Interleukin-1, interleukin-6, and interleukin-10 responses after antibiotic treatment in experimental chronic Staphylococcus aureus osteomyelitis

2006 ◽  
Vol 11 (4) ◽  
pp. 370-374 ◽  
Author(s):  
Felícito García-Alvarez ◽  
Marta Monzón ◽  
José María Grasa ◽  
Antonio Laclériga ◽  
Beatriz Amorena ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Antibiotic Treatment ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
Interleukin 10

scholarly journals Expression of Cytokines and Cytokine Receptors-Genes in Patients with Different Forms of Thyroid Pathology in Ukrainian Population

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Iryna Kamyshna ◽  
Aleksandr Kamyshnyi
Keyword(s):  
Autoimmune Thyroiditis ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
White Blood Cells ◽  
Elevated Serum ◽  
Interleukin 10 ◽  
Thyroid Peroxidase ◽  
Thyroid Peroxidase Antibodies ◽  
Interleukin 6 Receptor ◽  
Peripheral White Blood Cells

Abstract Multiple susceptibility genes can be involved in the development of Hashimoto’s thyroiditis. Some of these genes are implicated in other autoimmune diseases, while others are specific to thyroid autoimmune response. 153 patients with thyroid pathology were enrolled in the study (152 women and 1 man, the average age was 46,02±14,3). They were divided into 3 groups: 16 patients with postoperative hypothyroidism; 65 patients with hypothyroidism resulting from autoimmune thyroiditis, and 72 patients with both AIT and elevated serum an anti-thyroglobulin and anti-thyroid peroxidase antibodies. We used a pathway-specific real-time Polymerase chain reaction array to identify and verify cytokines and receptor pathway-associated gene expression in peripheral white blood cells in randomly selected 12 individuals from each group. In the patients with postoperative hypothyroidism and those with hypothyroidism resulting from autoimmune thyroiditis, the expression of Chemokine (C-X3-C motif) receptor 1, Chemokine (C-X-C motif) receptor 4, Interleukin 6, and Interleukin 6 receptor significantly decreased, while the expression of IL6ST and IL10RA increased. In contrast, mRNA levels of Chemokine (C-X3-C motif) receptor 1, Chemokine (C-X-C motif) receptor 4, Interleukin 6, and Interleukin 6 receptor increased in the autoimmune thyroiditis patients with elevated serum anti-thyroglobulin and anti-thyroid peroxidase antibodies, while the expression of Interleukin 6 signal transducer and Interleukin 10 receptor, alpha decreased in this group of patients. The patients with hypothyroidism resulting from autoimmune thyroiditis and patients with elevated serum anti-thyroglobulin and anti-thyroid peroxidase antibodies had significantly lowered expression of Interleukin 10, while the expression of Interleukin 1, beta and Interleukin 1 receptor, type I was elevated. autoimmune thyroiditis and hypothyroidism affect the mRNA-level expression of cytokines and cytokine receptor genes in a gene-specific manner, and these changes to gene expression can be among the triggers of autoimmune inflammation progression in the thyroid gland. Transcriptional activity of cytokines, inducer, and receptor genes in the peripheral white blood cells can be used as an important minimally invasive prognostic marker of the autoimmune thyroid disease severity.

scholarly journals Tiazofurin modulates lipopolysaccharide-activated microglia in vitro

2014 ◽  
Vol 66 (4) ◽  
pp. 1633-1640 ◽  
Author(s):  
Danijela Savic ◽  
Irena Lavrnja ◽  
Sanja Dacic ◽  
Ivana Bjelobaba ◽  
Nadezda Nedeljkovic ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Antitumor Action ◽  
Activated Microglia ◽  
Anti Inflammatory ◽  
Necrosis Factor

Tiazofurin is a purine nucleoside analogue, with a broad spectrum of antitumoral and anti-inflammatory properties. In the present study, we have investigated the effect of tiazofurin on microglial inflammatory response to lipopolysaccharide in vitro. The cytotoxic effect of the drug was examined by sulforhodamine B assay. The Griess method was used to quantify nitrite production. Microglial morphology was assessed by measuring cell body size. Release of the pro-inflammatory cytokines, tumor necrosis factor-?, interleukin-1?, interleukin-6, and the anti-inflammatory cytokine interleukin- 10, were evaluated by enzyme-linked immunosorbent assay. Our data showed that tiazofurin decreased the number of activated microglia, lowered nitric oxide production and reduced the average cell surface of these cells. Tiazofurin reduced tumor necrosis factor-?, interleukin-6 and increased interleukin-10 secretion. Conversely, this drug promoted the release of interleukin-1?. Results obtained in this study indicate that TR displayed both anti- and pro-inflammatory modulation of activated microglia that could be relevant for its antitumor action within the central nervous system.

