scholarly journals Staphylococcus aureus and Host Immunity in Recurrent Furunculosis

Dermatology ◽  
2019 ◽  
Vol 235 (4) ◽  
pp. 295-305 ◽  
Author(s):  
Danuta Nowicka ◽  
Ewelina Grywalska
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Bacterial Colonization ◽  
Clinical Findings ◽  
Host Immunity ◽  
Acquired Immunity ◽  
Host Immune Responses ◽  
Infection Susceptibility ◽  
Inflammatory Processes ◽  
Recurrent Furunculosis

Staphylococcus aureus is one of the severest and most persistent bacterial pathogens. The most frequent S. aureus infections include impetigo, folliculitis, furuncles, furunculosis, abscesses, hidradenitis suppurativa, and mastitis. S. aureus produces a great variety of cellular and extracellular factors responsible for its invasiveness and ability to cause pathological lesions. Their expression depends on the growth phase, environmental factors, and location of the infection. Susceptibility to staphylococcal infections is rooted in multiple mechanisms of host immune responses and reactions to bacterial colonization. Immunological and inflammatory processes of chronic furunculosis are based on the pathogenicity of S. aureus as well as innate and acquired immunity. In-depth knowledge about them may help to discover the whole pathomechanism of the disease and to develop effective therapeutic options. In this review, we focus on the S. aureus-host immune interactions in the pathogenesis of recurrent furunculosis according to the most recent experimental and clinical findings.

scholarly journals During the Early Stages of Staphylococcus aureus Biofilm Formation, Induced Neutrophil Extracellular Traps Are Degraded by Autologous Thermonuclease

2019 ◽  
Vol 87 (12) ◽  
Author(s):  
Andi R. Sultan ◽  
Tamara Hoppenbrouwers ◽  
Nicole A. Lemmens-den Toom ◽  
Susan V. Snijders ◽  
Johan W. van Neck ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Structural Stability ◽  
Biofilm Formation ◽  
Bacterial Colonization ◽  
Extracellular Dna ◽  
Content Type ◽  
Host Immune Responses ◽  
Early Stages ◽  
Biofilm Development

ABSTRACT Staphylococcus aureus extracellular DNA (eDNA) plays a crucial role in the structural stability of biofilms during bacterial colonization; on the contrary, host immune responses can be induced by bacterial eDNA. Previously, we observed production of S. aureus thermonuclease during the early stages of biofilm formation in a mammalian cell culture medium. Using a fluorescence resonance energy transfer (FRET)-based assay, we detected thermonuclease activity of S. aureus biofilms grown in Iscove’s modified Dulbecco’s medium (IMDM) earlier than that of widely studied biofilms grown in tryptic soy broth (TSB). The thermonuclease found was Nuc1, confirmed by mass spectrometry and competitive Luminex assay. These results indicate that biofilm development in IMDM may not rely on eDNA for structural stability. A bacterial viability assay in combination with wheat germ agglutinin (WGA) staining confirmed the accumulation of dead cells and eDNA in biofilms grown in TSB. However, in biofilms grown in IMDM, minimal amounts of eDNA were found; instead, polysaccharide intercellular adhesin (PIA) was detected. To investigate if this early production of thermonuclease plays a role in immune modulation by biofilm, we studied the effect of thermonuclease on human neutrophil extracellular trap (NET) formation using a nuc knockout and complemented strain. We confirmed that thermonuclease produced by early-stage biofilms grown in IMDM degraded biofilm-induced NETs. Additionally, neither the presence of biofilms nor thermonuclease stimulated an increase in reactive oxygen species (ROS) production by neutrophils. Our findings indicated that S. aureus, during the early stages of biofilm formation, actively evades the host immune responses by producing thermonuclease.

scholarly journals Roles of Host Immunity in Viral Myocarditis and Dilated Cardiomyopathy

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Lifang Zhao ◽  
Zhaoying Fu
Keyword(s):  
Innate Immunity ◽  
T Cell ◽  
Immune Responses ◽  
Viral Infection ◽  
Dilated Cardiomyopathy ◽  
Viral Myocarditis ◽  
Host Immunity ◽  
Host Immune Responses ◽  
Direct Damage ◽  
Working Together

The pathogenesis of viral myocarditis includes both the direct damage mediated by viral infection and the indirect lesion resulted from host immune responses. Myocarditis can progress into dilated cardiomyopathy that is also associated with immunopathogenesis. T cell-mediated autoimmunity, antibody-mediated autoimmunity (autoantibodies), and innate immunity, working together, contribute to the development of myocarditis and dilated cardiomyopathy.

scholarly journals Infection, Inflammation and Immunity in Covid-19 Infection

2021 ◽  
Vol 48 (3) ◽  
pp. 77-82
Author(s):  
R. Cherneva ◽  
Z. Cherneva
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Immune Responses ◽  
Systemic Inflammation ◽  
Multiple Organ ◽  
Host Immunity ◽  
Effective Prevention ◽  
Systemic Complications ◽  
Host Immune Responses ◽  
Prevention And Treatment

