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2021 ◽  
Vol 20 (10) ◽  
pp. 2235
Author(s):  
Shuhong Ding ◽  
Hongzhi Li ◽  
Xiaohui Li ◽  
Wenwen Wang ◽  
Xiuling Du ◽  
...  

This article previously published in Volume 17 Issue 16 of this journal in September 2017 has been retracted in line with the guidelines from the Committee on Publication Ethics (COPE,http://publicationethics.org/ resources/guidelines). Retraction: Ding S, Li H, Li X, Wang W, Du X, Dong G, Zhang P. Serum amyloid P down-regulates CCL-1 expression, and inhibits Ras/MAPK signaling and development of breast cancer. Trop J Pharm Res 2017; 16(9):2089-2095 doi: http://dx.doi.org/10.4314/tjpr.v16i9.7 To the editor: The figures in the paper were plagiarized partly from an earlier published article, Qi et al, P-selectinmediated tablet adhesion promoters tumor growth. Oncotarget 2015;30:6(9):6584–6596, and data from a master's thesis submitted by Bin Li under the supervision of Professor Lijing Wang and Professor Cuiling Qi. Sincerely, Cuiling Qi and Lijing Wang.


Author(s):  
Stephan Ellmerich ◽  
Graham W Taylor ◽  
Connor D Richardson ◽  
Thais Minett ◽  
A Floriaan Schmidt ◽  
...  

Abstract Despite many reported associations, the direct cause of neurodegeneration responsible for cognitive loss in Alzheimer’s disease and some other common dementias is not known. The normal human plasma protein, serum amyloid P component, a constituent of all human fibrillar amyloid deposits and present on most neurofibrillary tangles, is cytotoxic for cerebral neurones in vitro and in experimental animals in vivo. The neocortical content of serum amyloid P component was immunoassayed in 157 subjects aged 65 or more with known dementia status at death, in the large scale, population-representative, brain donor cohort of the Cognitive Function and Ageing Study, which avoids the biases inherent in studies of predefined clinico-pathological groups. The serum amyloid P component values were significantly higher in individuals with dementia, independent of serum albumin content measured as a control for plasma in the cortex samples. The odds ratio for dementia at death in the high serum amyloid P component tertile was 5.24 (95% CI 1.79–15.29) and was independent of Braak tangle stages and Thal amyloid-β phases of neuropathological severity. The strong and specific association of higher brain content of serum amyloid P component with dementia, independent of neuropathology, is consistent with a pathogenetic role in dementia.


Author(s):  
Mada Ghanem ◽  
Méline Homps-Legrand ◽  
Marc Garnier ◽  
Lise Morer ◽  
Tiphaine Goletto ◽  
...  

Increased blood fibrocytes are associated with a poor prognosis in fibrotic lung diseases. We aimed to determine whether the percentage of circulating fibrocytes could be predictive of severity and prognosis during Coronavirus disease 2019 (COVID-19) pneumonia. Blood fibrocytes were quantified by flow cytometry as CD45+/CD15-/CD34+/Collagen-1+cells in patients hospitalized for COVID-19 pneumonia. In a subgroup of patients admitted in ICU, fibrocytes were quantified in blood and broncho-alveolar lavage (BAL). Serum amyloid P (SAP), TGF-b1,CXCL12, CCL2, and FGF2 serum concentration were measured in serum. We included 57 patients in the Hospitalized group (median age 59 years [23-87]) and 16 Healthy controls. The median percentage of circulating fibrocytes was higher in patients compared to controls (3.6% [0.2-9.2] vs. 2.1% [0.9-5.1], p=0.04). Blood fibrocyte count was lower in the 6 patients who died compared to survivors (1.6% [0.2-4.4] vs. 3.7% [0.6-9.2], p=0.02). Initial fibrocyte count was higher in patients showing a complete lung CT resolution at 3 months. Circulating fibrocyte count was decreased in the ICU group (0.8% [0.1-2.0]) whereas BAL fibrocyte count was 6.7% [2.2-15.4]. Serum SAP and TGF-b1 concentrations were increased in Hospitalized patients. SAP was also increased in ICU patients. CXCL12 and CCL2 were increased in ICU patients, and negatively correlated with circulating fibrocyte count. We conclude that circulating fibrocytes were increased in patients hospitalized for COVID-19 pneumonia and a lower fibrocyte count was associated with an increased risk of death and a slower resolution of lung CT opacities.


