scholarly journals Complement Inactivation Strategy of Staphylococcus aureus Using Decay-Accelerating Factor and the Response of Infected HaCaT Cells

2021 ◽  
Vol 22 (8) ◽  
pp. 4015
Author(s):  
Kyoung Ok Jang ◽  
Youn Woo Lee ◽  
Hangeun Kim ◽  
Dae Kyun Chung
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Cells ◽  
Respiratory Infections ◽  
Food Poisoning ◽  
Surface Expression ◽  
Host Cells ◽  
Hacat Cells ◽  
Decay Accelerating Factor ◽  
Ligand Expression ◽  
The Complement System

Staphylococcus aureus is a species of Gram-positive staphylococcus. It can cause sinusitis, respiratory infections, skin infections, and food poisoning. Recently, it was discovered that S. aureus infects epithelial cells, but the interaction between S. aureus and the host is not well known. In this study, we confirmed S. aureus to be internalized by HaCaT cells using the ESAT-6-like protein EsxB and amplified within the host over time by escaping host immunity. S. aureus increases the expression of decay-accelerating factor (CD55) on the surfaces of host cells, which inhibits the activation of the complement system. This mechanism makes it possible for S. aureus to survive in host cells. S. aureus, sufficiently amplified within the host, is released through the initiation of cell death. On the other hand, the infected host cells increase their surface expression of UL16 binding protein 1 to inform immune cells that they are infected and try to be eliminated. These host defense systems seem to involve the alteration of tight junctions and the induction of ligand expression to activate immune cells. Taken together, our study elucidates a novel aspect of the mechanisms of infection and immune system evasion for S. aureus.

scholarly journals Nilgirianthus ciliatus mediated Environment friendly extracellular synthesis of AgNps for exacting its potential against the Dengue vector, Aedes aegypti and the Microbial pathogen, Staphylococcus aureus

2018 ◽  
Vol 50 (1) ◽  
Author(s):  
K. Meenambigai ◽  
R. Kokila ◽  
A. Naresh Kumar
Keyword(s):  
Staphylococcus Aureus ◽  
Silver Nanoparticles ◽  
Aedes Aegypti ◽  
Respiratory Infections ◽  
Food Poisoning ◽  
Bacterial Pathogen ◽  
Multidrug Resistant ◽  
Particle Dispersion ◽  
Dengue Vector ◽  
Microbial Pathogen

Aedes aegypti, the dengue vector is a menace continues since 1780’s due to development of resistant to synthetic insecticides and Staphylococcus aureus, the common microbial pathogen agent of food poisoning, skin infections and respiratory infections have developed multidrug resistant, which forced us to focus on novel agent for which the dengue vector and bacterial pathogen have not practiced to develop resistant and which cannot detoxify it using its usual enzyme activity as it did earlier. Silver nanoparticles a challenging insecticidal agents for the toxic degrading enzymes of both the insect and microbe was the target of our present study to excavate the potential in killing immature of dengue vector and bacterial pathogen. Green protocolled nanoparticles were successfully synthesized using leaf extract of Nilgirianthus ciliatus which act as reducing as well as capping agents. The UV-vis spectra observed at 441nm confirmed the presence of silver nanoparticles. XRD and FT-IR confirmed the crystalline nature and organic capping around the silver nanoparticles respectively. SEM and DLS showed the average size at 117nm and the particle dispersion was at -17.2mV zeta potential.

scholarly journals Immune System Evasion Mechanisms in Staphylococcus aureus: Current Understanding

2020 ◽  
Vol 14 (4) ◽  
pp. 2219-2234
Author(s):  
Hesham A. Malak ◽  
Hussein H. Abulreesh ◽  
Sameer R. Organji ◽  
Khaled Elbanna ◽  
Mohammed R. Shaaban ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune System ◽  
Soft Tissue ◽  
Immune Cells ◽  
Bloodstream Infections ◽  
Host Cells ◽  
Human Pathogen ◽  
Immune Systems ◽  
Wide Range ◽  
New Strategy