Induction of circulating interleukin 10 by interleukin 1 and interleukin 2, but not interleukin 6 immunotherapy

Cytokine ◽  
1995 ◽  
Vol 7 (7) ◽  
pp. 734-739 ◽  
Author(s):  
Herbert Tilg ◽  
Michael B. Atkins ◽  
Charles A. Dinarello ◽  
James W. Mier
Keyword(s):  
Interleukin 6 ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Interleukin 10

scholarly journals Analysis of Polymorphisms in Interleukin-10, Interleukin-6, and Interleukin-1 Receptor Antagonist in Mexican-Mestizo Women with Pre-eclampsia

2012 ◽  
Vol 16 (11) ◽  
pp. 1263-1269 ◽  
Author(s):  
Elith Yazmin Valencia Villalvazo ◽  
Thelma Canto-Cetina ◽  
Juan Fernando Romero Arauz ◽  
Ramón Mauricio Coral-Vázquez ◽  
Samuel Canizales-Quinteros ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Mexican Mestizo ◽  
Interleukin 1 Receptor Antagonist

scholarly journals Reduced Transferrin Levels in Active Inflammatory Bowel Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Malgorzata Matusiewicz ◽  
Katarzyna Neubauer ◽  
Paulina Lewandowska ◽  
Andrzej Gamian ◽  
Malgorzata Krzystek-Korpacka
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Interleukin 6 ◽  
Interleukin 1 ◽  
Interleukin 10 ◽  
Clinical Severity ◽  
Paraoxonase 1 ◽  
Inflammatory Bowel ◽  
And Oxidative Stress

Inflammatory bowel disease (IBD) is an inflammatory disease of unclear etiopathogenesis and challenging diagnosis, frequently complicated by anemia and malnutrition. C-reactive protein (CRP) remains the only biochemical marker of clinical relevance. The aim of this study was to test hypothesis that transferrin, coinfluenced by inflammation, malnutrition, anemia, and oxidative stress, may better reflect global IBD patient’s condition than any other more specific index. Transferrin and other indices of inflammation, anemia, malnutrition, and oxidative stress were measured in 137 IBD patients (Crohn’s disease (CD): n=63 and ulcerative colitis (UC): n=74) and 97 controls. Transferrin is reduced in active CD and UC and negatively correlates with the disease activity scores (CD: ρ=-0.49; UC: ρ=-0.52). In UC, transferrin correlates negatively with CRP, erythrocyte sedimentation rate (ESR), leukocytes, platelets, interleukin-6, interleukin-10, and TNF-α and positively with albumins, cholesterol, hemoglobin, hematocrit, erythrocytes, iron, and paraoxonase-1. In CD, transferrin correlates negatively with CRP, leukocytes, platelets, interleukin-1, and interleukin-6 and positively with albumins, iron, catalase, glutathione peroxidase-1, superoxide dismutase-1, and paraoxonase-1. The associations with inflammation and anemia/malnutrition were more pronounced in UC and with oxidative stress in CD. As UC activity marker, transferrin outperforms ESR and hemoglobin, indices used in calculating the disease clinical severity score.

scholarly journals Biomarkers of Post-COVID Depression

2021 ◽  
Vol 10 (18) ◽  
pp. 4142
Author(s):  
Piotr Lorkiewicz ◽  
Napoleon Waszkiewicz
Keyword(s):  
Interleukin 6 ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Interleukin 10 ◽  
Kynurenine Pathway ◽  
Monocyte Chemoattractant Protein 1 ◽  
After Effects ◽  
Amyloid A ◽  
Interleukin 6 Receptor ◽  
Factor Α

