scholarly journals Role of Bacterial Exopolymers and Host Factors on Adherence and Phagocytosis of Staphylococcus aureus in Foreign Body Infection

1987 ◽  
Vol 155 (3) ◽  
pp. 524-531 ◽  
Author(s):  
E. Falcieri ◽  
P. Vaudaux ◽  
E. Huggler ◽  
D. Lew ◽  
F. Waldvogel
Keyword(s):  
Staphylococcus Aureus ◽  
Foreign Body ◽  
Host Factors

scholarly journals Foreign Body Infection: Role of Fibronectin as a Ligand for the Adherence of Staphylococcus aureus

1984 ◽  
Vol 150 (4) ◽  
pp. 546-553 ◽  
Author(s):  
P. Vaudaux ◽  
R. Suzuki ◽  
F. A. Waldvogel ◽  
J. J. Morgenthaler ◽  
U. E. Nydegger
Keyword(s):  
Staphylococcus Aureus ◽  
Foreign Body

scholarly journals Bacterial virulence plays a crucial role in MRSA sepsis

2021 ◽  
Vol 17 (2) ◽  
pp. e1009369
Author(s):  
Gordon Y. C. Cheung ◽  
Justin S. Bae ◽  
Ryan Liu ◽  
Rachelle L. Hunt ◽  
Yue Zheng ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Quorum Sensing ◽  
Early Stage ◽  
Bacterial Virulence ◽  
Host Factors ◽  
Bacterial Sepsis ◽  
Critical Stage ◽  
Industrialized Nations ◽  
Device Associated Infection

Bacterial sepsis is a major global cause of death. However, the pathophysiology of sepsis has remained poorly understood. In industrialized nations, Staphylococcus aureus represents the pathogen most commonly associated with mortality due to sepsis. Because of the alarming spread of antibiotic resistance, anti-virulence strategies are often proposed to treat staphylococcal sepsis. However, we do not yet completely understand if and how bacterial virulence contributes to sepsis, which is vital for a thorough assessment of such strategies. We here examined the role of virulence and quorum-sensing regulation in mouse and rabbit models of sepsis caused by methicillin-resistant S. aureus (MRSA). We determined that leukopenia was a predictor of disease outcome during an early critical stage of sepsis. Furthermore, in device-associated infection as the most frequent type of staphylococcal blood infection, quorum-sensing deficiency resulted in significantly higher mortality. Our findings give important guidance regarding anti-virulence drug development strategies for the treatment of staphylococcal sepsis. Moreover, they considerably add to our understanding of how bacterial sepsis develops by revealing a critical early stage of infection during which the battle between bacteria and leukocytes determines sepsis outcome. While sepsis has traditionally been attributed mainly to host factors, our study highlights a key role of the invading pathogen and its virulence mechanisms.

scholarly journals IgG4-specific responses in patients with Staphylococcus aureus bone infections are not predictive of postoperative complications

2021 ◽  
Vol 42 ◽  
pp. 156-165
Author(s):  
JR Owen ◽  
◽  
MP Campbell ◽  
MD Mott ◽  
CA Beck ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Adverse Outcome ◽  
Host Factors ◽  
Healthy Controls ◽  
Complement Inhibitor ◽  
Inhibitory Protein ◽  
Blood Samples ◽  
Bone Infections ◽  
Prevalent Pathogen

The most prevalent pathogen in bone infections is Staphylococcus aureus; its incidence and severity are partially determined by host factors. Prior studies showed that anti-glucosaminidase (Gmd) antibodies are protective in animals, and 93.3 % of patients with culture-confirmed S. aureus osteomyelitis do not have anti-Gmd levels > 10 ng/mL in serum. Infection in patients with high anti-Gmd remains unexplained. Are anti-Gmd antibodies in osteomyelitis patients of the non-opsonising, non-complement-fixing IgG4 isotype? The relative amounts of IgG4 and total IgG against Gmd and 7 other S. aureus antigens: iron-surface determinants (Isd) IsdA, IsdB, and IsdH, amidase (Amd), α-haemolysin (Hla), chemotaxis inhibitory protein from S. aureus (CHIPS), and staphylococcal-complement inhibitor (SCIN) were determined in sera from healthy controls (Ctrl, n = 92), osteomyelitis patients whose surgical treatment resulted in infection control (IC, n = 95) or an adverse outcome (AD, n = 40), and post-mortem (PM, n = 7) blood samples from S. aureus septic-death patients. Anti-Gmd IgG4 levels were generally lower in infected patients compared to controls; however, levels among the infected were higher in AD than IC patients. Anti-IsdA, IsdB and IsdH IgG4 levels were increased in infected patients versus controls, and Jonckheere-Terpstra tests of levels revealed an increasing order of infection (Ctrl < IC < AD < PM) for anti-Isd IgG4 antibodies and a decreasing order of infection (Ctrl > IC > AD > PM) for anti-autolysin (Atl) IgG4 antibodies. Collectively, this does not support an immunosuppressive role of IgG4 in S. aureus osteomyelitis but is consistent with a paradigm of high anti-Isd and low anti-Atl responses in these patients.

