial repair, survival and growth and that such compensatory epithelial responses are mediated by autonomous non-inflammatory pathway. Therefore the outcome of the interaction between the host epithelium and microorganisms depends on multiple features

Invasion of the Host Epithelium by the Microorganisms: Good or Bad News for the Host?

The host epithelium has permanent contact with the environment and a multitude of diverse microorganisms, resulting in a network of the host's defense mechanisms. Pathogens use various strategies to invade epithelial barriers, to hijack eukaryotic host function to their own benefit and use the epithelium as a reservoir for dissemination throughout the host. Alteration of the host cell apoptosis, promotion of cell proliferation or conversely, inhibition of cell growth and modulation of the cell differentiation by blocking of cell cycle progression are some of them. The mechanisms all of the stratagems employed by the pathogens are not fully elucidated, but they can contribute to the virulence of those microorganisms. However, the latest investigation of the interaction between host epithelium and microorganisms suggest that the epithelium is not a simple mechanical barrier: epithelial cells recognize microorganisms and initiate appropriate signaling which contribute to the endocytosis of microorganisms. It appears that capture of microorganisms by the epithelial cells is selective and that the different endocytic mechanisms may be enhanced by proinflammatory cytokines. The specificity of the recognition is illustrated by the various studies, showing that the epithelial cells distinguish the different morphotypes of the microorganisms. Using the model of the infection of respiratory epithelium by opportunistic pathogen Aspergillus fumigatus, we have shown that the airway epithelial cells identify the most invasive fungal form that may be beneficial for the host defense. Moreover, host epithelium exposed to the microorganisms, express various cytokines and different protective substances, such as antimicrobial peptides, with direct microbicidal or chemotactic activities, which might contribute to the regulation of host adaptive immunity against microbial invasion. Autocrine mechanismes of antimicrobial peptides expression was shown with the epithelial cells exposed to Aspergillus fumigatus. Further study of the regulation of antimicrobial peptides expression might provide the new approaches that may enhance its expression for potential therapeutic use.Nevertheless, despite permanent exposure to a considerable amount of the microorganisms present in the environment, epithelium possesses the enormous capacity to keep its integrity, suggesting that some microbial strategies link to the mechanisms, which control the structural integrity of the tissue. Recent evidence supports the role of microbial factors in the maintenance of the integrity of the epithelial tissue: it was shown that Staphylococcus aureus as well as other microbial products induce epithelial repair, survival and growth and that such compensatory epithelial responses are mediated by autonomous non-inflammatory pathway. Therefore the outcome of the interaction between the host epithelium and microorganisms depends on multiple features

Invasion of the host epithelium by the microorganisms: Good or bad news for the host ?

absen

Inflammation, DNA damage and Staphylococcus aureus infection

Inflammation, DNA damage and Staphylococcus aureus infection. Meeting du LIA Bact-Infla

The secret weapon that allows Staphylococcus aureus to hijack your cell cycle

Statement of the Problem: Bacterial cyclomodulins are a growing family of microbial virulence factors that not only alter host cell cycle progression, but that also interfere with host cell activity, thus favoring the hijacking of host cell protective functions for their own benefit. Staphylococcus aureus (S. aureus), a highly versatile Gram-positive pathogen can cause life-threatening infections. The implications of S. aureus in the alteration of the eukaryotic cell cycle and the biological significance of such an alteration has not been fully investigated. The purpose of the study is to explore the mechanism and to identify staphylococcal compounds that caused host cell cycle arrest and to evaluate the benefit provided by cyclomodulins to bacteria. Methodology & Theoretical Orientation: Flow Cytometry analysis, size exclusion chromatography, mass spectroscopy analysis, Western blotting and immunofluorescence methods were used to identify staphylococcal cyclomodulins and characterize the mechanism. Findings: We demonstrated that S. aureus-induced G2/M transition delay was associated with the accumulation of inactive cyclin-dependent kinase Cdk1, a key inducer of mitosis entry, and with the accumulation of unphosphorylated histone H3. Phenol-soluble modulin a (PSMa) peptides were found responsible for this effect. The use of S. aureus mutants confirmed the findings. We showed that the G2 phase was preferential for bacterial proliferation and found that PSMa-induced G2/M transition delay correlated with a decrease in the defensins genes expression. We demonstrated that additionally to secreted staphylococcal cyclomodulins the membrane-anchored lipoprotein-like proteins exert cyclomodulin activity

Inflammation, DNA damage and Staphylococcus aureus infection

Inflammation, DNA damage and Staphylococcus aureus infection. Meeting du LIA Bact-Infla

Invasion of the host epithelium by the microorganisms: Good or bad news for the host ?

absen