scholarly journals The Effect of Synthetic C-Reactive Protein on the In Vitro Immune Response of Human PBMCs Stimulated with Bacterial Reagents

Inflammation ◽  
2013 ◽  
Vol 36 (4) ◽  
pp. 781-792 ◽  
Author(s):  
Atsushi Sato ◽  
Hiroyuki Nakashima ◽  
Manabu Kinoshita ◽  
Masahiro Nakashima ◽  
Yoshiko Ogawa ◽  
...  
2013 ◽  
Vol 47 (1) ◽  
pp. 31-39
Author(s):  
Atsushi Sato ◽  
Manabu Kinoshita ◽  
Hiroyuki Nakashima ◽  
Masahiro Nakashima ◽  
Masami Ikarashi ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Andreea Lorena Mateescu ◽  
Nicolae-Bogdan Mincu ◽  
Silvana Vasilca ◽  
Roxana Apetrei ◽  
Diana Stan ◽  
...  

AbstractThe purpose of the present study was to evaluate de influence of protein–sugar complexation on the stability and functionality of C-reactive protein, after exposure to constant high temperatures, in order to develop highly stable positive controls for in-vitro diagnostic tests. C-reactive protein is a plasmatic protein used as a biomarker for the diagnosis of a series of health problems such as ulcerative colitis, cardiovascular diseases, metabolic syndrome, due to its essential role in the evolution of chronic inflammation. The sugar–protein interaction was investigated using steady state and time resolved fluorescence. The results revealed that there are more than two classes of tryptophan, with different degree of accessibility for the quencher molecule. Our study also revealed that sugar–protein complexes have superior thermostability, especially after gamma irradiation at 2 kGy, the protein being stable and functional even after 22 days exposure to 40 °C.


1982 ◽  
Vol 156 (1) ◽  
pp. 230-242 ◽  
Author(s):  
F C de Beer ◽  
A K Soutar ◽  
M L Baltz ◽  
I M Trayner ◽  
A Feinstein ◽  
...  

C-reactive protein (CRP), the classical acute-phase protein, can bind phospholipids by virtue of its specific, calcium-dependent reactivity with phosphorylcholine residues. However, analysis of acute-phase serum by gel filtration and by density gradient ultracentrifugation showed that the CRP was in a free, uncomplexed form, despite the coexistent presence of the various classes of serum lipoproteins, all of which contain phospholipids. In contrast, when isolated CRP was aggregated by immobilization at a sufficient density on a solid phase and then exposed to normal human serum, it selectively bound low density lipoprotein (LDL) and traces of very low density lipoprotein. The reaction was calcium dependent and reversible by free phosphorylcholine but not by heparin. LDL isolated from normal plasma was also bound by aggregated CRP. CRP reacts in vitro with a wide variety of different ligands both of extrinsic and of autogenous origin, e.g., microbial products and damaged cell membranes, respectively. If CRP aggregated in vivo by complexing with these ligands than acquires the capacity to selectively bind LDL, the phenomenon may have significant implications for the function of CRP and for the metabolism, clearance, and deposition of LDL.


10.17816/cp66 ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 19-31
Author(s):  
Irina K. Malashenkova ◽  
Sergey A. Krynskiy ◽  
Daniil P. Ogurtsov ◽  
Nikita A. Hailov ◽  
Natalia V. Zakharova ◽  
...  

