SAA Versus CRP Serum Levels in Different Inflammatory Conditions, Studied by Elisa Using Polyclonal Anti-AA and Monoclonal Anti-SAA Antibodies

1988 ◽  
pp. 229-233 ◽  
Author(s):  
Bouke P. C. Hazenberg ◽  
Pieter C. Limburg ◽  
Johan Bijzet ◽  
Martin H. van Rijswijk
Keyword(s):  
Serum Levels ◽  
Inflammatory Conditions

scholarly journals Sustained high expression of multiple APOBEC3 cytidine deaminases in systemic lupus erythematosus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Danielle Perez-Bercoff ◽  
Hélène Laude ◽  
Morgane Lemaire ◽  
Oliver Hunewald ◽  
Valérie Thiers ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cell Death ◽  
Lupus Erythematosus ◽  
Immunosuppressive Treatment ◽  
Elevated Serum ◽  
Serum Levels ◽  
Chronic Inflammatory Disease ◽  
Mrna Levels ◽  
Systemic Lupus ◽  
Inflammatory Conditions

AbstractAPOBEC3 (A3) enzymes are best known for their role as antiviral restriction factors and as mutagens in cancer. Although four of them, A3A, A3B, A3F and A3G, are induced by type-1-interferon (IFN-I), their role in inflammatory conditions is unknown. We thus investigated the expression of A3, and particularly A3A and A3B because of their ability to edit cellular DNA, in Systemic Lupus Erythematosus (SLE), a chronic inflammatory disease characterized by high IFN-α serum levels. In a cohort of 57 SLE patients, A3A and A3B, but also A3C and A3G, were upregulated ~ 10 to 15-fold (> 1000-fold for A3B) compared to healthy controls, particularly in patients with flares and elevated serum IFN-α levels. Hydroxychloroquine, corticosteroids and immunosuppressive treatment did not reverse A3 levels. The A3AΔ3B polymorphism, which potentiates A3A, was detected in 14.9% of patients and in 10% of controls, and was associated with higher A3A mRNA expression. A3A and A3B mRNA levels, but not A3C or A3G, were correlated positively with dsDNA breaks and negatively with lymphopenia. Exposure of SLE PBMCs to IFN-α in culture induced massive and sustained A3A levels by 4 h and led to massive cell death. Furthermore, the rs2853669 A > G polymorphism in the telomerase reverse transcriptase (TERT) promoter, which disrupts an Ets-TCF-binding site and influences certain cancers, was highly prevalent in SLE patients, possibly contributing to lymphopenia. Taken together, these findings suggest that high baseline A3A and A3B levels may contribute to cell frailty, lymphopenia and to the generation of neoantigens in SLE patients. Targeting A3 expression could be a strategy to reverse cell death and the generation of neoantigens.

scholarly journals Passive immunization of mice against D factor blocks lethality and cytokine release during endotoxemia.

1993 ◽  
Vol 178 (3) ◽  
pp. 1085-1090 ◽  
Author(s):  
M I Block ◽  
M Berg ◽  
M J McNamara ◽  
J A Norton ◽  
D L Fraker ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Intraperitoneal Administration ◽  
Passive Immunization ◽  
Serum Levels ◽  
Acute Injury ◽  
Cytokine Release ◽  
Inflammatory Conditions ◽  
Inflammatory Cytokine Response ◽  
The Many ◽  
Necrosis Factor

D factor, also known as leukemia inhibitory factor, is a pleiotropic cytokine whose role during acute injury and inflammation is not known. Intraperitoneal administration of Escherichia coli endotoxin induced D factor gene expression in mice, and passive immunization against D factor protected them from the lethal effects of endotoxin and blocked endotoxin-induced increases in serum levels of interleukin 1 and 6. Peak levels of tumor necrosis factor and interferon gamma were not affected. These results indicate that D factor is an essential early mediator of the inflammatory cytokine response and therefore may be important in the pathogenesis of the many inflammatory conditions, such as sepsis, arthritis, allograft rejection, and cancer immunotherapy.

