A Porous CoII-MOF for CO2 Cycloaddition and the Protective Effect against Staphylococcus aureus Systemic Infection in the Department of Ultrasound

2020 ◽  
Author(s):  
Jin Cai ◽  
Peng-Fei Zou
Keyword(s):  
Staphylococcus Aureus ◽  
Protective Effect ◽  
Systemic Infection

scholarly journals Manipulation of Autophagy in Phagocytes Facilitates Staphylococcus aureus Bloodstream Infection

2015 ◽  
Vol 83 (9) ◽  
pp. 3445-3457 ◽  
Author(s):  
Kate M. O'Keeffe ◽  
Mieszko M. Wilk ◽  
John M. Leech ◽  
Alison G. Murphy ◽  
Maisem Laabei ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Systemic Infection ◽  
Critical Factor ◽  
Intracellular Survival ◽  
Autophagic Flux ◽  
Content Type ◽  
Bactericidal Effects ◽  
Staphylococcus Aureus Bloodstream Infection ◽  
Direct Killing

The capacity for intracellular survival within phagocytes is likely a critical factor facilitating the dissemination ofStaphylococcus aureusin the host. To date, the majority of work onS. aureus-phagocyte interactions has focused on neutrophils and, to a lesser extent, macrophages, yet we understand little about the role played by dendritic cells (DCs) in the direct killing of this bacterium. Using bone marrow-derived DCs (BMDCs), we demonstrate for the first time that DCs can effectively killS. aureusbut that certain strains ofS. aureushave the capacity to evade DC (and macrophage) killing by manipulation of autophagic pathways. Strains with high levels of Agr activity were capable of causing autophagosome accumulation, were not killed by BMDCs, and subsequently escaped from the phagocyte, exerting significant cytotoxic effects. Conversely, strains that exhibited low levels of Agr activity failed to accumulate autophagosomes and were killed by BMDCs. Inhibition of the autophagic pathway by treatment with 3-methyladenine restored the bactericidal effects of BMDCs. Using anin vivomodel of systemic infection, we demonstrated that the ability ofS. aureusstrains to evade phagocytic cell killing and to survive temporarily within phagocytes correlated with persistence in the periphery and that this effect is critically Agr dependent. Taken together, our data suggest that strains ofS. aureusexhibiting high levels of Agr activity are capable of blocking autophagic flux, leading to the accumulation of autophagosomes. Within these autophagosomes, the bacteria are protected from phagocytic killing, thus providing an intracellular survival niche within professional phagocytes, which ultimately facilitates dissemination.

scholarly journals Making the Most of the Host; Targeting the Autophagy Pathway Facilitates Staphylococcus aureus Intracellular Survival in Neutrophils

2021 ◽  
Vol 12 ◽  
Author(s):  
Emilio G. Vozza ◽  
Michelle E. Mulcahy ◽  
Rachel M. McLoughlin
Keyword(s):  
Staphylococcus Aureus ◽  
Therapeutic Potential ◽  
Systemic Infection ◽  
Opportunistic Pathogen ◽  
Intracellular Survival ◽  
Innate Immune ◽  
Pathogenic Role ◽  
New Host ◽  
Increased Risk ◽  
Autophagy Pathway

The success of Staphylococcus aureus as a human commensal and an opportunistic pathogen relies on its ability to adapt to several niches within the host. The innate immune response plays a key role in protecting the host against S. aureus infection; however, S. aureus adeptness at evading the innate immune system is indisputably evident. The “Trojan horse” theory has been postulated to describe a mechanism by which S. aureus takes advantage of phagocytes as a survival niche within the host to facilitate dissemination of S. aureus to secondary sites during systemic infection. Several studies have determined that S. aureus can parasitize both professional and non-professional phagocytes by manipulating the host autophagy pathway in order to create an intracellular survival niche. Neutrophils represent a critical cell type in S. aureus infection as demonstrated by the increased risk of infection among patients with congenital neutrophil disorders. However, S. aureus has been repeatedly shown to survive intracellularly within neutrophils with evidence now supporting a pathogenic role of host autophagy. By manipulating this pathway, S. aureus can also alter the apoptotic fate of the neutrophil and potentially skew other important signalling pathways for its own gain. Understanding these critical host-pathogen interactions could lead to the development of new host directed therapeutics for the treatment of S. aureus infection by removing its intracellular niche and restoring host bactericidal functions. This review discusses the current findings surrounding intracellular survival of S. aureus within neutrophils, the pathogenic role autophagy plays in this process and considers the therapeutic potential for targeting this immune evasion mechanism.

scholarly journals Engineered biomimetic platelet membrane-coated nanoparticles block staphylococcus aureus cytotoxicity and protect against lethal systemic infection