Abstract The COVID-19 pandemic caused by the SARS-CoV-2 has increased the burden on healthcare system. Despite some progress in its diagnostics has been made, effective prevention and treatment are still insufficient. Since SARS-CoV-2 infections often cause systemic inflammation and multiple organ failure, the therapeutic options aimed at modulating the host immune responses to prevent subsequent systemic complications are demanding. The review provides a summary of the SARS-CoV-2 virus infection and underlines the current perception of pulmonary host’s immune response and its contributions to disease severity and systemic inflammation. Signaling pathways which have the potential to manipulate host immunity and improve clinical outcomes are also presented.

scholarly journals Staphylococcus aureus synthesizes adenosine to escape host immune responses

2009 ◽  
Vol 206 (11) ◽  
pp. 2417-2427 ◽  
Author(s):  
Vilasack Thammavongsa ◽  
Justin W. Kern ◽  
Dominique M. Missiakas ◽  
Olaf Schneewind
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Immune Responses ◽  
Virulence Factor ◽  
Adenosine Monophosphate ◽  
Healthy Individuals ◽  
Subsequent Formation ◽  
Host Immune Responses ◽  
A Cell ◽  
Exogenous Supply

Staphylococcus aureus infects hospitalized or healthy individuals and represents the most frequent cause of bacteremia, treatment of which is complicated by the emergence of methicillin-resistant S. aureus. We examined the ability of S. aureus to escape phagocytic clearance in blood and identified adenosine synthase A (AdsA), a cell wall–anchored enzyme that converts adenosine monophosphate to adenosine, as a critical virulence factor. Staphylococcal synthesis of adenosine in blood, escape from phagocytic clearance, and subsequent formation of organ abscesses were all dependent on adsA and could be rescued by an exogenous supply of adenosine. An AdsA homologue was identified in the anthrax pathogen, and adenosine synthesis also enabled escape of Bacillus anthracis from phagocytic clearance. Collectively, these results suggest that staphylococci and other bacterial pathogens exploit the immunomodulatory attributes of adenosine to escape host immune responses.

Bromophenazine derivatives with potent inhibition, dispersion and eradication activities against Staphylococcus aureus biofilms

RSC Advances ◽  
2015 ◽  
Vol 5 (2) ◽  
pp. 1120-1124 ◽  
Author(s):  
Aaron T. Garrison ◽  
Fang Bai ◽  
Yasmeen Abouelhassan ◽  
Nicholas G. Paciaroni ◽  
Shouguang Jin ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Bacterial Biofilms ◽  
Host Immune Responses ◽  
Potent Inhibition ◽  
Human Infections

Bacterial biofilms are surface-attached communities of bacteria that are: (1) highly prevalent in human infections, and (2) resistant to conventional antibiotic treatments and host immune responses.

scholarly journals Staphylococcus aureus internalisation enhances bacterial survival through modulation of host immune responses and mast cell activation

Allergy ◽  
2020 ◽  
Author(s):  
Timothy C. Biggs ◽  
Rana S. Abadalkareem ◽  
Stephen M. Hayes ◽  
Rebecca E. Holding ◽  
Laurie C. Lau ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mast Cell ◽  
Immune Responses ◽  
Cell Activation ◽  
Mast Cell Activation ◽  
Bacterial Survival ◽  
Host Immune Responses

scholarly journals Identifying protective antigens of Staphylococcus aureus , a pathogen that suppresses host immune responses

2011 ◽  
Vol 25 (10) ◽  
pp. 3605-3612 ◽  
Author(s):  
Hwan Keun Kim ◽  
Hye‐Young Kim ◽  
Olaf Schneewind ◽  
Dominique Missiakas
Keyword(s):  
Staphylococcus Aureus ◽  
Immune Responses ◽  
Host Immune Responses ◽  
Protective Antigens

scholarly journals The IL-2 Defect in Systemic Lupus Erythematosus Disease Has an Expansive Effect on Host Immunity

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Linda A. Lieberman ◽  
George C. Tsokos
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Cell Function ◽  
Host Immunity ◽  
Systemic Lupus Erythematosus Disease ◽  
Systemic Lupus ◽  
Host Immune Responses ◽  
Activation Induced Cell Death ◽  
Immune Defects

IL-2 production is decreased in systemic lupus erythematosus (SLE) patients and affects T cell function and other aspects of host immunity. Transcription factors regulating IL-2 production behave aberrantly in SLE T cells. In addition to IL-2 dysregulation, other IL-2 family members (IL-15 and IL-21) are abnormally expressed in SLE. Decreased IL-2 production in SLE patients leads to many immune defects such as decreasedTregproduction, decreased activation-induced cell death (AICD), and decreased cytotoxicity. IL-2 deficiency results in systemic dysregulation of host immune responses in patients suffering from SLE disease.

scholarly journals Tailoring host immune responses toListeriaby manipulation of virulence genes – the interface between innate and acquired immunity

2003 ◽  
Vol 35 (3) ◽  
pp. 243-253 ◽  
Author(s):  
Christian Peters ◽  
Eugen Domann ◽  
Abdelhak Darbouche ◽  
Trinad Chakraborty ◽  
Martin E.A Mielke
Keyword(s):  
Immune Responses ◽  
Virulence Genes ◽  
Acquired Immunity ◽  
Host Immune Responses
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