Staphylococcus aureus is a major human pathogen that may cause a wide range of infections and is a frequent cause of soft tissue and bloodstream infections. It is a successful pathogen due to its collective virulence factors and its ability to evade the host immune systems. The review aims to highlight how S. aureus destroys and damage the host cells and explains how immune cells can respond to this pathogen. This review may also provide new insights that may be useful for developing new strategy for combating MRSA and its emerging clones such as community-associated methicillin-resistant S. aureus (CA-MRSA).

scholarly journals Decay-accelerating factor in the periovulatory rat ovary

2005 ◽  
Vol 186 (2) ◽  
pp. 303-313 ◽  
Author(s):  
Mary C Gieske ◽  
Gi Youn Na ◽  
Yongbum Koo ◽  
Misung Jo ◽  
Thomas E Curry ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Complement System ◽  
Northern Blot ◽  
Ovarian Tissue ◽  
Host Cells ◽  
Control Activity ◽  
Decay Accelerating Factor ◽  
Rat Ovary ◽  
The Complement System

One of the most prominent inflammatory reactions is the activation of the complement system. The activated complement system does not distinguish between pathogens and the host cell. In order to prevent autologous complement-mediated attack, host cells express a variety of both membrane-bound and fluid-phase complement regulatory proteins which control activity of the complement cascade by acting on convertase enzymes or the membrane-attack complex. Although the process of ovulation is facilitated by the inflammatory reaction, this reaction has the potential to cause serious damage to growing follicles, ovulated follicles, and other important ovarian tissues. This study was undertaken to characterize the expression and regulation of decay-accelerating factor (DAF), a complement regulator, as a potential mediator of ovarian tissue protection from ovulatory inflammation. DNA microarray and Northern blot analyses showed that an ovulatory gonadotropin stimulus dramatically yet transiently induced DAF mRNA expression in the immature rat ovary. Northern blot and PCR analyses revealed that of the three known DAF isoforms, glycosylphosphatidylinositol (GPI)-, soluble-, and transmembrane-(TM) DAF, GPI-DAF was the predominant form. In situ hybridization localized GPI-DAF mRNA expression in the theca-interstitial cells of the periovulatory ovary. Neither the anti-progestin RU486 nor the cyclooxygenase inhibitor indomethacin significantly inhibited human chorionic gonadotropin (hCG)-induced GPI-DAF mRNA expression in vivo. In vitro theca cell culture studies indicated that hCG induces GPI-DAF mRNA expression through the protein kinase A pathway. This study suggests that gonadotropin-induced GPI-DAF may be involved in the protection of ovarian tissues from the potential attack by the complement system activated by the inflammatory response associated with ovulation.

scholarly journals Consequences of Metabolic Interactions during Staphylococcus aureus Infection

Toxins ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 581
Author(s):  
Tania Wong Fok Lung ◽  
Alice Prince
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Cells ◽  
Infection Process ◽  
Host Cells ◽  
Metabolic Adaptation ◽  
Cell Death Pathways ◽  
Innate Immune Signaling ◽  
Bacterial Mutants ◽  
Metabolic Interactions ◽  
Metabolic Activities

Staphylococcus aureus is a metabolically flexible pathogen that causes infection in diverse settings. An array of virulence factors, including the secreted toxins, enables S. aureus to colonize different environmental niches and initiate infections by any of several discrete pathways. During these infections, both S. aureus and host cells compete with each other for nutrients and remodel their metabolism for survival. This metabolic interaction/crosstalk determines the outcome of the infection. The reprogramming of metabolic pathways in host immune cells not only generates adenosine triphosphate (ATP) to meet the cellular energy requirements during the infection process but also activates antimicrobial responses for eventual bacterial clearance, including cell death pathways. The selective pressure exerted by host immune cells leads to the emergence of bacterial mutants adapted for chronicity. These host-adapted mutants are often characterized by substantial changes in the expression of their own metabolic genes, or by mutations in genes involved in metabolism and biofilm formation. Host-adapted S. aureus can rewire or benefit from the metabolic activities of the immune cells via several mechanisms to cause persistent infection. In this review, we discuss how S. aureus activates host innate immune signaling, which results in an immune metabolic pressure that shapes S. aureus metabolic adaptation and determines the outcome of the infection.

