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Yin and yang of inflammation – play opposite roles in infection and serious diseases

Yin and yang of inflammation – play opposite roles in infection and serious diseases

Get an infected cut or sprain an ankle and you will experience the healing benefit of inflammation. However, with the benefit also come the redness, swelling, heat and pain that are inflammation’s hallmarks. Although unpleasant, these symptoms dissipate rapidly and are reassuring that the immune system is doing its job to clear infection and guide repair of damaged tissue.
The journal  Science  had a recent review of inflammation as it pertains to chronic diseases. The review looked at new research in three major areas: Type 2 diabetes, cardiovascular disease and neurodegenerative disease. A common factor to all three is the inability of the immune system to clear away the stimulus that triggers the inflammation. Hence, there is a chronic inflammatory state that causes the disease to progress. In the case of Type 2 diabetes, obesity with the resultant saturated fatty acids is the “nonclearable” stimulus to inflammation which leads to insulin resistance, and thereby elevated blood sugars.  In the case of cardiovascular disease it is apolipoprotein B, containing lipoproteins which can’t be cleared by the immune system. The resulting chronic inflammation can be measured by a test called C-reactive protein, and it leads to laying down of arteryblocking plaque or atherosclerosis. And in the case of the neurodegenerative disease (Alzheimer’s disease, Parkinson’s, prion disease and traumatic brain injury), it is the formation of protein aggregates that can’t be cleared.
In Alzheimer’s the protein that aggregates is B amyloid, and its presence stimulates immune cells unique to the brain called microglial cells. The chronic inflammation leads to loss of brain cells and thus, dementia.  Luckily, understanding these mechanisms is leading to fruitful research. One example is altering JNK molecules. These are the enzymes that cause the diabetes-related inflammation. Drugs to modify these JNK enzymes have proven very successful in curing diabetes in mice models.