Interleukin-1, Interleukin-6: Messengers in the Neuroendocrine Immune System?

Background: Increasing incidence of diabetes due to strees inducing life-style, involves dearrangement of carbohydrate, fat, protein metabolism characterized by hyperglycemia, hyperlipidimia and negative nitrogen balance respectively. Causing morbidity and mortality, effects gestational diabetes. Pregnancy, capacity to secrete insulin increases with gestational age, has effect in last trimester of pregnancy. Maternal glycemic-status influences neonates leucocyte profile.Methods: Fully automated haematology analyzer ABXMICROsot used to analyze cord blood of neonates born to 40 diabetic (known to be diabetic at pregnancy) and 40 non-diabetic mothers, collected in EDTA tubes. Diabetic group was sub divided into D1 and D2. D1 as 100-150 mg/dcl, D2 as above 150 mg/dcl. Statistical treatment of Levene's test of equality of variances applied to the data.Results: WBC count, granulocyte percent and monocyte percent were significantly lower, lymphocyte percent was higher in neonates to diabetic mothers. Significantly higher in D2 then D1group. The prognosis for the child of a pregnant diabetic is related to the degree of control of mother’s glycemic status, reflected higher indices in D2 then D1.Conclusions: Neonates immune system depends on the mother's immune system i.e.; immunological properties are practically under control of interleukin-1 and interleukin-6. Interleukin-6 potentiates action of interleukin-1 synergistically, such action of interleukin converts non-committed stem cells to committed stem cells. Immunosuppressant status in diabetic mother (i.e.; non-priming of neonatal interleukin-6 by immunosuppressant diabetic mother’s interleukin-6, main cause for altered counts) modulating neonatal interleukin-6 it decreases haematopoietic potential in the neonates, ECF in infants of diabetic mother is reduced leading to haemo-concentration, increasing cell count. Pictures as increase cell count at birth in neonates of diabetic mother.

Download Full-text

Erythrocyte profile in cordblood of newborns to diabetic and non-diabetic mothers

International Journal of Research in Medical Sciences ◽

10.18203/2320-6012.ijrms20210422 ◽

2021 ◽

Vol 9 (2) ◽

pp. 449

Author(s):

Nazima Thaseen ◽

Shivakumar Veeraiah

Keyword(s):

Stem Cells ◽

Immune System ◽

Interleukin 6 ◽

Interleukin 1 ◽

Hemoglobin Concentration ◽

Diabetic Mother ◽

Mean Corpuscular Hemoglobin ◽

Corpuscular Hemoglobin ◽

Cell Counts ◽

Diabetic Mothers

Background: Diabetes, an endocrinal disorder causing morbidity and mortality has its effect on gestational diabetes. Intrapartum stress, maternal hyperglycemia leads to fetal hyperglycemia. The maternal glycaemic status has influence on neonates erythrocyte profile.Methods: Cord blood of neonates born to 40 diabetic (known to be diabetic at pregnancy) and 40 non-diabetic mothers were selected. A fully automated hematology analyzer ABXMICROsot was used to analyze whole blood collected in EDTA tubes. The diabetic group was subdivided into D1 and D2. D1 as 100-150 mg/dcl, D2 as above 150 mg/dcl.Results: Hemoglobin, hematocrit, MCV, MCH, RDW were significantly higher, RBC count were comparatively insignificant. Hemoglobin (Hb), hematocrit (HCT), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), Mean corpuscular hemoglobin concentration (MCHC) were significantly higher in D2 than D1 group. The prognosis for the child of a pregnant diabetic is related to the degree of control of mother’s glycemic status, reflected as higher indices in D2 than D1.Conclusions: Neonatal immune system depends on maternal immune system i.e, all the immunological properties are practically under the control of interleukin-1 and interleukin-6. Interleukin-6 potentiates the action of interleukin-1 synergistically, such action of interleukin converts noncommitted stem cells to committed stem cells. Immunosuppressant status in diabetic mother (i.e., non-priming of neonatal interleukin-6 by immunosuppressant diabetic mother`s interleukin-6, the main cause for these altered count). By modulating neonatal interleukin-6 it decreases hematopoietic potential in the neonates, on the other hand ECF in infants of diabetic mother is reduced leading to hemoconcentration and increase in cell counts. Giving a picture as if polycythemia at birth in neonates of diabetic mothers.

