scholarly journals Basil Polysaccharide Reverses Development of Experimental Model of Sepsis-Induced Secondary Staphylococcus aureus Pneumonia

2021 ◽  
Vol 2021 ◽  
pp. 1-21
Author(s):  
Xi Chen ◽  
Yue He ◽  
Qiang Wei ◽  
Chuanjiang Wang
Keyword(s):  
Staphylococcus Aureus ◽  
Bacterial Pneumonia ◽  
Cecal Ligation ◽  
Intratracheal Instillation ◽  
Signal Transduction Pathway ◽  
Treated Group ◽  
Protective Role ◽  
Dual Model ◽  
Secondary Bacterial Pneumonia

Background. Basil polysaccharide (BPS) represents a main active ingredient extracted from basil (Ocimum basilicum L.), which can regulate secondary bacterial pneumonia development in the process of sepsis-mediated immunosuppression. Methods. In this study, a dual model of sepsis-induced secondary pneumonia with cecal ligation and puncture and intratracheal instillation of Staphylococcus aureus or Pseudomonas aeruginosa was constructed. Results. The results indicated that BPS-treated mice undergoing CLP showed resistance to secondary S. aureus pneumonia. Compared with the IgG-treated group, BPS-treated mice exhibited better survival rate along with a higher bacterial clearance rate. Additionally, BPS treatment attenuated cell apoptosis, enhanced lymphocyte and macrophage recruitment to the lung, promoted pulmonary cytokine production, and significantly enhanced CC receptor ligand 4 (CCL4). Notably, recombinant CCL4 protein could enhance the protective effect on S. aureus-induced secondary pulmonary infection of septic mice, which indicated that BPS-induced CCL4 partially mediated resistance to secondary bacterial pneumonia. In addition, BPS priming markedly promoted the phagocytosis of alveolar macrophages while killing S. aureus in vitro, which was related to the enhanced p38MAPK signal transduction pathway activation. Moreover, BPS also played a protective role in sepsis-induced secondary S. aureus pneumonia by inducing Treg cell differentiation. Conclusions. Collectively, these results shed novel lights on the BPS treatment mechanism in sepsis-induced secondary S. aureus pneumonia in mice.

scholarly journals Basil Polysaccharide Reverses Development of Experimental Model of Sepsis-Induced Secondary Staphylococcus Aureus Pneumonia

2021 ◽  
Author(s):  
Xi Chen ◽  
Yue He ◽  
Qiang Wei ◽  
Chuanjiang Wang
Keyword(s):  
Staphylococcus Aureus ◽  
Bacterial Pneumonia ◽  
Cecal Ligation ◽  
Intratracheal Instillation ◽  
Signal Transduction Pathway ◽  
Treated Group ◽  
Protective Role ◽  
Dual Model ◽  
Secondary Bacterial Pneumonia

Abstract Background: Basil polysaccharide (BPS) represents a main active ingredient extracted from Basil (Ocimum basilicum L.), which can regulate secondary bacterial pneumonia development in the process of sepsis-mediated immunosuppression.Methods: In this study, a dual model of sepsis-induced secondary pneumonia with cecal ligation and puncture and intratracheal instillation of Staphylococcus aureus or Pseudomonas aeruginosa was constructed.Results: The results indicated that BPS treated mice undergoing CLP showed resistance to secondary S. aureus pneumonia. Compared with the IgG treated group, BPS treated mice exhibited better survival rate along with higher bacterial clearance rate. Additionally, BPS treatment attenuated cell apoptosis, enhanced lymphocytes and macrophages recruitment to the lung, promoted pulmonary cytokine production, and significantly enhanced CC receptor ligand 4 (CCL4). Notably, recombinant CCL4 protein could enhance the protective effect on S. aureus-induced secondary pulmonary infection of septic mice, which indicated that BPS induced CCL4 partially mediated resistance to secondary bacterial pneumonia. In addition, BPS priming markedly promoted the phagocytosis of alveolar macrophages while killing S. aureus in vitro, which was related to the enhanced p38MAPK signal transduction pathway activation. Moreover, BPS also played a protective role in sepsis-induced secondary S. aureus pneumonia by inducing Treg cell differentiation.Conclusions: Collectively, these results shed novel lights on the BPS treatment mechanism in sepsis-induced secondary S. aureus pneumonia in mice.