Introduction. Associations of disturbances in innate and adaptive immunity during the clinical course of schizophrenia have been found in a number of studies. Yet, the relationship of immune parameters and systemic inflammation in relation to the clinical course of the disease and its prognosis, remains poorly understood, which highlights an interesting topic for further research. The goal of this study was to research the immuno-inflammatory changes in patients with clinical continuous and episodic paranoid schizophrenia, to assess the pathogenetic significance of these changes. Methods. Thirty-six patients with paranoid schizophrenia, of which 20 had episodic symptoms and 16 had continuous symptoms, consented to participate in the study, together with 30 healthy volunteers. In the study we assessed the parameters of innate immune response (serum levels of key pro-inflammatory and anti-inflammatory cytokines, C-reactive protein) and the adaptive immune response, including humoral-mediated immunity (serum immunoglobulins IgA, IgM, IgG, circulating immune complexes), as well as the cell link of adaptive immunity (key lymphocyte subpopulations). Positive and negative symptoms were assessed with the positive and negative symptoms scale; frontal dysfunction was assessed by Frontal Assessment Battery (FAB). Results. Both patient groups had higher than normal levels of C-reactive protein and IL-8. There was a significant elevation of circulating immune complexes among patients with continuous symptoms of schizophrenia, compared to patients with episodic symptoms and healthy controls. Levels of CD45+CD3+ lymphocytes (T-cells) differed between clinical groups, with higher values identified among patients with episodic symptoms and lower values among those with continuous symptoms. In addition, patients with episodic symptoms had significantly increased levels of CD45+CD3+CD4+CD25+CD127- regulatory T-cells. Finally, the level of CD45+CD3-CD19+ B-cells was significantly higher among patients with continuous symptoms vs. patients with episodic symptoms and the control groups. Markers of activation of humoral immunity were associated with the severity of frontal disorders in these patients. Discussion. Comprehensive data on the serum level of cytokines and the parameters of adaptive immunity among individuals with continuous schizophrenia, by comparison with patients with episodic schizophrenia, are practically absent in the literature. We have shown that among those with continuous schizophrenia, there are signs of systemic inflammation and chronic activation of the adaptive humoral immune response, while among patients with episodic symptoms of the disease, there are signs of systemic inflammation and certain activation of cell-mediated immunity, without significant changes in the humoral link of adaptive immunity. Conclusion. More studies are needed, but the data obtained in this study are important for subsequent clinical studies of new treatment methods, based on various immunophenotypes of schizophrenia.


1990 ◽  
Vol 20 (3) ◽  
pp. 165-174 ◽  
Author(s):  
A.B. Singh ◽  
K. Hiehle ◽  
P. Casale ◽  
S. Gerber ◽  
S. Nayar ◽  
...  

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Nicholas Parchim ◽  
Wei Wang ◽  
Chen Liu ◽  
Athar Siddiqui ◽  
Rodney Kellems ◽  
...  

Introduction: C-Reactive Protein (CRP) is an important immunomodulatory molecule. Early studies have indicated that CRP is elevated in preeclamptic patient sera, but its function remains unclear. CRP is known to bind with phosphocholine (PC) of bacteria membrane to kill bacteria by triggering innate immune response. Phosphocholination is a post-translational modification mediated by PC transferase, an enzyme reported expressed only in two tissues, including placenta and testis. Recent studies identified that Neurokinin B (NKB), a known, placenta-enriched pathogenic molecule for preeclampsia (PE), is phosphocholinated. This modification increases its stability, preferentially activates NK3 receptor (NK3R) and promotes PE features. Given CRP can bind to PC on bacterial membranes, the role that phosphocholination plays is a mystery. In light of NKB, being phosphocholinated in the endoplasmic reticulum and signals via the NK3R in the pathogenesis of PE, we feel that elevated CRP may be associated with NKB and contributes to the pathophysiology of PE via NK3R activation. Results: ELISA results show that CRP is significantly elevated in PE vs. control sera_65 ug/mL vs. 10 ug/ml; p<0.0001. Western blot analysis reveals that CRP, NKB, and NK3R are significantly increased in PE vs. control placental tissue. Immunohistochemistry studies indicate that all of these three molecules are abundant in syncytiotrophoblast cells. Co-immunoprecipitation demonstrates an interaction between CRP and NKB. In vitro , we provide the first evidence that CRP decreased the invasion of trophoblast cells from 0.7 ± 0.06 to 0.06 ± 0.001 invasion index; p<0.005, while treatment with SB222200 ameliorates shallow invasion from 0.28 ± 0.09 to 0.55 ± 0.07 invasion index; p<0.05. Significantly, infusion of CRP into pregnant mice induces hypertension (169.152 ± 14.7 mmHg vs. 141.916 ± 6.93 mmHg; p<0.05) and proteinuria (28.78 ± 13.56 mg albumin/μg Cr vs. 13.87 ± 3.277 mg albumin/μg Cr; p<0.05). Conclusion: Our findings demonstrate elevated CRP contributes to PE and NKB/NK3R is a new mechanism underlying CRP-mediated shallow invasion and disease development. These studies suggest novel pathogenic biomarkers and innovative therapies for PE.


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