The inflammation is a defence reaction of the organism against an inner or outer triggered and potential harmful stimulus. The purpose of this immune response is to remove the harmful agent, to stop the propagation of the stimulus and to repair damages in the organism. Extending the capillary vessels is one of the reactions of the body. This is because more inflammation-mediators and cellular components of the immune system (e.g. neutrophils granulocytes and monocytes) are washed up by chemotactic signals to the affected parts of the body.

An inflammation is transmitted by a heterogeneous group of various solvable factors and signalling molecules, the so called Cytokines. Cytokines are small molecules, produced naturally in the body, which are produced and distributed by certain cells of the immune system. The cytokines are acting pro-inflammatory (supporting inflammations) or anti-inflammatory (inhibiting inflammations). Within the cytokine-family there are 5 main groups: interferon, interleukin, colony stimulating factors, tumor necrosis factors and chemokine.

Interleukins (IL) are the communication substances between cells of the immune system for a more effective fight against pathogens or tumor cells. Important represantatives of this group are Interleukin 1A (IL-1A), Interleukin 1B (IL-1B), Interleukin 4 (IL-4), Interleukin 6, (IL-6) und Interleukin 10 (IL-10). Another group of the cytokines are the tumor necrosis factor Alpha (TNFa). TNFa is a body own, multifunctional transmitter of the immune system, that is interacting by local or systemic inflammations. TNFa is mostly distributed by the macrophages. The biological function of interleukins and TNFa is the infection defence. They are activating enzyme systems, nitrous gases, prostaglandin, leukotriene, collagenase and other metalloproteases of the matrix and the production of the thrombocyte-activating factor. Plenty of these different cytokines and their receptors and receptor-antagonists form a fine coordinated, sophisticated system of regulation. This regulation balances the immune defence between an effective system and a system which is not to harmful against body own cells. The interleukins IL-1A, IL-1B and TNFa are the main mediators of the local answer of the host against bacterial infections. The respective roles of IL-1A, IL-1B and TNFa are hard to differentiate. The overproduction of cytokines and/or the functional impairment of the controllproteins can end up in important tissue damage.

Interleukin 6 takes part in the regulation of the acute phase reaction, in the immune answers and the haemopoiesis. It guides cells of the immune defence to the center of inflammation, for example the monocytes to the subendothelium of the vessels, which is the first step of arteriosclerosis. The pro-inflammatory acting IL-6 is connected with a lot of diseases like coronary heart diseases, early appearing forms of chronic arthritis and some kinds of cancer (e.g. Kaposi-Sarcoma)..

The cytokines and TNFa are important mediators of inflammation reactions and take part, as we know today, as a central role in the pathogenesis of a variety chronic inflammable disease processes. Their genetic variants show stable inheritable activity levels. That is why the existence of regulatory or structural changes in the DNA sequence allows us a risk assessment in relation to infection-dependencies or the immune system concerning diseases. Scientific studies of twins showed us for example, that the interleukins (IL-1) are highly significant for a heavy periodontitis. Of course pathogenic bacteria in the oral flora causes this disease, but there are some more factors like smoking, psychosomatic stress and systemic diseases (e.g. Diabetes mellitus), which influence the periodontitis in progressivity and severity. Patients with periodontitis have a higher concentration of IL-1A and IL-1B in their oral mucosa. These are activating the breakdown of extracellular matrix and the bones in the periodontal tissue. Over this is IL-1 a high inductor for TNFa.

Against this, Il-4 is an anti-inflammatory interleukin, which stimulates the B-Cell-activation and IgE-production. It is involved at the formation of atopic diseases.

IL-10 is also an anti-inflammatory interleukin that has immunomodulatory properties. It inhibits the pro-inflammatory cytokines, like TNFa and Il-1. The point mutation on position -1082 of the IL-10 gene is put in context of a lower production of Il-10. A lack together with an assessment will end up in chronic inflammatory diseases like Morbus Crohn, autoimmune thyroiditis, colitis ulcerosa and skin diseases.

Recommended tests:

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