Thursday, July 05, 2007

News dump: inflammation

I've already done one news dump on the subject of inflammation (here), and there's been a lot of interesting stuff since then. This is just the first installment of new stuff, in reverse chronological order.

Schizophrenia may be linked to inflammation: study (3/21/07)
Many patients with schizophrenia also have autoimmune diseases. Using a technique called whole genome association researchers have located a gene variant common to many schizophrenics. The variant is located close to genes that produce receptors for two cytokines, which are immune system signals whose production is a first step in causing inflammation. Although the result is intriguing, the evidence for a relation to inflammation is still circumstantial.

Why Aerobic Exercise Is Good For The Heart (3/21/07)
The biological mechanisms connecting exercise and cardiovascular health are not fully understood. This study shows how exercise decreases inflammation, which reduces the risk of atherosclerosis, which in turn causes most cases of heart disease. Blood samples were taken from experimental volunteers before and after aerobic exercise. The samples were stimulated with an infectious agent and then analyzed for levels of tumor necrosis factor (TNF), an initial step in the inflammatory cascade. Substantially lower levels of TNF were found after aerobic training

Inflammation May Play Role In Metastasis Of Prostate Cancer (3/19/07)
This research strongly suggests that inflammation associated with the progression of tumors plays a key role in the metastasis of prostate cancer. It appears that inflammation in the tumor may lead to production of a cytokine called RANK. This eventually results in turning down the expression of a gene called Maspin, which has well-established anti-metastatic activity in breast and prostate cancers.

Researchers Identify Molecular Basis Of Inflammatory Bowel Disease (3/15/07)
The category of inflammatory bowel diseases includes Crohn's disease and ulcerative colitis. A likely molecular basis for such diseases has been identified in a mouse model. It appears that there is an underproduction of the signaling molecule NF-kB, which helps cells cope with stress, in the intestinal epithelium. With insufficient NF-kB, epithelial cells are more likely to die, and as a result bacteria can penetrate the epithelium. This results in activation of the intestinal immune system, producing a strong immune response and inflammation. The inflammation leads to death of more epithelial cells due to lack of NF-kB, perpetuating the cycle.

Obstructive Sleep Apnea Patients Show Silent Brain Infarction Lesions (3/15/07)
Patients with sleep apnea often have high levels in their blood of inflammatory markers. Cardiovascular disease is commonly characterized by ongoing inflammatory responses that can enhance blood platelet activation and increase the risk of silent brain infarction (stroke). Treatment of patients with obstructive sleep apnea using devices to create positive airway pressure led to lower blood levels of C-reactive protein and levels of two markers of platelet activation, suggesting that the apnea played a causal role in inflammation.

Belly Fat May Drive Inflammatory Processes Associated With Disease (3/14/07)
This research strongly suggests that visceral fat present in significant amounts surrounding organs in the midsection of the body may be a major source of inflammatory molecules. The resulting inflammation is suspected to play an important role in diseases such as insulin resistance, hypertension, type 2 diabetes, and atherosclerosis, and possibly Alzheimer's, cancer, and general aging. The study was done by analyzing blood taken from the portal vein (which drains organs surrounded by visceral fat) during gastric bypass surgery. Elevated levels of the inflammatory cytokine IL-6 were found, along with higher levels of C-reactive protein.

C-Reactive Protein Liver Protein Induces Hypertension, Researchers Find (2/22/07)
Researchers claim to have found that C-reactive protein is not merely a marker of the risk of hypertension, it actually induces hypertension. Using a mouse model having an engineered gene for CRP that was regulated by another gene responsive to carbohydrate in the diet, the researchers determined that raising CRP levels increased blood pressure, while lowering CRP levels lowered blood pressure. (It has been known for some time that high CRP levels are correlated with risk of hypertension and atherosclerosis.) Further investigation showed that the experimental mice were highly sensitive to the blood pressure regulating protein angiotensin II, and this was due to alterations in key proteins in the vascular wall that are involved with angiotensin II. The mechanism involves a lack of nitric oxide in the artery wall, and a connection was found between nitric oxide and proteins responsible for angiotensin II activity. Remaining to be shown is whether the same mechanism operates in humans.

Inflammatory Genes Linked To Salt-sensitive Hypertension (12/30/06)
A team of researchers is investigating interrelations among genetic variations, stress, inflammation, and hypertension. One hypothesis is that sodium handling goes awry because of mutations in genes for the inflammation-related proteins IL-6, IL-6 receptor, cytokine signal transducer, and C-reactive protein. Stress is involved because of a suspicion that the connection between stress, inflammation and hypertension is the kidneys’ ability to release sodium. When stress activates the sympathetic nervous system, the body increases production of IL-6, which ultimately leads to production of other inflammatory factors such as CRP. Stress also prompts the body to hold onto sodium to help temporarily raise blood pressure in order to deal with the situation.

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