Central Nervous System inflammation

La Flamme AC, Ruddenklau K, Backstrom BT Schistosomiasis decreases central nervous system inflammation and alters the progression of experimental autoimmune encephalomyelitis. Infect Immun 2003 71 4996-5004. 

Kielian, T., and Drew, P. D. (2003). Effects of peroxisome proliferator-activated receptor-gamma agonists on central nervous system inflammation. J. Neurosci. Res. 71, 315-325. 

Dale Shenk, Ph.D., at Elan Pharmaceuticals in San Francisco reported that the initial results of vaccination were very promising (Psychiatric Mews, August 18,2000). Unfortunately, he stopped the trial because of central nervous system inflammation in some of the subjects. There is still hope that a P-amyloid vaccine might eventually be a safe and effective treatment for AD, and many are pursuing research in this direction. Some peptides that bind to amyloid plaques are not toxic to human neurons in tissue culture. Other investigators are developing compounds that inhibit the enzymes involved in the production of P-amyloid, namely, P- and y-secretase. 

Van der Veen RC, Hinton DR, Incardonna F et al. Extensive peroxynitrite activity during progressive stages of central nervous system inflammation. J Neuroimmunol 1997 77 1-7. 

Exposure to helminths inhibits central nervous system inflammation in experimental autoimmune encephahtis (EAE). a rodent model of MS. Exposure of mice to viable S. mansoni or dead (freeze-thawed) S. mansoni s protects from EAE. Schistosome exposure reduces proinflammatory IL12/23p40, IFNy and TNFa and promotes r ulatory TGPp, ILIO and IL4 expression by splenocytes and CNS immune cells. Protection against EAE appears to require intact IL4 signaling. ... 

Pashenkov, M., Soderstrom, M., and Link, H. (2003). Secondary lymphoid organ chemokines are elevated in the cerebrospinal fluid during central nervous system inflammation. J. Neuroimmunol 135, 154-160. 

Bromothiophenes are toxic materials by aU routes. Inhalation toxicity of 2-bromothiophene is significant. Ecotoxicity is also noted for these materials, particularly for 2-bromo-3-methylthiophene. 2-Thiophenecarboxaldehyde and the 3-methyl derivative can cause minor irritation to the skin and eyes of rabbits. The former is a sensitizer to guinea pig skin, the latter is not. 2-Acetylthiophene is toxic in aU modes of contact. Severe exposure causes serious inflammation of the lung, damage to many organs, and depression of the central nervous system. 

Histamine is a biogenic amine that is widely distributed in the body and functions as a major mediator of inflammation and allergic reactions, as a physiological regulator of gastric acid secretion in the stomach, as a neurotransmitter in the central nervous system (CNS) and may also have a role in tissue growth and repair. 

Etiology Trauma, viral infections, ischemia, inflammation, genetic defects Neuropathy, genetic defects Peripheral inflammation, peripheral neuropathy, trauma, genetic defects, spinal cord injury, inflammation in the central nervous system ... 

Prostaglandins are a group of lipid autacoids known as eicosanoids. They are produced from membrane phospholipids and found in almost every tissue and body fluid. They are involved in a number of physiological processes including inflammation, smooth muscle tone and gastrointestinal secretion. In the central nervous system they have been reported to produce both excitation and inhibition of neuronal activity. 

Cartier L, Hartley O, Dubois-Dauphin M, Krause KH (2005) Chemokine receptors in the central nervous system role in brain inflammation and neurodegenerative diseases. Brain Res Brain Res Rev 48 16-42... 

Headache, tachypnea, dizziness, confusion, and chest pain. The casualty may also experience palpitations, dyspnea on exertion, drowsiness, lethargy, hallucination, agitation, nausea, vomiting, diarrhea, and coma. If metal carbonyls have been released, there may be complaints of irritation of the eyes, mucous membrane, and respiratory system. Inflammation of lung tissue (pneumonitis) caused by metal carbonyls can may be delayed 12-36 hours. They may also cause injury to the liver, kidneys, and lungs as well as degenerative changes in the central nervous system. 

Signs and Symptoms Symptoms in immunocompromised individuals may include fever, difficulty breathing (dyspnea), nonproductive cough, bloody sputum (hemoptysis), bloody nose (epistaxis), a vague feeling of bodily discomfort (malaise), pneumonia, weakness, chest pain, and anorexia. May progress to inflammation of the eyes (endophthalmitis), sensitivity to light (photophobia), and/or inflammation of the heart (endocarditis). May also cause abscesses in the heart, kidneys, liver, spleen, other soft tissue, or the bone. If the central nervous system becomes involved, can cause altered mental states and seizures. 

Although histamine is not stored in neurons outside of the central nervous system, mast-cell-derived histamine can modify peripheral sensory nerve function. Both acute and chronic pain states can result from inflammation or peripheral nerve cell injury, and there is substantial evidence that mast cell histamine participates in these disorders. 

Since the identification of PAF in the early 1970 s, the autacoid has steadily emerged as a crucial mediator of diverse pathologies. Indeed, PAF is a potent mediator of anaphylaxis and inflammation and is also implicated in shock, graft rejection, renal disease, ovoimplantation and certain disorders of the central nervous system (CNS) [36,44]. There is also accumulating evidence that PAF is capable of modulating the immune response [45, 46]. 

Monshouwer M, Agnello D, Ghezzi P, Villa P. 2000. Decrease in brain cytochrome P450 enzyme activities during infection and inflammation of the central nervous system. Neu-roimmunomodulation 8 142-147. 

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