Analysis of Extracellular Proteome of Staphylococcus aureus: A Mass Spectrometry based Proteomics Method of Exotoxin Characterisation

2020 ◽  
Vol 17 (1) ◽  
pp. 3-9
Author(s):  
Rajdeep Das ◽  
Nisha D`souza ◽  
Surya K. Choubey ◽  
Sethumadhavan Murlidharan ◽  
Anura V. Kurpad ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Staphylococcus Aureus ◽  
Food Poisoning ◽  
Extracellular Proteins ◽  
Host Cells ◽  
Dependent Manner ◽  
Extracellular Proteome ◽  
Cytoplasmic Proteins ◽  
Wide Range

Background: Staphylococcus aureus (S. aureus), an important pathogen, causes a wide range of infections in human starting from food poisoning to septicemia. It affects the host cells with various exotoxins, known as virulence factors, which are synthesized in growth phase-dependent manner of the bacteria. S. aureus has been reported to become resistant to antibiotics rapidly. Among two common clinical isolates, Methicillin-sensitive S. aureus (MSSA) and Methicillin-resistant S. aureus (MRSA), MRSA pose major problems across hospitals around the world. Objective: The objective of the present study was to profile the exoproteins of Methicillin-sensitive S. aureus (ATCC 25293) and subsequently to establish a proteomics-based method of characterization of S. aureus that is crucial in treating hospital-acquired infections. Methods: We used two-dimensional nanoLC/ESI-MS based proteomic platform to characterize and quantify the exoproteins isolated from Methicillin-sensitive S. aureus (ATCC 25293) strain. Results: A total of 69 proteins were identified from extracellular proteome pool of ATCC 25293 strain that includes 18 extracellular proteins, 40 cytoplasmic proteins, 2 membrane proteins, 3 cell wall proteins and 6 uncharacterized proteins. Conclusion: We propose that this mass spectrometry-based proteomics method of characterization of exoproteins might be useful to identify S. aureus strains that are resistant to antibiotics.

Phylogeny Characterization of Seb Gene Encoding Enterotoxins in Staphylococcus aureus Isolated from Raw Milk and Cheese

2019 ◽  
Vol 9 (o3) ◽  
Author(s):  
Fatima N. Aziz ◽  
Laith Abdul Hassan Mohammed-Jawad
Keyword(s):  
Staphylococcus Aureus ◽  
Food Poisoning ◽  
Raw Milk ◽  
Staphylococcal Enterotoxin B ◽  
Human Pathogen ◽  
Conventional Pcr ◽  
Biochemical Tests ◽  
Specific Primers ◽  
Gene Encoding

Food poisoning due to the bacteria is a big global problem in economically and human's health. This problem refers to an illness which is due to infection or the toxin exists in nature and the food that use. Milk is considered a nutritious food because it contains proteins and vitamins. The aim of this study is to detect and phylogeny characterization of staphylococcal enterotoxin B gene (Seb). A total of 200 milk and cheese samples were screened. One hundred ten isolates of Staphylococcus aureus pre-confirmed using selective and differential media with biochemical tests. Genomic DNA was extracted from the isolates and the SEB gene detects using conventional PCR with specific primers. Three staphylococcus aureus isolates were found to be positive for Seb gene using PCR and confirmed by sequencing. Sequence homology showed variety range of identity starting from (100% to 38%). Phylogenetic tree analyses show that samples (6 and 5) are correlated with S. epidermidis. This study discovered that isolates (A6-RLQ and A5-RLQ) are significantly clustered in a group with non- human pathogen Staphylococcus agnetis.

