High levels of C-reactive protein in the peripheral blood during visceral leishmaniasis predict subsequent development of post kala-azar dermal leishmaniasis

Acta Tropica ◽  
2000 ◽  
Vol 75 (1) ◽  
pp. 35-38 ◽  
Author(s):  
Soha Gasim ◽  
Thor G Theander ◽  
Ahmed M ElHassan
2019 ◽  
Vol 17 ◽  
pp. 205873921882268
Author(s):  
Shiping Qu ◽  
Chunyi Yu ◽  
Qian Xing ◽  
Haisheng Hu ◽  
Haiyan Jin

The aim of this study is to investigate the expression of CD62P and CD154 in peripheral blood of patients with rheumatoid arthritis (RA) and their correlation with the clinical indexes of RA. A total of 60 RA patients diagnosed and treated in the Department of Rheumatism in our hospital from January to December 2016 were selected as the RA group, and 60 cases of healthy subjects were selected as the control group. CD62P and CD154 levels in peripheral blood were determined by flow cytometry using the FACS Vantage flow cytometer, and the correlation analysis with the clinical indexes of RA patients were conducted. The levels of CD62P and CD154 in the peripheral blood of RA group were 28.75% ± 1.48% and 26.84% ± 1.03%, respectively, which were significantly higher than those of the control group ( P < 0.05). The levels of white blood cell (WBC), platelet (PLT), erythrocyte sedimentation rate (ESR), rheumatoid factor (RF), C-reactive protein (CRP), and interleukin (IL)-37 in the RA group were significantly higher than those in the control group ( P < 0.05). Pearson test showed that CD62P and CD154 levels in the peripheral blood in the RA group were positively correlated with serum WBC, PLT, ESR, RF, CRP, IL-37, and disease activity score 28 (DAS28) ( P < 0.05), but not correlated with disease course ( P > 0.05). The expression of CD62P and CD154 in peripheral blood of patients with RA was upregulated, and their expression levels were correlated with the activity of RA and the degree of joint lesion.


2018 ◽  
Vol 261 ◽  
pp. 383-390 ◽  
Author(s):  
Klaus Munkholm ◽  
Anne Sophie Jacoby ◽  
Toke Lenskjold ◽  
Helle Bruunsgaard ◽  
Maj Vinberg ◽  
...  

Blood ◽  
1993 ◽  
Vol 82 (2) ◽  
pp. 513-520 ◽  
Author(s):  
J Cermak ◽  
NS Key ◽  
RR Bach ◽  
J Balla ◽  
HS Jacob ◽  
...  

The acute inflammatory response is frequently accompanied by serious thrombotic events. We show that C-reactive protein (CRP), an acute- phase reactant that markedly increases its serum concentration in response to inflammatory stimuli, induced monocytes to express tissue factor (TF), a potent procoagulant. Purified human CRP in concentrations commonly achieved in vivo during inflammation (10 to 100 micrograms/mL) induced a 75-fold increase in TF procoagulant activity (PCA) of human peripheral blood mononuclear cells (PBM), with a parallel increase in TF antigen levels. CRP-induced PCA was completely blocked by a monoclonal antibody against human TF but not by irrelevant murine IgG. Dot blot analysis showed a significant increase of TF mRNA after 4 hours of incubation with CRP, followed by a peak of PCA within 6 and 8 hours. Actinomycin D and cycloheximide blocked CRP-stimulated PCA, suggesting that de novo TF protein synthesis was required. Endotoxin (LPS) contamination of CRP was excluded as the mediator of TF synthesis because: (1) CRP was Limulus assay negative; (2) induction of TF PCA by CRP was not blocked by Polymyxin B, in contrast to LPS- induced PCA; (3) antihuman CRP IgG inhibited CRP-induced PCA, but not LPS-induced PCA; (4) CRP was able to stimulate TF production in LPS- pretreated PBM refractory to additional LPS stimulation; and, (5) unlike LPS, CRP was incapable of inducing TF in human umbilical vein endothelial cells. We suggest that CRP-mediated TF production in monocytes may contribute to the development of disseminated intravascular coagulation and thrombosis in inflammatory states.


Author(s):  
Julia J. Schubert ◽  
Mattia Veronese ◽  
Tim D. Fryer ◽  
Roido Manavaki ◽  
Manfred G. Kitzbichler ◽  
...  

ABSTRACTBACKGROUNDImmune mechanisms have been implicated in the pathogenesis of depression, and translocator-protein (TSPO) targeted positron emission tomography (PET) has been used to assess neuroinflammation in major depressive disorder. We aimed to: (i) test the prior hypothesis of significant case-control differences in TSPO binding in anterior cingulate (ACC), prefrontal (PFC) and insular (INS) cortical regions; and (ii) explore the relationship between cerebral TSPO binding and peripheral blood concentration of C-reactive protein (CRP).METHODS51 depressed cases with Hamilton Depression Rating Scale score > 13 (median 17; IQR 16-22) and 25 healthy matched controls underwent dynamic brain 11C-PK11195 PET and peripheral blood immune marker characterisation. Depressed cases were divided into high CRP (>3mg/L;N=20) and low CRP (<3mg/L;N=31).RESULTSAcross the three regions, TSPO binding was significantly increased in cases vs controls (; F(1,71)=6.97, P=0.01). which was not influenced by differences in body mass index (BMI). The case-control difference was greatest in ACC (d=0.49; t(74)=2.00, .P=0.03) and not significant in PFC or INS (d=0.27; d=0.36). Following CRP stratification, significantly higher TSPO binding was observed in low CRP depression compared to controls (d=0.53; t(54)=1.96, P=0.03). These effect sizes are comparable to prior MDD case-control TSPO PET data. No significant correlations were observed between TSPO and CRP measures.CONCLUSIONSConsistent with previous findings, there is a modest increase in TSPO binding in depressed cases compared to healthy controls. The lack of a significant correlation between brain TSPO binding and blood CRP concentration or BMI poses questions about the interactions between central and peripheral immune responses in the pathogenesis of depression.


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