A large variety of proteins are involved in inflammation, and any one of them is open to a genetic mutation which impairs or otherwise dysregulates the normal function and expression of that protein.
Examples of disorders associated with inflammation include:
* Acne vulgaris
* Asthma
* Autoimmune diseases
* Chronic prostatitis
* Glomerulonephritis
* Hypersensitivities
* Inflammatory bowel diseases
* Pelvic inflammatory disease
* Reperfusion injury
* Rheumatoid arthritis
* Sarcoidosis
* Transplant rejection
* Vasculitis
* Interstitial cystitis
Allergies
An allergic reaction, formally known as type 1 hypersensitivity, is the result of an inappropriate immune response triggering inflammation. A common example is hay fever, which is caused by a hypersensitive response by skin mast cells to allergens. Pre-sensitised mast cells respond by degranulating, releasing vasoactive chemicals such as histamine. These chemicals propagate an excessive inflammatory response characterised by blood vessel dilation, production of pro-inflammatory molecules, cytokine release, and recruitment of leukocytes. Severe inflammatory response may mature into a systemic response known as anaphylaxis.Other hypersensitivity reactions (''type 2'' and ''type 3'') are mediated by antibody reactions and induce inflammation by attracting leukocytes which damage surrounding tissue.
Myopathies
Inflammatory myopathies are caused by the immune system inappropriately attacking components of muscle, leading to signs of muscle inflammation. They may occur in conjunction with other immune disorders, such as systemic sclerosis, and include dermatomyositis, polymyositis, and inclusion body myositis.Leukocyte defects
Due to the central role of leukocytes in the development and propagation of inflammation, defects in leukocyte function often result in a decreased capacity for inflammatory defense with subsequent vulnerability to infection. Dysfunctional leukocytes may be unable to correctly bind to blood vessels due to surface receptor mutations, digest bacteria (Chediak-Higashi syndrome), or produce microbicides (chronic granulomatous disease). Additionally, diseases affecting the bone marrow may result in abnormal or few leukocytes.Pharmacological
Certain drugs or exogenic chemical compounds are known to affect inflammation. Vitamin A deficiency causes an increase in inflammatory responses, and anti-inflammatory drugs work specifically by inhibiting normal inflammatory components.Cancer
Inflammation orchestrates the microenvironment around tumours, contributing to proliferation, survival and migration. Cancer cells use selectins, chemokines and their receptors for invasion, migration and metastasis. On the other hand, many cells of the immune system contribute to cancer immunology, suppressing cancer.Resolution of inflammation
The inflammatory response must be actively terminated when no longer needed to prevent unnecessary "bystander" damage to tissues. Failure to do so results in chronic inflammation, and cellular destruction. Resolution of inflammation occurs by different mechanisms in different tissues.Mechanisms which serve to terminate inflammation include:
* Short half-life of inflammatory mediators ''in vivo''.
* Production and release of Transforming growth factor beta from macrophages
* Production and release of Interleukin 10 (IL-10)
* Production of anti-inflammatory lipoxins
* Downregulation of pro-inflammatory molecules, such as leukotrienes
* Upregulation of anti-inflammatory molecules such as the Interleukin 1 receptor antagonist or the soluble tumor necrosis factor receptor (TNFR)
* Apoptosis of pro-inflammatory cells
* Desensitization of receptors
* Increased survival of cells in regions of inflammation due to their interaction with the extracellular matrix (ECM)
* Downregulation of receptor activity by high concentrations of ligands
* Cleavage of chemokines by matrix metalloproteinases (MMPs) might lead to production of anti-inflammatory factors.
Adapted from the Wikipedia article Inflammation, under the G. N. U. Free Documentation License. Please also see http://en.wikipedia.org/wiki