The Role of the Coagulase-negative Staphylococci (CoNS) in Infective Endocarditis; A Narrative Review from 2000 to 2020

2020 ◽  
Vol 21 (12) ◽  
pp. 1140-1153 ◽  
Author(s):  
Mohammad A. Noshak ◽  
Mohammad A. Rezaee ◽  
Alka Hasani ◽  
Mehdi Mirzaii
Keyword(s):  
Foreign Body ◽  
Infective Endocarditis ◽  
Prosthetic Valve ◽  
Human Life ◽  
Prosthetic Valve Endocarditis ◽  
Surgical Site Infections ◽  
Coagulase Negative Staphylococci ◽  
Native Valve ◽  
Native Valve Endocarditis

Coagulase-negative staphylococci (CoNS) are part of the microbiota of human skin and rarely linked with soft tissue infections. In recent years, CoNS species considered as one of the major nosocomial pathogens and can cause several infections such as catheter-acquired sepsis, skin infection, urinary tract infection, endophthalmitis, central nervous system shunt infection, surgical site infections, and foreign body infection. These microorganisms have a significant impact on human life and health and, as typical opportunists, cause peritonitis in individuals undergoing peritoneal dialysis. Moreover, it is revealed that these potential pathogens are mainly related to the use of indwelling or implanted in a foreign body and cause infective endocarditis (both native valve endocarditis and prosthetic valve endocarditis) in patients. In general, approximately eight percent of all cases of native valve endocarditis is associated with CoNS species, and these organisms cause death in 25% of all native valve endocarditis cases. Moreover, it is revealed that methicillin-resistant CoNS species cause 60 % of all prosthetic valve endocarditis cases. In this review, we describe the role of the CoNS species in infective endocarditis, and we explicated the reported cases of CoNS infective endocarditis in the literature from 2000 to 2020 to determine the role of CoNS in the process of infective endocarditis.

scholarly journals GSDMD contributes to host defence against Staphylococcus aureus skin infection by suppressing the Cxcl1–Cxcr2 axis

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Zhen-Zhen Liu ◽  
Yong-Jun Yang ◽  
Feng-Hua Zhou ◽  
Ke Ma ◽  
Xiao-Qi Lin ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Skin Infection ◽  
Bacterial Colonization ◽  
Critical Role ◽  
Host Defence ◽  
Skin Damage ◽  
Microbial Infection ◽  
Caspase 1 ◽  
Deficient Mice

AbstractGasdermin D (GSDMD), a member of the gasdermin protein family, is a caspase substrate, and its cleavage is required for pyroptosis and IL-1β secretion. To date, the role and regulatory mechanism of GSDMD during cutaneous microbial infection remain unclear. Here, we showed that GSDMD protected against Staphylococcus aureus skin infection by suppressing Cxcl1–Cxcr2 signalling. GSDMD deficiency resulted in larger abscesses, more bacterial colonization, exacerbated skin damage, and increased inflammatory cell infiltration. Although GSDMD deficiency resulted in defective IL-1β production, the critical role of IL-1β was counteracted by the fact that Caspase-1/11 deficiency also resulted in less IL-1β production but did not aggravate disease severity during S. aureus skin infection. Interestingly, GSDMD-deficient mice had increased Cxcl1 secretion accompanied by increased recruitment of neutrophils, whereas Caspase-1/11-deficient mice presented similar levels of Cxcl1 and neutrophils as wild-type mice. Moreover, the absence of GSDMD promoted Cxcl1 secretion in bone marrow-derived macrophages induced by live, dead, or different strains of S. aureus. Corresponding to higher transcription and secretion of Cxcl1, enhanced NF-κB activation was shown in vitro and in vivo in the absence of GSDMD. Importantly, inhibiting the Cxcl1–Cxcr2 axis with a Cxcr2 inhibitor or anti-Cxcl1 blocking antibody rescued host defence defects in the GSDMD-deficient mice. Hence, these results revealed an important role of GSDMD in suppressing the Cxcl1–Cxcr2 axis to facilitate pathogen control and prevent tissue damage during cutaneous S. aureus infection.

scholarly journals The Phosphoarginine Phosphatase PtpB from Staphylococcus aureus Is Involved in Bacterial Stress Adaptation during Infection