The COVID-19 pandemic is spreading around the world and 187 million people have already been affected. One of its after-effects is post-COVID depression, which, according to the latest data, affects up to 40% of people who have had SARS-CoV-2 infection. A very important issue for the mental health of the general population is to look for the causes of this complication and its biomarkers. This will help in faster diagnosis and effective treatment of the affected patients. In our work, we focused on the search for major depressive disorder (MDD) biomarkers, which are also present in COVID-19 patients and may influence the development of post-COVID depression. For this purpose, we searched PubMed, Scopus and Google Scholar scientific literature databases using keywords such as ‘COVID-19’, ‘SARS-CoV-2’, ‘depression’, ‘post-COVID’, ‘biomarkers’ and others. Among the biomarkers found, the most important that were frequently described are increased levels of interleukin 6 (IL-6), soluble interleukin 6 receptor (sIL-6R), interleukin 1 β (IL-1β), tumor necrosis factor α (TNF-α), interferon gamma (IFN-γ), interleukin 10 (IL-10), interleukin 2 (IL-2), soluble interleukin 2 receptor (sIL-2R), C-reactive protein (CRP), Monocyte Chemoattractant Protein-1 (MCP-1), serum amyloid a (SAA1) and metabolites of the kynurenine pathway, as well as decreased brain derived neurotrophic factor (BDNF) and tryptophan (TRP). The biomarkers identified by us indicate the etiopathogenesis of post-COVID depression analogous to the leading inflammatory hypothesis of MDD.

Schwere systemische juvenile idiopathische Arthritis und familiäres Mittelmeerfieber mit homozygoter Mutation im MEFV-Gen

2016 ◽  
Vol 36 (01) ◽  
pp. 49-51
Author(s):  
T. Geikowski ◽  
D. Peters ◽  
J. Peitz ◽  
G. Horneff ◽  
S. Wintrich
Keyword(s):  
Interleukin 6 ◽  
Interleukin 1 ◽  
Juvenile Idiopathische Arthritis ◽  
Familiäres Mittelmeerfieber ◽  
Systemische Juvenile Idiopathische Arthritis

ZusammenfassungDie systemische juvenile idiopathische Arthritis (sJIA) und das familiäre Mittelmeerfieber (FMF) zeigen mit Fieber, Arthritis, Exanthem, generalisierter Lymphadenopathie und Sero sitis viele Gemeinsamkeiten. Therapieoptio-nen bei der sJIA sind neben Glukokortikoi-den, nichtsteroidalen Antirheumatika und Methotrexat, Biologika wie Interleukin-1-und Interleukin-6-Antagonisten. Firstline Therapie des FMF ist Colchicin. Bei Therapie resistenz oder -unverträglichkeit können aber auch bei dieser Erkrankung Interleukin-1-und Interleukin-6-Antagonisten erfolgreich eingesetzt werden.Berichtet wird über einen elf Jahre alten Jungen, geboren in Armenien. Im Alter von zwei Jahren kam es zu anhaltendem Fieber mit ausgeprägter Arthritis. Die Diagnose sJIA wurde gestellt und das Vorliegen eines FMF genetisch nachgewiesen. Unter Therapie mit Kortikosteroiden, Sulfasalazin und Colchicin entwickelte der Patient eine deutliche Dystro phie und ausgeprägte Destruktionen der Hüft-, Knie- und Sprunggelenke mit resultie-render Laufunfähigkeit. Die Halswirbelsäule war durch Ankylosen kyphotisch fixiert. La borchemisch waren die Entzündungszeichen deutlich erhöht. Röntgen- und CT-Aufnah-men zeigten das Ausmaß der Gelenkzer -störung. Nach einem Jahr unter intravenöser Tocilizumab-Therapie liegen CRP, SAA und BSG im Normbereich. Bestehende Kontraktu ren sind unter intensiver Physiotherapie rück-läufig. Der Patient ist mit eigenem Rollstuhl mobil.Bei diesem Patient liegt sowohl eine systemische JIA als auch ein familiäres Mittelmeerfieber vor. Tocilizumab ist bereits seit mehreren Jahren für die Behandlung der systemischen JIA zugelassen. Unser Patient zeigt unter Tocilizumab eine Remission beider Erkrankungen.

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