scholarly journals Streptococcus pneumoniae Modulates Staphylococcus aureus Biofilm Dispersion and the Transition from Colonization to Invasive Disease

mBio ◽  
2018 ◽  
Vol 9 (1) ◽  
Author(s):  
Ryan M. Reddinger ◽  
Nicole R. Luke-Marshall ◽  
Shauna L. Sauberan ◽  
Anders P. Hakansson ◽  
Anthony A. Campagnari
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Influenza A Virus ◽  
Bacterial Pneumonia ◽  
Influenza A ◽  
Bacterial Species ◽  
Invasive Disease ◽  
Secondary Bacterial Pneumonia

ABSTRACTStreptococcus pneumoniaeandStaphylococcus aureusare ubiquitous upper respiratory opportunistic pathogens. Individually, these Gram-positive microbes are two of the most common causative agents of secondary bacterial pneumonia following influenza A virus infection, and they constitute a significant source of morbidity and mortality. Since the introduction of the pneumococcal conjugate vaccine, rates of cocolonization with both of these bacterial species have increased, despite the traditional view that they are antagonistic and mutually exclusive. The interactions betweenS. pneumoniaeandS. aureusin the context of colonization and the transition to invasive disease have not been characterized. In this report, we show thatS. pneumoniaeandS. aureusform stable dual-species biofilms on epithelial cellsin vitro. When these biofilms are exposed to physiological changes associated with viral infection,S. pneumoniaedisperses from the biofilm, whereasS. aureusdispersal is inhibited. These findings were supported by results of anin vivostudy in which we used a novel mouse cocolonization model. In these experiments, mice cocolonized in the nares with both bacterial species were subsequently infected with influenza A virus. The coinfected mice almost exclusively developed pneumococcal pneumonia. These results indicate that despite our previous report thatS. aureusdisseminates into the lungs of mice stably colonized with these bacteria following influenza A virus infection, cocolonization withS. pneumoniae in vitroandin vivoinhibitsS. aureusdispersal and transition to disease. This study provides novel insight into both the interactions betweenS. pneumoniaeandS. aureusduring carriage and the transition from colonization to secondary bacterial pneumonia.IMPORTANCEIn this study, we demonstrate thatStreptococcus pneumoniaecan modulate the pathogenic potential ofStaphylococcus aureusin a model of secondary bacterial pneumonia. We report that host physiological signals related to viral infection cease to elicit a dispersal response fromS. aureuswhile in a dual-species setting withS. pneumoniae, in direct contrast to results of previous studies with each species individually. This study underscores the importance of studying polymicrobial communities and their implications in disease states.

scholarly journals The Synergistic Effect of Nicotine and Staphylococcus aureus on Peri-Implant Infections

2021 ◽  
Vol 9 ◽  
Author(s):  
Yao Hu ◽  
Wen Zhou ◽  
Chengguang Zhu ◽  
Yujie Zhou ◽  
Qiang Guo ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Synergistic Effects ◽  
Protein A ◽  
Treated Group ◽  
Combination Group ◽  
Staphylococcal Protein A ◽  
Receptor Activator ◽  
And Staphylococcus Aureus

Smoking is considered a key risk factor for implant survival; however, how it interacts with the pathogens in peri-implant infections is not clear. Here, we identified that nicotine, the key component of cigarette smoking, can interact with Staphylococcus aureus and synergistically induce peri-implant infections in a rat osteolysis model. The nicotine–S. aureus combination group increased the gross bone pathology, osteolysis, periosteal reactions, and bone resorption compared to the nicotine or S. aureus single treated group (p < 0.05). Nicotine did not promote the proliferation of S. aureus both in vitro and in vivo, but it can significantly upregulate the expression of staphylococcal protein A (SpA), a key virulence factor of S. aureus. The nicotine–S. aureus combination also synergistically activated the expression of RANKL (receptor activator of nuclear factor-kappa B ligand, p < 0.05) to promote the development of peri-implant infections. The synergistic effects between nicotine and S. aureus infection can be a new target to reduce the peri-implant infections.

scholarly journals Protective Role of Coenzyme Q10 in Acute Sepsis-Induced Liver Injury in BALB/c Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Qian-wei Li ◽  
Qin Yang ◽  
Hong-Yang Liu ◽  
Yu-ling Wu ◽  
Yu-Hua Hao ◽  
...  
Keyword(s):  
Liver Injury ◽  
Coenzyme Q10 ◽  
Cecal Ligation ◽  
Protective Role ◽  
Hepatic Tissue ◽  
Control Group ◽  
Cecal Ligation And Puncture ◽  
Sequestosome 1

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1β, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor-α expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.