scholarly journals Fetuin-A – Alpha2-Heremans-Schmid Glycoprotein: From Structure to a Novel Marker of Chronic Diseases Part 2. Fetuin-A – A Marker of Insulin Resistance and Related Chronic Diseases

2018 ◽  
Vol 11 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Regina S. Komsa-Penkova ◽  
Katya S. Kovacheva ◽  
Georgy M. Golemanov ◽  
Veselin P. Penkov ◽  
Zdravka V. Radionova ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Chronic Diseases ◽  
Polycystic Ovary ◽  
Serum Levels ◽  
Fetuin A ◽  
Inflammatory Conditions ◽  
Increased Risk ◽  
Proliferative Signaling

Summary Fetuin-A is a secretory liver glycoprotein with multiple physiological functions such as regulation of insulin resistance, tissue calcification, bone metabolism, cellular proteolytic activity, and self-proliferative signaling. Fetuin-A is a unique molecule which binds to the insulin receptor, modulating its sensitivity, and transducing “the physiological conditions” (serum levels of the metabolites like glucose, free fatty acids, inflammatory signals) from outside into inside the cells. Plasma fetuin-A levels correlate with reduced glucose tolerance and insulin resistance. Impaired insulin sensitivity leads to the development of metabolic syndrome, an increased risk for type 2 diabetes (T2DM), dyslipidaemias and cardiovascular diseases (CVDs). Furthermore, fetuin-A inversely correlates with inflammatory and activation biomarkers, e.g. in patients with T2DM. Thus, circulatory fetuin-A levels may have plausible predictive importance as a biomarker of risk of diabetes and negative acute phase protein. Dysregulated, it plays a crucial role in the pathogenesis of some metabolic disorders and clinical inflammatory conditions like metabolic syndrome, T2DM, CVDs, polycystic ovary syndrome (PCOS), etc.

scholarly journals Gut Microbiome and Common Variable Immunodeficiency: Few Certainties and Many Outstanding Questions

2021 ◽  
Vol 12 ◽  
Author(s):  
Gilda Varricchi ◽  
Remo Poto ◽  
Gianluca Ianiro ◽  
Alessandra Punziano ◽  
Gianni Marone ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Common Variable Immunodeficiency ◽  
Cell Activation ◽  
Immune Cell ◽  
Serum Levels ◽  
Therapeutic Interventions ◽  
Polygenic Inheritance ◽  
Alpha And Beta Diversity ◽  
Inflammatory Conditions ◽  
Common Variable

Common variable immunodeficiency (CVID) is the most common symptomatic primary antibody immunodeficiency, characterized by reduced serum levels of IgG, IgA, and/or IgM. The vast majority of CVID patients have polygenic inheritance. Immune dysfunction in CVID can frequently involve the gastrointestinal tract and lung. Few studies have started to investigate the gut microbiota profile in CVID patients. Overall, the results suggest that in CVID patients there is a reduction of alpha and beta diversity compared to controls. In addition, these patients can exhibit increased plasma levels of lipopolysaccharide (LPS) and markers (sCD14 and sCD25) of systemic immune cell activation. CVID patients with enteropathy exhibit decreased IgA expression in duodenal tissue. Mouse models for CVID unsatisfactorily recapitulate the polygenic causes of human CVID. The molecular pathways by which gut microbiota contribute to systemic inflammation and possibly tumorigenesis in CVID patients remain poorly understood. Several fundamental questions concerning the relationships between gut microbiota and the development of chronic inflammatory conditions, autoimmune disorders or cancer in CVID patients remain unanswered. Moreover, it is unknown whether it is possible to modify the microbiome and the outcome of CVID patients through specific therapeutic interventions.

scholarly journals Serum fetuin-A levels following recombinant human thyroid-stimulating hormone stimulation