2021 ◽  
Vol 10 (17) ◽  
pp. 3879
Author(s):  
María Insenser ◽  
Nuria Vilarrasa ◽  
Joan Vendrell ◽  
Héctor F. Escobar-Morreale

Bariatric surgery restores glucose tolerance in many, but not all, severely obese subjects with type 2 diabetes (T2D). We aimed to evaluate the plasma protein profiles associated with the T2D remission after obesity surgery. We recruited seventeen women with severe obesity submitted to bariatric procedures, including six non-diabetic patients and eleven patients with T2D. After surgery, diabetes remitted in 7 of the 11 patients with T2D. Plasma protein profiles at baseline and 6 months after bariatric surgery were analyzed by two-dimensional differential gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight coupled to mass spectrometry (MALDI-TOF/TOF MS). Remission of T2D following bariatric procedures was associated with changes in alpha-1-antichymotrypsin (SERPINA 3, p < 0.05), alpha-2-macroglobulin (A2M, p < 0.005), ceruloplasmin (CP, p < 0.05), fibrinogen beta chain (FBG, p < 0.05), fibrinogen gamma chain (FGG, p < 0.05), gelsolin (GSN, p < 0.05), prothrombin (F2, p < 0.05), and serum amyloid p-component (APCS, p < 0.05). The resolution of diabetes after bariatric surgery is associated with specific changes in the plasma proteomic profiles of proteins involved in acute-phase response, fibrinolysis, platelet degranulation, and blood coagulation, providing a pathophysiological basis for the study of their potential use as biomarkers of the surgical remission of T2D in a larger series of severely obese patients.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Qiu Qin ◽  
Ronghua Song ◽  
Peng Du ◽  
Chaoqun Gao ◽  
Qiuming Yao ◽  
...  

Objective. Rheumatoid arthritis (RA) is a complex disease with unknown pathogenesis. In recent years, fewer have paid attention to the broad spectrum of systemic markers of RA. The aim of this study was to identify exosomal candidate proteins in the pathogenesis of RA. Methods. Totally, 12 specimens of plasma from 6 RA patients and 6 age- and gender-matched controls from the Chinese population were obtained for nanoscale liquid chromatography coupled to tandem mass spectrometry (nano-LC-MS/MS) analysis to identify exosomal profiles. Results. A total of 278 exosomal proteins were detected. Among them, 32 proteins were significantly upregulated ( FC ≥ 2.0 and P < 0.05 ) and 5 proteins were downregulated ( FC ≤ 0.5 and P < 0.05 ). Bioinformatics analysis revealed that transthyretin (TTR), angiotensinogen (AGT), lipopolysaccharide-binding protein (LBP), monocyte differentiation antigen CD14 (CD14), cartilage oligomeric matrix protein (COMP), serum amyloid P (SAP/APCS), and tenascin (TNC) can interact with each other. Subsequently, these cross-linked proteins may be mainly involved in the inflammatory-related pathways to mediate the onset of RA. Noteworthy, the LBP/CD14 complex can promote the expression of IL-8 and TNF-α, eventually leading to the development of RA. Conclusions. Our findings suggest distinct plasmatic exosomal protein profiles in RA patients. These proteins not only take important parts in the vicious circle in the pathogenic process of RA but also serve as novel biomarkers in RA diagnosis and prognosis.


Author(s):  
Nathella Pavan Kumar ◽  
Aishwarya Venkataraman ◽  
Luke Elizabeth Hanna ◽  
Sulochana Putlibai ◽  
M Karthick ◽  
...  