Download Full-text

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

Arthritis und Rheuma ◽

10.1055/s-0037-1616801 ◽

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.

Download Full-text

Die medikamentöse Therapie der juvenilen idiopathischen Arthritis bei Kindern

Arthritis und Rheuma ◽

10.1055/s-0037-1620152 ◽

2009 ◽

Vol 29 (02) ◽

pp. 81-93 ◽

Cited By ~ 1

Author(s):

G. Horneff

Keyword(s):

Interleukin 6 ◽

Medikamentöse Therapie ◽

Interleukin 1 ◽

Therapeutische Optionen

ZusammenfassungDie Therapie der juvenilen idiopathischen Arthritis erfolgt durch eine Kombination von nichtsteroidalen Antirheumatika, systemischen und/oder intraartikulären Glukokortikoiden, klassischen Basistherapeutika, Immunsupressiva und Biologika. Die neuen bio-logischen Medikamente erwiesen sich als au-ßerordentlich wirksam, auch bei schweren oder bislang therapierefraktären Verläufen. Drei Tumor-Nekrose-Faktor-Inhibitoren (Eta-nercept, Adalimumab und Infliximab) wurden bereits untersucht. Weitere therapeutische Optionen bestehen durch Inhibition von Interleukin-1 durch Anakinra, Canakinumab und Rilonacept, Interleukin 6 durch Tocilizumab oder der Inhibition der T-Zellaktivierung durch Abatacept. In dieser Übersichtsarbeit werden die pharmakologischen Therapieoptionen orientierend an der Existenz von kontrollierten randomisierten Studien dargestellt.

Download Full-text

Increased Fibrinogen Synthesis in Mice During the Acute Phase Response: Co-Operative Interaction of Interleukin 1, Interleukin 6, and Interleukin 1 Receptor Antagonist

10.21236/ada280464 ◽

1993 ◽

Author(s):

Hanna Rokita ◽

Ruta Neta ◽

Jean D. Sipe

Keyword(s):

Receptor Antagonist ◽

Acute Phase ◽

Interleukin 6 ◽

Acute Phase Response ◽

Interleukin 1 ◽

Phase Response ◽

Interleukin 1 Receptor Antagonist

Download Full-text

There is an Association of Synovial Interleukin-6 Levels With Chondral Damage in Anterior Cruciate Ligament–Deficient Knees

HSS Journal ® ◽

10.1177/1556331621992006 ◽

2021 ◽

pp. 155633162199200

Author(s):

Ravi Gupta ◽

Anil Kapoor ◽

Sourabh Khatri ◽

Dinesh Sandal ◽

Gladson David Masih

Keyword(s):

Anterior Cruciate Ligament ◽

Synovial Fluid ◽

Acl Reconstruction ◽

Inflammatory Cytokines ◽

Interleukin 6 ◽

Cruciate Ligament ◽

Interleukin 1 ◽

Chondral Damage ◽

Anterior Cruciate ◽

Acl Deficient

Background: Osteoarthritis (OA) in the anterior cruciate ligament (ACL)–deficient knee is seen in approximately 50% of affected patients. Possible causes include biochemical or biomechanical changes. Purpose: We sought to study the correlation between inflammatory cytokines and chondral damage in ACL-deficient knees. Methods: Seventy-six male patients who underwent ACL reconstruction were enrolled in a cross-sectional study. Synovial fluid was aspirated before surgery and analyzed for levels of the inflammatory cytokines tumor necrosis factor-α, interleukin-1 (IL-1), and interleukin-6 (IL-6). At the time of ACL reconstruction, the severity of chondral damage was documented as described by the Outerbridge classification. Results: Patients with grade 2 or higher chondral damage were observed to have elevated IL-6 levels when compared to patients who had no chondral damage. Interleukin-6 levels had no correlation with the duration of injury. Conclusion: Elevated levels of IL-6 in synovial fluid were associated with chondral damage in ACL-deficient knees. Further study is warranted to determine whether inflammatory cytokines contribute to the development of OA of the knee after ACL injury.

Download Full-text