2013 ◽  
Vol 36 (5) ◽  
pp. 264 ◽  
Author(s):  
AnneMarie Gagnon ◽  
Hussein Abujrad ◽  
Clara Irobi ◽  
Heather A Lochnan ◽  
Alexander Sorisky
Keyword(s):  
Thyroid Cancer ◽  
Cancer Recurrence ◽  
Serum Levels ◽  
Thyroid Stimulating Hormone ◽  
Human Thyroid ◽  
Fetuin A ◽  
Thyroxine Therapy ◽  
Inflammatory Conditions ◽  
Thyroid Cancer Recurrence ◽  
Stimulating Hormone

Purpose: Fetuin-A is a hepatokine that is linked to lipid metabolism, obesity, insulin resistance, type 2 diabetes and cardiovascular disease. Elevated thyroid-stimulating hormone (TSH) levels are associated with metabolic and cardiovascular disturbances. Our aim was to determine if TSH can regulate fetuin-A levels. Methods: Fetuin-A serum levels were examined in 26 subjects (19 women; previous thyroidectomy and radioactive iodine ablation) undergoing recombinant human TSH (rhTSH) stimulation to screen for thyroid cancer recurrence. Their age was 49±10 years, and body mass index (BMI) was 28±6 (both expressed as mean±SD). The patients received two doses of rhTSH (0.9 mg), administered 24 hours apart on days 1 and 2, without discontinuation of ongoing L-thyroxine therapy. Morning blood samples were obtained on days 1 (prior to the first dose of rhTSH), 3 and 5. Results: The baseline value of fetuin-A (mean±SD) for all participants was 527±186 mg/L. Values of fetuin-A did not change in response to rhTSH administration. The lack of response was not dependent on gender, age, baseline free thyroxine level or BMI. Conclusion: Fetuin-A has been implicated in metabolic and inflammatory conditions, but there have been no reports on whether fetuin-A is influenced by TSH. Within the context of rhTSH administration for surveillance of thyroid cancer recurrence, there was no effect on serum levels of fetuin-A.

Potential relevance of cerebrospinal fluid and serum levels and intrathecal synthesis of active matrix metalloproteinase-2 (MMP-2) as markers of disease remission in patients with multiple sclerosis

2009 ◽  
Vol 15 (5) ◽  
pp. 547-554 ◽  
Author(s):  
E Fainardi ◽  
M Castellazzi ◽  
C Tamborino ◽  
A Trentini ◽  
MC Manfrinato ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Matrix Metalloproteinase ◽  
Serum Levels ◽  
Recovery Phase ◽  
Matrix Metalloproteinase 2 ◽  
Mean Values ◽  
Active Matrix ◽  
Intrathecal Synthesis ◽  
Inflammatory Conditions

Background Little is known about the involvement of matrix metalloproteinase-2 (MMP-2) and its tissue inhibitor TIMP-2 in multiple sclerosis (MS). Objective To elucidate the actual implication of MMP-2 and TIMP-2 in MS. Methods Cerebrospinal fluid (CSF) and serum levels of active MMP-2 and TIMP-2 were measured by activity assay system and ELISA, respectively, in 67 patients with relapsing–remitting MS (RRMS), categorized according clinical and magnetic resonance imaging (MRI), and in 129 controls. Results Cerebrospinal fluid and serum active MMP-2/TIMP-2 ratio mean values and an intrathecal active MMP-2 production were more increased in RRMS than in non-inflammatory conditions ( P < 0.001, P < 0.05, and P < 0.0001, respectively) and in MRI inactive than in MRI active RRMS ( P < 0.02, P < 0.01 and P < 0.001, respectively). An intrathecal synthesis of active MMP-2 was more frequent in RRMS than in inflammatory disorders ( P < 0.01). Serum active MMP-2/TIMP-2 ratio and MS disease duration were positively correlated ( P < 0.02). Conclusion These findings suggest a potential role for MMP-2 activity in the termination of MS neuroinflammation related to remission of the disease and seem to indicate that serum MMP-2/TIMP-2 ratio may represent a useful biomarker for monitoring MS recovery phase.

