Potential Role of Trimethoprim-Sulfamethoxazole in the Treatment of Serious Hospital-Acquired Bacterial Infections

1987 ◽  
Vol 9 (Supplement_2) ◽  
pp. S160-S165 ◽  
Author(s):  
Richard Quintiliani ◽  
Robert E. Levitz ◽  
Charles H. Nightingale
Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Kentaro Ueno

Objective: Circulating platelet-neutrophil aggregates play a crucial role in amplifying acute inflammation and could promote adverse effects involving vascular injury. The aim of this study was to clarify the role of platelet-neutrophil aggregates in patients with Kawasaki disease (KD). Methods: We analyzed 40 patients with KD (30 intravenous immunoglobulin [IVIG] responders and 10 IVIG non-responders), 7 febrile patients with bacterial infections, and 9 normal volunteers. Thirty-three patients with KD were treated with IVIG alone, and remaining seven were treated with IVIG plus prednisolone. We evaluated the rate of platelet-neutrophil aggregates and measured the platelet factor 4 (PF4) and β-thromboglobulin (β-TG) levels in patients with KD. Results: The rate of platelet-neutrophil aggregates was significantly higher in patients with KD than in both patients with bacterial infection and normal volunteers. There was a trend toward increased rate of platelet-neutrophil aggregates within 2 or 3 days after IVIG than before IVIG. The rate of platelet-neutrophil aggregates was significantly higher in patients who showed coronary artery abnormalities (CAA) than in those who showed without CAA and was correlated with PF4 and β-TG levels in patients with KD. Comparing time course analysis, the rate of platelet-neutrophil aggregates was significantly decreased in patients treated with IVIG plus prednisolone than in those treated with IVIG alone. Conclusions: Our findings demonstrate that platelet-neutrophil aggregates play a crucial role in regulating vasculitis, and are involved in the development of CAA. Additional prednisolone treatment in the acute phase of KD might have a potential role in inhibiting amplified reciprocal inflammatory activation by suppressing platelet-neutrophil aggregates.


2010 ◽  
Vol 79 (1) ◽  
pp. 342-352 ◽  
Author(s):  
Natalia Malachowa ◽  
Petra L. Kohler ◽  
Patrick M. Schlievert ◽  
Olivia N. Chuang ◽  
Gary M. Dunny ◽  
...  

ABSTRACTStaphylococcus aureusis a prominent human pathogen and a leading cause of community- and hospital-acquired bacterial infections worldwide. Herein, we describe the identification and characterization of theS. aureus67.6-kDa hypothetical protein, named for thesurface factor promoting resistance tooxidativekilling (SOK) in this study. Sequence analysis showed that the SOK gene is conserved in all sequencedS. aureusstrains and homologous to the myosin cross-reactive antigen ofStreptococcus pyogenes.Immunoblotting and immunofluorescence analysis showed that SOK was copurified with membrane fractions and was exposed on the surface ofS. aureusNewman and RN4220. Comparative analysis of wild-typeS. aureusand an isogenic deletion strain indicated that SOK contributes to both resistance to killing by human neutrophils and to oxidative stress. In addition, theS. aureus sokdeletion strain showed dramatically reduced aortic valve vegetation and bacterial cell number in a rabbit endocarditis model. These results, plus the suspected role of the streptococcal homologue in certain diseases such as acute rheumatic fever, suggest that SOK plays an important role in cardiovascular and other staphylococcal infections.


1997 ◽  
Vol 65 (8) ◽  
pp. 3300-3303 ◽  
Author(s):  
M Bakhiet ◽  
A Diab ◽  
Mahamustafa ◽  
Jiezhu ◽  
L Lindqvist ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Savino Sciascia ◽  
Massimo Radin ◽  
Mario Bazzan ◽  
Barbara Montaruli ◽  
Domenico Cosseddu ◽  
...  

