Researchers at the University of Illinois report that a plant compound found in abundance in celery and green peppers can disrupt a key component of the inflammatory response in the brain. The findings have implications for research on aging and diseases such as Alzheimer’s and multiple sclerosis.
According to ScienceDaily, inflammation can be a blessing or a blight. It is a critical part of the body’s immune response that in normal circumstances reduces injury and promotes healing. When it goes awry, however, the inflammatory response can lead to serious physical and mental problems.
Inflammation plays a key role in many neurodegenerative diseases and is also implicated in the cognitive and behavioral impairments seen in aging.
The new study looked at luteolin (LOO-tee-OH-lin), a plant flavonoid known to impede the inflammatory response in several types of cells outside the central nervous system. The purpose of the study was to determine if luteolin could also reduce inflammation the brain, said animal sciences professor and principal investigator Rodney Johnson.

Inflammation plays a key role in many neurodegenerative diseases and is also implicated in the cognitive and behavioral impairments seen in aging.

“One of the questions we were interested in is whether something like luteolin, or other bioactive food components, can be used to mitigate age-associated inflammation and therefore improve cognitive function and avoid some of the cognitive deficits that occur in aging,“ Johnson said.
The researchers first studied the effect of luteolin on microglia. These brain cells are a key component of the immune defense. When infection occurs anywhere in the body, microglia respond by producing inflammatory cytokines, chemical messengers that act in the brain to orchestrate a whole-body response that helps fight the invading microorganism.
This response is associated with many of the most obvious symptoms of illness: sleepiness, loss of appetite, fever and lethargy, and sometimes a temporary diminishment of learning and memory. Neuroinflammation can also lead some neurons to self-destruct, with potentially disastrous consequences if it goes too far.
Graduate research assistant Saebyeol Jang studied the inflammatory response in microglial cells. She spurred inflammation by exposing the cells to lipopolysaccharide (LPS), a component of the cell wall of many common bacteria.
Those cells that were also exposed to luteolin showed a significantly diminished inflammatory response. Jang showed that luteolin was shutting down production of a key cytokine in the inflammatory pathway, interleukin-6 (IL-6). The effects of luteolin exposure were dramatic, resulting in as much as a 90 percent drop in IL-6 production in the LPS-treated cells.
“This was just about as potent an inhibition as anything we had seen previously,“ Johnson said. But how was luteolin inhibiting production of IL-6?
Jang began by looking at a class of proteins involved in intracellular signaling, called transcription factors, which bind to specific “promoter“ regions on DNA and increase their transcription into RNA and translation into proteins.
Using electromobility shift assays, which measure the binding of transcription factors to DNA promoters, Jang eventually determined that luteolin inhibited IL-6 production by preventing activator protein-1 (AP-1) from binding the IL-6 promoter.
AP-1 is in turn activated by JNK, an upstream protein kinase. Jang found that luteolin inhibited JNK phosphorylation in microglial cell culture. The failure of the JNK to activate the AP-1 transcription factor prevented it from binding to the promoter region on the IL-6 gene and transcription came to a halt.
To see if luteolin might have a similar effect in vivo, the researchers gave mice luteolin-laced drinking water for 21 days before injecting the mice with LPS.
Those mice that were fed luteolin had significantly lower levels of IL-6 in their blood plasma four hours after injection with the LPS. Luteolin also decreased LPS-induced transcription of IL-6 in the hippocampus, a brain region that is critical to spatial learning and memory.

New spray-on films developed by UC San Diego chemists will be the basis of portable devices that can quickly reveal trace amounts of nitrogen-based explosives.
Contaminated fingerprints leave dark shadows on the films, which glow blue under ultraviolet light. One of the films can distinguish between different classes of explosive chemicals, a property that could provide evidence to help solve a crime, or prevent one, ScienceDaily wrote.
Detection relies on fluorescent polymers developed at UCSD by chemistry and biochemistry professor William Trogler and graduate student Jason Sanchez. “It’s a very intuitive detection method that doesn’t require a scientist to run,“ Trogler said.
The polymers emit blue light when excited by ultraviolet radiation. Nitrogen-based explosive chemicals such as TNT quench that glow by soaking up electrons.
Because the polymers fluoresce brightly, no special instruments are needed to read the results. Only a very thin film sprayed on a suspect surface is needed to reveal the presence of a dangerous chemical.
A single layer of the polymer, about one thousandth of a gram, is enough to detect minute amounts of some explosives, as little as a few trillionths of a gram (picograms) on a surface a half-foot in diameter. Handling explosives can leave 1,000 times that quantity or more stuck to fingers or vehicles.

Nothing may feel lonelier than trying to quit smoking, but in fact, people kick the habit in clusters, US researchers said.
The same team of experts who found that obesity may be socially contagious said they found similar patterns among smokers, with people clearly influencing others in their social and family networks, Reuters reported.
In fact, the most isolated people are now those who remain the most addicted as their personal networks get pushed to the fringes, they wrote in the New England Journal of Medicine.
“This study tells us that social relationships have a critical impact on health behaviors and decisions, and that people are strongly influenced by those in their social sphere,“ said National Institute on Aging director Dr. Richard Hodes, whose institute paid for the study.
Dr. Nicholas Christakis of Harvard Medical School in Boston and Dr. James Fowler of the University of California, San Diego, studied 12,067 people who have been taking part in the Framingham study--a study of the health and habits of nearly an entire town in Massachusetts--for the past 32 years.
“We’ve found that when you analyze large social networks, entire pockets of people who might not know each other all quit smoking at once,“ Christakis said in a statement. “What appears to happen is that people quit in droves.“