scholarly journals Pseudomonas aeruginosa PA14 Enhances the Efficacy of Norfloxacin against Staphylococcus aureus Newman Biofilms

2020 ◽  
Vol 202 (18) ◽  
Author(s):  
Giulia Orazi ◽  
Fabrice Jean-Pierre ◽  
George A. O’Toole
Keyword(s):  
Cystic Fibrosis ◽  
Staphylococcus Aureus ◽  
Pseudomonas Aeruginosa ◽  
Antimicrobial Agents ◽  
Respiratory Infections ◽  
Multiple Infection ◽  
Bacterial Biofilms ◽  
Interspecies Interactions ◽  
Chronic Infections ◽  
Content Type

ABSTRACT The thick mucus within the airways of individuals with cystic fibrosis (CF) promotes frequent respiratory infections that are often polymicrobial. Pseudomonas aeruginosa and Staphylococcus aureus are two of the most prevalent pathogens that cause CF pulmonary infections, and both are among the most common etiologic agents of chronic wound infections. Furthermore, the ability of P. aeruginosa and S. aureus to form biofilms promotes the establishment of chronic infections that are often difficult to eradicate using antimicrobial agents. In this study, we found that multiple LasR-regulated exoproducts of P. aeruginosa, including 2-heptyl-4-hydroxyquinoline N-oxide (HQNO), siderophores, phenazines, and rhamnolipids, likely contribute to the ability of P. aeruginosa PA14 to shift S. aureus Newman norfloxacin susceptibility profiles. Here, we observe that exposure to P. aeruginosa exoproducts leads to an increase in intracellular norfloxacin accumulation by S. aureus. We previously showed that P. aeruginosa supernatant dissipates the S. aureus membrane potential, and furthermore, depletion of the S. aureus proton motive force recapitulates the effect of the P. aeruginosa PA14 supernatant on shifting norfloxacin sensitivity profiles of biofilm-grown S. aureus Newman. From these results, we hypothesize that exposure to P. aeruginosa PA14 exoproducts leads to increased uptake of the drug and/or an impaired ability of S. aureus Newman to efflux norfloxacin. Surprisingly, the effect observed here of P. aeruginosa PA14 exoproducts on S. aureus Newman susceptibility to norfloxacin seemed to be specific to these strains and this antibiotic. Our results illustrate that microbially derived products can alter the ability of antimicrobial agents to kill bacterial biofilms. IMPORTANCE Pseudomonas aeruginosa and Staphylococcus aureus are frequently coisolated from multiple infection sites, including the lungs of individuals with cystic fibrosis (CF) and nonhealing diabetic foot ulcers. Coinfection with P. aeruginosa and S. aureus has been shown to produce worse outcomes compared to infection with either organism alone. Furthermore, the ability of these pathogens to form biofilms enables them to cause persistent infection and withstand antimicrobial therapy. In this study, we found that P. aeruginosa-secreted products dramatically increase the ability of the antibiotic norfloxacin to kill S. aureus biofilms. Understanding how interspecies interactions alter the antibiotic susceptibility of bacterial biofilms may inform treatment decisions and inspire the development of new therapeutic strategies.

scholarly journals 87. Utilization of Methicillin-Sensitive/Resistant Staphylococcus aureus Nares Screen to Decrease Vancomycin and Linezolid Use in Hospitalized Patients with Respiratory Infections

2020 ◽  
Vol 7 (Supplement_1) ◽  
pp. S60-S60
Author(s):  
Noor F Zaidan ◽  
Rachel S Britt ◽  
David Reynoso ◽  
R Scott Ferren
Keyword(s):  
Staphylococcus Aureus ◽  
Respiratory Infections ◽  
Intervention Group ◽  
Kidney Injury ◽  
Post Intervention ◽  
Gram Positive ◽  
Stewardship Program ◽  
Screening Protocol ◽  
The Impact ◽  
Post Intervention Group