Engineering ◽  
2020 ◽  
Author(s):  
Jwa-Kyung Kim ◽  
Satoshi Uchiyama ◽  
Hua Gong ◽  
Alexandra Stream ◽  
Liangfang Zhang ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Systemic Infection ◽  
Platelet Membrane ◽  
Coated Nanoparticles

scholarly journals Interleukin-10 (IL-10) Produced by Mutant Toxic Shock Syndrome Toxin 1 Vaccine-Induced Memory T Cells Downregulates IL-17 Production and Abrogates the Protective Effect against Staphylococcus aureus Infection

2019 ◽  
Vol 87 (10) ◽  
Author(s):  
Kouji Narita ◽  
Dong-Liang Hu ◽  
Krisana Asano ◽  
Akio Nakane
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Infectious Diseases ◽  
Protective Effect ◽  
Toxic Shock Syndrome ◽  
Long Term Memory ◽  
Toxic Shock ◽  
Content Type ◽  
Memory Phase ◽  
Toxic Shock Syndrome Toxin

ABSTRACT Development of long-term memory is crucial for vaccine-induced adaptive immunity against infectious diseases such as Staphylococcus aureus infection. Toxic shock syndrome toxin 1 (TSST-1), one of the superantigens produced by S. aureus, is a possible vaccine candidate against infectious diseases caused by this pathogen. We previously reported that vaccination with less toxic mutant TSST-1 (mTSST-1) induced T helper 17 (Th17) cells and elicited interleukin-17A (IL-17A)-mediated protection against S. aureus infection 1 week after vaccination. In the present study, we investigated the host immune response induced by mTSST-1 vaccination in the memory phase, 12 weeks after the final vaccination. The protective effect and IL-17A production after vaccination with mTSST-1 were eliminated because of IL-10 production. In the presence of IL-10-neutralizing monoclonal antibody (mAb), IL-17A production was restored in culture supernatants of CD4+ T cells and macrophages sorted from the spleens of vaccinated mice. Vaccinated mice treated with anti-IL-10 mAb were protected against systemic S. aureus infection in the memory phase. From these results, it was suggested that IL-10 produced in the memory phase suppresses the IL-17A-dependent vaccine effect through downregulation of IL-17A production.

scholarly journals THE IN VIVO INTERACTION BETWEEN STAPHYLOCOCCUS BACTERIOPHAGE AND STAPHYLOCOCCUS AUREUS

1963 ◽  
Vol 118 (1) ◽  
pp. 13-26 ◽  
Author(s):  
P. F. Bartell ◽  
I. S. Thind ◽  
T. Orr ◽  
W. S. Blakemore
Keyword(s):  
Staphylococcus Aureus ◽  
Protective Effect ◽  
Host Defense ◽  
Defense Mechanisms ◽  
Protective Role ◽  
Protection Time ◽  
Determining Factors ◽  
Specific Bacteriophage ◽  
And Staphylococcus Aureus

Staphylococcus bacteriophage 81 is capable of in vivo interaction with Staphylococcus aureus, Type 80/81. This is immediately made evident by increased levels of bacteriophage and concomitant survival of 81 per cent infected mice. The reaction is dependent upon the use of active, type-specific bacteriophage. The maximal protective effect is observed at a bacteriophage to bacteria ratio of 1:2 and decreased quantities of bacteriophage result in decreased protection. Time and sequence of administration are also determining factors. It is evident that bacteriophage administered intravenously is capable of interaction with the infecting bacterial cell at the site of infection. In vivo produced bacteriophage is apparently eliminated or otherwise rendered nondetectable fairly rapidly, occurring within a period of 5 to 10 days. However, it appears that host defense mechanisms are stimulated in the process and actively play a protective role against subsequent challenge inocula administered up to 3 weeks later.

scholarly journals Protective effect of acidic mannan fraction of bakers' yeast against Staphylococcus aureus infection in mice.

1985 ◽  
Vol 8 (11) ◽  
pp. 942-947 ◽  
Author(s):  
YOSHIO OKAWA ◽  
YASUSHI OKURA ◽  
KAZUHIKO HASHIMOTO ◽  
KO SUZUKI ◽  
SHIGEO SUZUKI ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Protective Effect ◽  
Aureus Infection

Protective Effect of Furocoumarins Against 254-nm Ultraviolet in Staphylococcus aureus

2005 ◽  
Vol 52 (1) ◽  
pp. 40-44 ◽  
Author(s):  
Humberto M. Barreto ◽  
José P. Siqueira-Junior
Keyword(s):  
Staphylococcus Aureus ◽  
Protective Effect
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