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 645
Author(s):  
Mohamed Ibrahem Elhawy ◽  
Sylvaine Huc-Brandt ◽  
Linda Pätzold ◽  
Laila Gannoun-Zaki ◽  
Ahmed Mohamed Mostafa Abdrabou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Treatment Strategies ◽  
Physiological Role ◽  
Aureus Strain ◽  
Stress Adaptation ◽  
Cellular Mechanisms ◽  
Host Interaction ◽  
Liver And Kidney

Staphylococcus aureus continues to be a public health threat, especially in hospital settings. Studies aimed at deciphering the molecular and cellular mechanisms that underlie pathogenesis, host adaptation, and virulence are required to develop effective treatment strategies. Numerous host-pathogen interactions were found to be dependent on phosphatases-mediated regulation. This study focused on the analysis of the role of the low-molecular weight phosphatase PtpB, in particular, during infection. Deletion of ptpB in S. aureus strain SA564 significantly reduced the capacity of the mutant to withstand intracellular killing by THP-1 macrophages. When injected into normoglycemic C57BL/6 mice, the SA564 ΔptpB mutant displayed markedly reduced bacterial loads in liver and kidney tissues in a murine S. aureus abscess model when compared to the wild type. We also observed that PtpB phosphatase-activity was sensitive to oxidative stress. Our quantitative transcript analyses revealed that PtpB affects the transcription of various genes involved in oxidative stress adaptation and infectivity. Thus, this study disclosed first insights into the physiological role of PtpB during host interaction allowing us to link phosphatase-dependent regulation to oxidative bacterial stress adaptation during infection.

scholarly journals The Abstruse Side of Type I Interferon Immunotherapy for COVID-19 Cases with Comorbidities

2021 ◽  
Vol 1 (1) ◽  
pp. 49-59
Author(s):  
Selvakumar Subbian
Keyword(s):  
Infectious Diseases ◽  
Disease Severity ◽  
Type I Interferon ◽  
Host Factors ◽  
Type I ◽  
The Novel ◽  
Inflammatory Drugs ◽  
Precautionary Measures ◽  
Inducible Genes

The Coronavirus Disease-2019 (COVID-19) pandemic, caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has claimed 1.2 million people globally since December 2019. Although the host factors underpinning COVID-19 pathology are not fully understood, type I interferon (IFN-I) response is considered crucial for SARS-CoV-2 pathogenesis. Perturbations in IFN-I signaling and associated interferon-inducible genes (ISG) are among the primary disease severity indicators in COVID-19. Consequently, IFN-I therapy, either alone or in- combination with existing antiviral or anti-inflammatory drugs, is tested in many ongoing clinical trials to reduce COVID-19 mortality. Since signaling by the IFN-I family of molecules regulates host immune response to other infectious and non-infectious diseases, any imbalance in this family of cytokines would impact the clinical outcome of COVID-19, as well as other co-existing diseases. Therefore, it is imperative to evaluate the beneficial-versus-detrimental effects of IFN-I immunotherapy for COVID-19 patients with divergent disease severity and other co-existing conditions. This review article summarizes the role of IFN-I signaling in infectious and non-infectious diseases of humans. It highlights the precautionary measures to be considered before administering IFN-I to COVID-19 patients having other co-existing disorders. Finally, suggestions are proposed to improve IFN-I immunotherapy to COVID-19.

scholarly journals A Narrative Review of Early Oral Stepdown Therapy for the Treatment of Uncomplicated Staphylococcus aureus Bacteremia: Yay or Nay?

2020 ◽  
Vol 7 (6) ◽  
Author(s):  
Michael Dagher ◽  
Vance G Fowler ◽  
Patty W Wright ◽  
Milner B Staub
Keyword(s):  
Staphylococcus Aureus ◽  
Hospital Readmission ◽  
Potential Role ◽  
Review Article ◽  
Narrative Review ◽  
Oral Antibiotics ◽  
Staphylococcus Aureus Bacteremia ◽  
Complete Treatment

Abstract Historically, intravenous (IV) antibiotics have been the cornerstone of treatment for uncomplicated Staphylococcus aureus bacteremia (SAB). However, IV antibiotics are expensive, increase the rates of hospital readmission, and can be associated with catheter-related complications. As a result, the potential role of oral antibiotics in the treatment of uncomplicated SAB has become a subject of interest. This narrative review article aims to summarize key arguments for and against the use of oral antibiotics to complete treatment of uncomplicated SAB and evaluates the available evidence for specific oral regimens. We conclude that evidence suggests that oral step-down therapy can be an alternative for select patients who meet the criteria for uncomplicated SAB and will comply with medical treatment and outpatient follow-up. Of the currently studied regimens discussed in this article, linezolid has the most support, followed by fluoroquinolone plus rifampin.

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