Letters to the Editor

PEDIATRICS ◽  
1980 ◽  
Vol 66 (1) ◽  
pp. 154-155
Author(s):  
Charles M. Ginsburg ◽  
John D. Nelson
Keyword(s):  
Staphylococcus Aureus ◽  
Haemophilus Influenzae ◽  
Bacterial Pneumonia ◽  
Hospitalized Patients ◽  
Haemophilus Influenzae Type ◽  
Haemophilus Influenzae Type B ◽  
Type B ◽  
Letters To The Editor ◽  
And Staphylococcus Aureus

We do not disagree with the recommendations of Drs Fischer, Bass, and Arthur for treating hospitalized patients with pneumonia. They might have mentioned, additionally, the possible utility of cefamandole as an alternative to a penicillinase-resistant penicillin plus chloramphenicol for hospitalized infants with presumed bacterial pneumonia. We are currently evaluating cefuroxime, which has a similar in vitro spectrum, and are finding it effective in patients with pneumonia due to Haemophilus influenzae type b, pneumococci and Staphylococcus aureus.

scholarly journals Amniotic fluid stem cells ameliorate cisplatin-induced acute renal failure through induction of autophagy and inhibition of apoptosis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ekta Minocha ◽  
Rohit Anthony Sinha ◽  
Manali Jain ◽  
Chandra Prakash Chaturvedi ◽  
Soniya Nityanand
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Amniotic Fluid ◽  
Cell Types ◽  
Treated Group ◽  
Protective Role ◽  
Protective Effects ◽  
Amniotic Fluid Stem Cells

Abstract Background We have recently demonstrated that amniotic fluid stem cells (AFSC) express renal progenitor markers and can be differentiated in vitro into renal lineage cell types, viz, juxtaglomerular and renal proximal tubular epithelial-like cells. Here, we have evaluated the therapeutic efficacy of AFSC in a cisplatin-induced rat model of acute renal failure (ARF) and investigated the underlying mechanisms responsible for their renoprotective effects. Methods ARF was induced in Wistar rats by intra-peritoneal injection of cisplatin (7 mg/kg). Five days after cisplatin injection, rats were randomized into two groups and injected with either AFSC or normal saline intravenously. On days 8 and 12 after cisplatin injection, the blood biochemical parameters, histopathological changes, apoptosis and expression of pro-apoptotic, anti-apoptotic, and autophagy-related proteins in renal tissues were studied in both groups of rats. To further confirm whether the protective effects of AFSC on cisplatin-induced apoptosis were dependent on autophagy, chloroquine, an autophagy inhibitor, was administered by the intra-peritoneal route. Results Administration of AFSC in ARF rats resulted in improvement of renal function and attenuation of renal damage as reflected by significant decrease in blood urea nitrogen, serum creatinine levels, tubular cell apoptosis as assessed by Bax/Bcl2 ratio, and expression of the pro-apoptotic proteins, viz, PUMA, Bax, cleaved caspase-3, and cleaved caspase-9, as compared to the saline-treated group. Furthermore, in the AFSC-treated group as compared to the saline-treated group, there was a significant increase in the activation of autophagy as evident by increased expression of LC3-II, ATG5, ATG7, Beclin1, and phospho-AMPK levels with a concomitant decrease in phospho-p70S6K and p62 expression levels. Chloroquine administration led to significant reduction in the anti-apoptotic effects of the AFSC therapy and further deterioration in the renal structure and function caused by cisplatin. Conclusion AFSC led to amelioration of cisplatin-induced ARF which was mediated by inhibition of apoptosis and activation of autophagy. The protective effects of AFSC were blunted by chloroquine, an inhibitor of autophagy, highlighting that activation of autophagy is an important mechanism of action for the protective role of AFSC in cisplatin-induced renal injury.

scholarly journals Staphylococcus aureus Infection Induced Oxidative Imbalance in Neutrophils: Possible Protective Role of Nanoconjugated Vancomycin

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Subhankari Prasad Chakraborty ◽  
Panchanan Pramanik ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Cell Damage ◽  
Treated Group ◽  
Protective Role ◽  
Control Group ◽  
Similar Dose ◽  
Cellular Components

Staphylococcus aureus infection causes oxidative stress in neutrophils. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The present study was aimed to test the protective role of nanoconjugated vancomycin against vancomycin-sensitive Staphylococcus aureus (VSSA) and vancomycin-resistant Staphylococcus aureus (VRSA) infection induced oxidative stress in neutrophils. VSSA- and VRSA-infection were developed in Swiss mice by intraperitoneal injection of 5×106 CFU/mL bacterial solutions. Nanoconjugated vancomycin was treated to VSSA- and VRSA-infected mice at its effective dose for 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result reveals that in vivo VSSA and VRSA infection significantly increases the level of lipid peroxidation, protein oxidation, oxidized glutathione level, and nitrite generation and decreases the level of reduced glutathione, antioxidant enzyme status, and glutathione-dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in nanoconjugated vancomycin-treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative imbalance in neutrophils.