Abstract Background Pharmacist-driven protocols for utilization of methicillin-resistant Staphylococcus aureus (MRSA) nares screenings have shown to decrease duration of empiric gram-positive therapy and rates of acute kidney injury (AKI) in patients with respiratory infections. This study evaluated the impact of a pharmacist-driven MRSA nares screening protocol on duration of vancomycin or linezolid therapy (DT) in respiratory infections. Methods Patients aged 18 years and older with a medication order of vancomycin or linezolid for respiratory indication(s) were included. The MRSA nares screening protocol went into effect in October 2019. The protocol allowed pharmacists to order an MRSA nares polymerase chain reaction (PCR) for included patients, while the Antimicrobial Stewardship Program (ASP) made therapeutic recommendations for de-escalation of empiric gram-positive coverage based on negative MRSA nares screenings, if clinically appropriate. Data for the pre-intervention group was collected retrospectively for the months of October 2018 to March 2019. The post-intervention group data was collected prospectively for the months of October 2019 to March 2020. Results Ninety-seven patients were evaluated within both the pre-intervention group (n = 50) and post-intervention group (n = 57). Outcomes for DT (38.2 hours vs. 30.9 hours, P = 0.601) and AKI (20% vs. 14%, P = 0.4105) were not different before and after protocol implementation. A subgroup analysis revealed a significant reduction in DT within the pre- and post-MRSA PCR groups (38.2 hours vs. 24.8 hours, P = 0.0065) when pharmacist recommendations for de-escalation were accepted. Conclusion A pharmacist-driven MRSA nares screening protocol did not affect the duration of gram-positive therapy for respiratory indications. However, there was a reduction in DT when pharmacist-driven recommendations were accepted. Disclosures All Authors: No reported disclosures

scholarly journals The potential role of chemotaxis and the complement system in the formation and progression of thoracic aortic aneurysms inferred from the weighted gene coexpression network analysis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Chuxiang Lei ◽  
Dan Yang ◽  
Wenlin Chen ◽  
Haoxuan Kan ◽  
Fang Xu ◽  
...  
Keyword(s):  
Network Analysis ◽  
Clinical Significance ◽  
Immune Cells ◽  
Complement System ◽  
Aortic Wall ◽  
Gene Coexpression Network ◽  
Hub Genes ◽  
Gene Coexpression ◽  
The Complement System ◽  
Coexpression Network Analysis

Abstract Background Thoracic aortic aneurysm (TAA) can be life-threatening due to the progressive weakening and dilatation of the aortic wall. Once the aortic wall has ruptured, no effective pharmaceutical therapies are available. However, studies on TAA at the gene expression level are limited. Our study aimed to identify the driver genes and critical pathways of TAA through gene coexpression networks. Methods We analyzed the genetic data of TAA patients from a public database by weighted gene coexpression network analysis (WGCNA). Modules with clinical significance were identified, and the differentially expressed genes (DEGs) were intersected with the genes in these modules. Gene Ontology and pathway enrichment analyses were performed. Finally, hub genes that might be driving factors of TAA were identified. Furthermore, we evaluated the diagnostic accuracy of these genes and analyzed the composition of immune cells using the CIBERSORT algorithm. Results We identified 256 DEGs and two modules with clinical significance. The immune response, including leukocyte adhesion, mononuclear cell proliferation and T cell activation, was identified by functional enrichment analysis. CX3CR1, C3, and C3AR1 were the top 3 hub genes in the module correlated with TAA, and the areas under the curve (AUCs) by receiver operating characteristic (ROC) analysis of all the hub genes exceeded 0.7. Finally, we found that the proportions of infiltrating immune cells in TAA and normal tissues were different, especially in terms of macrophages and natural killer (NK) cells. Conclusion Chemotaxis and the complement system were identified as crucial pathways in TAA, and macrophages with interactive immune cells may regulate this pathological process.

Sign in / Sign up

Export Citation Format

Share Document