The CX3C-Chemokine Fractalkine (CX3CL1) is Detectable in Serum of Patients Affected by the Inflammatory Diseases Allergic Rhinitis and/or Asthma

2005 ◽  
Vol 3 (3) ◽  
pp. 149-152
Author(s):  
P.L. Minciullo ◽  
M. Patafi ◽  
L. Giannetto ◽  
R.A. Merendino ◽  
G. Di Pasquale ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Potential Role ◽  
Inflammatory Diseases ◽  
Allergic Diseases ◽  
Serum Levels ◽  
Airway Disease ◽  
High Serum ◽  
Allergic Airway Disease ◽  
Inflammatory Conditions ◽  
Healthy Donors

Fractalkine (FKN) is a chemokine able to mediate the initial capture, firm adhesion, and activation of circulating leukocytes. Many tissues express FKN mRNA and FKN expression is increased during inflammatory conditions. To assess a possible involvement in allergic airway disease, we detected serum levels of FKN in a group of patients affected by allergic rhinitis and/or asthma and found high serum levels of FKN in all patients and in only 26% of healthy donors at lower concentrations. The present results underscore the potential role that this chemokine may play in the pathogenesis of respiratory allergic diseases.

Alkaline Phosphatase Levels Before and After Nonsurgical Periodontal Therapy

2019 ◽  
Vol 3 (2) ◽  
pp. 62-65
Author(s):  
Shaili Pradhan ◽  
Pramod Kumar Koirala
Keyword(s):  
Alkaline Phosphatase ◽  
Chronic Periodontitis ◽  
Correct Diagnosis ◽  
Serum Levels ◽  
Periodontal Therapy ◽  
Inflammatory Conditions ◽  
Nonsurgical Periodontal Therapy ◽  
Before And After ◽  
Periodontal Destruction ◽  
Supporting Structures

Introduction: Chronic periodontitis is a multifactorial disease resulting in the inflammation and destruction of the supporting structures. Early detection of periodontal changes, prognosis and efficacy of treatment have been monitored by Alkaline Phosphatase Levels (ALP) levels. Objective: This study was carried out to determine level of ALP in saliva and serum before and after periodontal therapy. Methods: This pretest posttest study included 22 patients with generalised chronic periodontitis (GCP). The patients received nonsurgical periodontal therapy (NSPT). Saliva and serum levels of ALP were measured at baseline and after two months of periodontal therapy. Results: Twenty-two patients of mean age 44 years were analysed. Participants had significantly better periodontal parameters after two months. Salivary ALP levels, which were high at baseline, decreased after periodontal treatment. A significant positive correlation (0.0001) was found between the salivary levels of ALP and periodontal inflammatory conditions. Gingival index was found directly proportional with salivary ALP level but not with serum ALP. Conclusion: Periodontal therapy lowered the levels of ALP saliva in GCP patients with high ALP levels. Biochemical analysis of enzymes found in saliva may help in patients’ evaluation to determine the control and progression of periodontal destruction and aid in a correct diagnosis, prognosis and, consequently, better treatment.

scholarly journals Elevated IL-38 Serum Levels in Newly Diagnosed Multiple Sclerosis and Systemic Sclerosis Patients

2020 ◽  
pp. 1-8
Author(s):  
Maryam Zarrabi ◽  
Mohammadali Nazarinia ◽  
Abbas Rahimi Jaberi ◽  
Nasser Gholijani ◽  
Zahra Amirghofran
Keyword(s):  
Multiple Sclerosis ◽  
Systemic Sclerosis ◽  
Serum Levels ◽  
Healthy Controls ◽  
Newly Diagnosed ◽  
Inflammatory Conditions ◽  
Probable Role ◽  
Previously Treated ◽  
Inflammatory Profile