Secondary bacterial pneumonia due to Staphylococcus aureus complicating 2009 influenza A (H1N1) viral infection

Infection ◽  
2010 ◽  
Vol 38 (3) ◽  
pp. 237-239 ◽  
Author(s):  
C. Tsigrelis ◽  
M. Mohammad ◽  
H. S. Fraimow ◽  
R. P. Dellinger ◽  
D. Marchesani ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Viral Infection ◽  
Bacterial Pneumonia ◽  
Influenza A ◽  
Influenza A H1n1 ◽  
Secondary Bacterial Pneumonia

scholarly journals Plasma gelsolin improves lung host defense against pneumonia by enhancing macrophage NOS3 function

2015 ◽  
Vol 309 (1) ◽  
pp. L11-L16 ◽  
Author(s):  
Zhiping Yang ◽  
Terry Ting-Yu Chiou ◽  
Thomas P. Stossel ◽  
Lester Kobzik
Keyword(s):  
Host Defense ◽  
Bacterial Pneumonia ◽  
Secondary Infection ◽  
Bacterial Clearance ◽  
Bacterial Killing ◽  
Plasma Gelsolin ◽  
Patients At Risk ◽  
Secondary Bacterial Pneumonia

Plasma gelsolin (pGSN) functions as part of the “extracellular actin-scavenging system,” but its potential to improve host defense against infection has not been studied. In a mouse model of primary pneumococcal pneumonia, recombinant human pGSN (rhu-pGSN) caused enhanced bacterial clearance, reduced acute inflammation, and improved survival. In vitro, rhu-pGSN rapidly improved lung macrophage uptake and killing of bacteria ( Streptococcus pneumoniae, Escherichia coli, and Francisella tularensis). pGSN triggers activating phosphorylation (Ser1177) of macrophage nitric oxide synthase type III (NOS3), an enzyme with important bactericidal functions in lung macrophages. rhu-pGSN failed to enhance bacterial killing by NOS3−/− macrophages in vitro or bacterial clearance in NOS3−/− mice in vivo. Prophylaxis with immunomodulators may be especially relevant for patients at risk for secondary bacterial pneumonia, e.g., after influenza. Treatment of mice with pGSN challenged with pneumococci on postinfluenza day 7 (the peak of enhanced susceptibility to secondary infection) caused a ∼15-fold improvement in bacterial clearance, reduced acute neutrophilic inflammation, and markedly improved survival, even without antibiotic therapy. pGSN is a potential immunomodulator for improving lung host defense against primary and secondary bacterial pneumonia.

scholarly journals Antibacterial Activity of Lefamulin against Pathogens Most Commonly Causing Community-Acquired Bacterial Pneumonia: SENTRY Antimicrobial Surveillance Program (2015–2016)

2019 ◽  
Vol 63 (4) ◽  
Author(s):  
Susanne Paukner ◽  
Steven P. Gelone ◽  
S. J. Ryan Arends ◽  
Robert K. Flamm ◽  
Helio S. Sader
Keyword(s):  
Staphylococcus Aureus ◽  
Bacterial Pneumonia ◽  
Oral Treatment ◽  
Multidrug Resistant ◽  
Surveillance Program ◽  
Content Type ◽  
Highly Active ◽  
Antimicrobial Surveillance ◽  
Drug Resistant Strains

ABSTRACTLefamulin, the first semisynthetic pleuromutilin antibacterial for intravenous and oral treatment of community-acquired bacterial pneumonia (CABP), and comparators were evaluated forin vitroactivity against a global collection of pathogens commonly causing CABP (n= 8595) from the 2015 and 2016 SENTRY Antimicrobial Surveillance Program. Lefamulin was highly active against the pathogensStreptococcus pneumoniae, including multidrug-resistant and extensively drug-resistant strains (MIC50/90for total and resistant subsets, 0.06/0.12 μg/ml; 100% inhibited at ≤1 μg/ml),Staphylococcus aureus, including methicillin-resistantStaphylococcus aureus(MRSA; both MIC50/90, 0.06/0.12 μg/ml; 99.8% and 99.6% inhibited at ≤1 μg/ml, respectively),Haemophilus influenzae(MIC50/90, 0.5/1 μg/ml; 93.8% inhibited at ≤1 μg/ml), andMoraxella catarrhalis(MIC50/90, 0.06/0.12 μg/ml; 100% inhibited at ≤0.25 μg/ml), and its activity was unaffected by resistance to other antibacterial classes.

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