The clinical significance of antiphospholipid antibodies (aPL) in the context of infections has attracted attention since their first discovery in patients with syphilis. In fact, the recognition of aPL in patients with infections has been described in parallel to the understating of the syndrome. Since the first description of aPL-positive tests in three patients with COVID-19 diagnosed in January 2020 in Wuhan, China, a large number of studies took part in the ongoing debate on SARS-2-Cov 2 induced coagulopathy, and many following reports speculated a potential role for aPL. In order to get further insights on the effective role of detectable aPL in the pro-thrombotic status observed in COVID-19 patients, we performed an observational age-sex controlled study to compare the aPL profile of hospitalized patients with COVID with those observed in a) patients with thrombotic APS and b) patients with cultural/serologically-proved infections. Our data showed positive aPL testing in about half of the patients (53%) with COVID-19 and patients with other viral/bacterial infections (49%). However, aPL profile was different when comparing patients with overt APS and patients with aPL detected in the contest of infections. Caution is therefore required in the interpretation and generalization of the role of aPL s in the management of patients with COVID-19. Before introducing aPL testing as a part of the routine testing in patients with COVID-19, larger well-designed clinical studies are required. While the pro-thrombotic status in patients with COVID-19 is now unquestionable, different mechanisms other than aPL should be further investigated.


2021 ◽  
Vol 11 ◽  
Author(s):  
Valerio Nardone ◽  
Rocco Giannicola ◽  
Giovanna Bianco ◽  
Diana Giannarelli ◽  
Paolo Tini ◽  
...  

Peripheral-immune-checkpoint blockade (P-ICB) with mAbs to PD-1 (nivolumab and pembrolizumab) or PD-L1 (atezolizumab, durvalumab, avelumab) alone or combination with chemotherapy represents a novel active treatment for mNSCLC patients. However, this therapy can be associated to immune-related adverse events (irAEs) and high cost. Therefore, finding reliable biomarkers of response and irAEs is strongly encouraged to accurately select patients who may potentially benefit from the immuno-oncological treatment. This is a retrospective multi-institutional analysis performed on ninety-five mNSCLC patients who received real-world salvage therapy with nivolumab or atezolizumab between December 2015 and April 2020. The outcome of these patients in term of PFS and OS was evaluated in comparison with different serum levels of C-reactive protein (CRP), Erythrocyte Sedimention Rate (ESR) and Procalcitonin (PCT) by performing Kaplan–Meier and Log-rank test and multivariate analysis. We found that high baseline levels of CRP, ESR, and PCT were strongly predictive of poor outcome (P <0.05) with the worse prognosis detected in those patients with a baseline levels of both ESR and PCT over the pre-established cut off (median OS recorded in patients with no marker over the cut off vs. those with just one marker over the cut off vs. those with both markers over the cut off: 40 ± 59 vs. 15.5 ± 5.5 vs. 5.5 ± 1.6 months, respectively; P <0.0001). Our results suggest the predictive value of systemic inflammation and suggest a potential role of PCT in predicting a poor outcome in mNSCLC receiving PD-1/PD-L1 blocking mAbs. This finding also suggests a potential role of subclinical bacterial infections in defining the response to PD-1/PD-L1 blocking mAbs that deserves further and more specific investigations.


2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Zihe Yan ◽  
Junjun Yang ◽  
Renjing Hu ◽  
Xichi Hu ◽  
Kong Chen

Acinetobacter baumanniiis a significant cause of severe hospital-acquired infections with a recent rise in multidrug-resistant infections involving traumatic wounds of military personnel. The interleukin-17 (IL-17) pathway is essential for neutrophil recruitment in response to a variety of pathogens, while the control ofA. baumanniiinfection is known to be dependent on neutrophils. This suggests that IL-17 may play an important role inA. baumanniiinfection; however, this has yet to be studied. Here, we summarize the recent advances in understanding the host-pathogen interaction ofA. baumanniiand propose a potential role of the IL-17 pathway in generating a protective immune response.


2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Gabriella Wojewodka ◽  
Juan B. De Sanctis ◽  
Danuta Radzioch

Patients with cystic fibrosis (CF) are afflicted with many symptoms but the greatest challenge is the fight against chronic bacterial infections, leading to decreased lung function and ultimately death. Our group has recently found reduced levels of ceramides in CF patients and mice. Ceramides are sphingolipids involved in the structure of cell membranes but also participate in the inflammatory response, in cell signalling through membrane microdomains (lipid rafts), and in apoptosis. These characteristics of ceramides make them strong candidates for therapeutic intervention in CF. As more studies have come to evaluate the role of ceramide in CF, conflicting results have been described. This paper discusses various views regarding the potential role of ceramide in CF, summarizes methods of ceramide detection and their role in the regulation of cellular and molecular processes.


2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.


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