<b><i>Objective:</i></b> Interleukin (IL)-38 is a newly discovered member of the IL-1 cytokine family with a proposed anti-inflammatory profile. We studied the probable role of this cytokine in the pathogenesis of two autoimmune diseases: multiple sclerosis (MS) and systemic sclerosis (SSc). <b><i>Subjects and Methods:</i></b> A total of 87 MS patients and 86 SSc patients (40 new and recently untreated cases and 46 treated cases) were selected for this study. Eighty-seven and 80 age- and sex-matched healthy subjects were included as controls for MS and SSc, respectively. Clinical and paraclinical features of the patients were recorded at the time of sampling. Serum IL-38 was measured by ELISA. <b><i>Results:</i></b> Levels of serum IL-38 did not significantly differ between the total MS or SSc patients compared to controls. However, levels of IL-38 were significantly higher in newly diagnosed patients of MS (206.43 ± 38.97 pg/mL, <i>p</i> &#x3c; 0.0001) than in those previously treated (158.04 ± 39.45 pg/mL). Similarly, new/recently untreated cases of SSc patients showed increased IL-38 levels (185.19 ± 36.27 pg/mL, <i>p</i> = 0.001) compared to treated patients (166.82 ± 33.08 pg/mL). IL-38 levels in newly diagnosed MS patients (<i>p</i> = 0.007) and new/recently untreated SSc patients (<i>p</i> = 0.032) were significantly higher than those in healthy controls. <b><i>Conclusion:</i></b> The higher serum levels of IL-38 in new or recently untreated cases of MS and SSc patients than in treated patients and healthy controls suggest the possible role of this cytokine in the development of these diseases or as part of a feedback loop to attenuate the inflammatory conditions in early stages of these diseases.

scholarly journals Vaspin in atherosclerotic disease and cardiovascular risk in axial spondyloarthritis: a genetic and serological study

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Javier Rueda-Gotor ◽  
Raquel López-Mejías ◽  
Sara Remuzgo-Martínez ◽  
Verónica Pulito-Cueto ◽  
Alfonso Corrales ◽  
...  
Keyword(s):  
Axial Spondyloarthritis ◽  
Subclinical Atherosclerosis ◽  
Serum Levels ◽  
High Serum ◽  
Normal Weight ◽  
Minor Allele ◽  
Atherosclerotic Disease ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Conditions ◽  
Cv Disease

Abstract Background Vaspin is a novel anti-inflammatory adipokine associated with cardiovascular (CV) disease and inflammation in chronic inflammatory conditions different from axial spondyloarthritis (axSpA). Given the high incidence of CV disease (mainly due to accelerated atherosclerosis) exhibited by axSpA patients, we wondered if vaspin could also be a key molecule in this process. However, data on the role of vaspin regarding atherosclerotic disease in the context of axSpA is scarce. For this reason, we aimed to evaluate the implication of vaspin, at the genetic and serological level, in subclinical atherosclerosis and CV risk in axSpA. Methods This study included 510 patients diagnosed with axSpA. Carotid ultrasound (US) was performed to evaluate the presence of subclinical atherosclerosis. Three vaspin gene variants (rs2236242, rs7159023, and rs35262691) were genotyped by TaqMan probes. Serum vaspin levels were assessed by enzyme-linked immunosorbent assay. Statistical analysis was performed using STATA® v.11.1. Results Serum vaspin levels were significantly higher in female patients than in males and also in obese patients when compared to those with normal weight (p < 0.05). At the genetic level, we disclosed that the minor allele of rs2236242 (A) was associated with lower serum vaspin levels in axSpA, while the rs7159023 minor allele (A) was linked to higher serum levels (p < 0.05). When the three polymorphisms assessed were combined conforming haplotypes, we disclosed that the TGC haplotype related to high serum levels of vaspin (p = 0.01). However, no statistically significant association was observed between vaspin and markers of subclinical atherosclerosis, both at the genetic and serological level. Conclusions Our results revealed that vaspin is linked to CV risk factors that may influence on the atherosclerotic process in axSpA. Additionally, we disclosed that serum vaspin concentration is genetically modulated in a large cohort of patients with axSpA.

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