Inflammation reaction macrophages

SLE. An early hypothesis is that the prosthesis or injected silicone plays an adjuvant role by enhancing the immune response through increased macrophage and T-cell helper function. There is currently controversy as to whether silicone, as a foreign body, induces a nonspecific inflammation reaction, a specific cell-mediafed immunological reaction, or no reaction at all. However, there is strong support to indicate that silicone microparticles can act as haptens to produce a delayed hypersensitivity reaction in a genetically susceptible population of people. 

The particle size is the most important factor that contributes to the clearance of particles. For particles deposited in the anterior parts of the nose, wiping and blowing are important mechanisms whereas particles on the other areas of the nose are removed with mucus. The cilia move the mucus toward the glottis where the mucus and the particles are swallowed. In the tracheobronchial area, the mucus covering the tracheobronchial tree is moved upward by the cilia beating under the mucus. This mucociliary escalator transports deposited particles and particle-filled macrophages to the pharynx, where they are also swallowed. Mucociliary clearance is rapid in healthy adults and is complete within one to two days for particles in the lower airways. Infection and inflammation due to irritation or allergic reaction can markedly impair this form of clearance. 

Type III reactions are the result of antigen-antibody (IgG or IgM) complexes that accumulate in tissues or the circulation, activate macrophages and the complement system, and trigger the influx of granulocytes and lymphocytes (inflammation). Examples include an Arthrus reaction when soluble antigen is injected into the skin of a sensitized individual and serum sickness, which occurs 7 to 10 days following the administration... 

There are thus various autoantibodies present, and if the auto-antigens are released by cellular breakdown, a type III immune reaction can occur where an immune complex is formed, which is deposited in small blood vessels and joints, giving rise to many of the symptoms. The immunoglobulins IgG and IgE act as both autoantibody and antigen, and hence immune complexes form. Such complexes stimulate the complement system leading to inflammation, infiltration by polymorphs and macrophages, and the release of lysosomal enzymes. 

Once deposited, there are multiple mechanisms by which an immune complex initiates an inflammatory reaction (Fig. 2). Foremost among these is activation of the complement system. Immune complexes can activate the classical complement pathway as well as, indirectly or directly, the alternative complement pathway. The biologic activities of complement activation which are relevant to tissue inflammation include the generation of anaphylatoxins C5a and C3a (H29) and chemotactic peptide C5a (H29, T6), direct and indirect membrane lysis by the terminal complement components C56789 (T17), leukocytosis by C3e (G8), macrophage activation by Bb (G12), immune complex solubilization by C3b (C21), and immune adherence, the binding and activation of cells bearing complement receptors. 

Implantation-related acute inflammatory reactions are usually caused by neutrophil adsorption onto the surfaces of synthetic implants, which is mostly intermediated by the strong promoters of Csa and Leukotrienc B4 etc. Monocytes in blood circulation are also prone to adsorb to the sites of blood vessel defects or endothelium regeneration. With the stimulation by miscellaneous activating factors in serum, monocytes tend to differentiate into macrophages [M0] and become one of the major participators for host chronic inflammation. 

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