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Inflammation is a basic immune response to the introduction of a foreign antigen into the body. It involves a complex series of reactions, initiated through damage
of endothelial cells, that:
- increases circulation to the area of injury through the release of
vasodilators by cells such as mast cells or basophils;
- increases the concentration of plasma proteins involved in the Acute
Phase Response. One such protein, C-reactive protein, can function as a
non-specific opsonin;
- results in tissue swelling via leakage of plasma into the area of
injury;
- activates the classical complement system via the proteolytic enzyme
plasmin resulting in the lysis of the parasite or its' opsonization and
removal
via
phagocytosis;
phagocytosis II;
- results in the release of cytokines by endothelial cells
and platelets that attract immune system cells (lymphocytes,
polymorphonuclear cells, and monocytes) to the area of injury.
The inflammatory response, while eliminating the foreign antigen or
parasite, can, as well, result in local tissue damage. In cases of
hypersensitivity, the response may result in anaphylaxis; if directed at
a self antigen, in an autoimmune disease.
Hovever in recent studies, the inflammatory process has ben linked to the progress of cancer, heart and central nervous system disease: - "Recent data have expanded the concept that inflammation is a critical component of tumour
progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is
now becoming clear that the tumour microenvironment, which is largely orchestrated by
inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation,
survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of
the innate immune system, such as selectins, chemokines and their receptors for invasion,
migration and metastasis. These insights are fostering new anti-inflammatory therapeutic
approaches to cancer development.",
- "Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we
appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte
recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and
malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory
pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for
myocardial infarctions and most strokes. The new appreciation of the role of inflammation in
atherosclerosis provides a mechanistic framework for understanding the clinical benefits of
lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of
inflammatory pathways may eventually furnish new therapeutic targets.", and
- "The spectrum of inflammatory diseases of the central nervous system has been steadily expanding
from classical autoimmune disorders such as multiple sclerosis to far more diverse diseases.
Evidence now suggests that syndromes such as Alzheimer's disease and stroke have important
inflammatory and immune components and may be amenable to treatment by anti-inflammatory and
immunotherapeutic approaches. The notion of 'vaccinating' individuals against a neurodegenerative
disorder such as Alzheimer's disease is a marked departure from classical thinking about
mechanism and treatment, and yet therapeutic vaccines for both Alzheimer's disease and multiple
sclerosis have been validated in animal models and are in the clinic. Such approaches, however,
have the potential to induce unwanted inflammatory responses as well as to provide benefit."
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