Abstract Background Multisystem Inflammatory Syndrome in children (MIS-C) is a rare manifestation of SARS-CoV2 infection in children that can result in increased morbidity and mortality. The inflammatory underpinnings of MIS-C have not been examined in detail. Methods We examined the plasma levels of acute phase proteins and microbial translocation markers in MIS-C, acute COVID-19 infection (COVID-19), SARS-CoV-2 seropositive and control children. Findings MIS-C children exhibited significantly higher levels of C-reactive protein (CRP), alpha2 macroglobulin (a2M), Serum Amyloid P (SAP), lipopolysaccharide (LPS), sCD14 and LPS binding protein (LBP) and significantly lower levels of haptoglobin (Hp) in comparison to seropositive, control and/or COVID-19 children. In addition, COVID-19 children exhibited significantly higher levels of most of the above markers in comparison to seropositive and control children. PCA analysis using a set of these markers could clearly discriminate MIS-C and COVID-19 from seropositive and control children. MIS-C children requiring PICU admission and COVID-19 children with severe disease had higher levels of CRP, SAP and/or sCD14 at admission. Conclusion Our study describes the role of systemic inflammation and microbial translocation markers in children with MIS-C and COVID-19 and therefore helps in advancing our understanding of the pathogenesis of different presentations of SARS-CoV-2 infection in children.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Andrea Doni ◽  
Raffaella Parente ◽  
Ilaria Laface ◽  
Elena Magrini ◽  
Cristina Cunha ◽  
...  

AbstractSerum amyloid P component (SAP, also known as Pentraxin 2; APCS gene) is a component of the humoral arm of innate immunity involved in resistance to bacterial infection and regulation of tissue remodeling. Here we investigate the role of SAP in antifungal resistance. Apcs−/− mice show enhanced susceptibility to A. fumigatus infection. Murine and human SAP bound conidia, activate the complement cascade and enhance phagocytosis by neutrophils. Apcs−/− mice are defective in vivo in terms of recruitment of neutrophils and phagocytosis in the lungs. Opsonic activity of SAP is dependent on the classical pathway of complement activation. In immunosuppressed mice, SAP administration protects hosts against A. fumigatus infection and death. In the context of a study of hematopoietic stem-cell transplantation, genetic variation in the human APCS gene is associated with susceptibility to invasive pulmonary aspergillosis. Thus, SAP is a fluid phase pattern recognition molecule essential for resistance against A. fumigatus.


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245924
Author(s):  
Tejas R. Karhadkar ◽  
Darrell Pilling ◽  
Richard H. Gomer

SARS-CoV-2 is a single stranded RNA (ssRNA) virus and contains GU-rich sequences distributed abundantly in the genome. In COVID-19, the infection and immune hyperactivation causes accumulation of inflammatory immune cells, blood clots, and protein aggregates in lung fluid, increased lung alveolar wall thickness, and upregulation of serum cytokine levels. A serum protein called serum amyloid P (SAP) has a calming effect on the innate immune system and shows efficacy as a therapeutic for fibrosis in animal models and clinical trials. Here we show that aspiration of the GU-rich ssRNA oligonucleotide ORN06 into mouse lungs induces all of the above COVID-19-like symptoms. Men tend to have more severe COVID-19 symptoms than women, and in the aspirated ORN06 model, male mice tended to have more severe symptoms than female mice. Intraperitoneal injections of SAP starting from day 1 post ORN06 aspiration attenuated the ORN06-induced increase in the number of inflammatory cells and formation of clot-like aggregates in the mouse lung fluid, reduced ORN06-increased alveolar wall thickness and accumulation of exudates in the alveolar airspace, and attenuated an ORN06-induced upregulation of the inflammatory cytokines IL-1β, IL-6, IL-12p70, IL-23, and IL-27 in serum. SAP also reduced D-dimer levels in the lung fluid. In human peripheral blood mononuclear cells, SAP attenuated ORN06-induced extracellular accumulation of IL-6. Together, these results suggest that aspiration of ORN06 is a simple model for both COVID-19 as well as cytokine storm in general, and that SAP is a potential therapeutic for diseases with COVID-19-like symptoms and/or a cytokine storm.


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