Could compound in red wine, grapes treat acne?

New study published in the journal Dermatology and Therapy claims a compound derived from red grapes and found in red wine – resveratrol – may be an effective treatment for acne, particularly when combined with an already existing medication for the disorder.

Acne affects 40-50 million Americans, and around 85% of us develop acne at some point in our lives. The condition is characterized by pimples, blocked pores and/or cysts that can appear on the face, neck, chest, back, shoulders and upper arms.

Acne can be caused overproduction of oil in the skin, blockage of hair follicles from which the oil is released, and growth of bacteria called Propionibacterium acnes in the hair follicles.

There are medications that help treat acne, such as benzoyl peroxide – an oxidant that produces free radicals that kill P. acnes bacteria.

But the researchers of this latest study – including first author Dr. Emma Taylor of the division of dermatology at the David Geffen School of Medicine, the University of California-Los Angeles – note that this medication can sometimes cause skin irritation, such as redness, itching and peeling skin.

Past research has indicated that resveratrol – an antioxidant found naturally in red grapes that prevents free radicals from forming – may be effective against acne, but the mechanisms behind this have been unclear. Dr. Taylor and colleagues set out to investigate.

A ‘two-pronged attack’ on acne bacteria

The team applied resveratrol, benzoyl peroxide, and a combination of both compounds to colonies of P. acnesbacteria, and assessed their antibacterial effects for 10 days. They also cultured human skin cells and blood cells with the compounds.

They found that all concentrations of benzoyl peroxide were able to kill P. acnes, but this effect lasted no longer than 24 hours.

Resveratrol, however, appeared to kill P. acnes by weakening the outer membrane of the bacteria. Such effects lasted for 48 hours, although a concentration of at least 50 ug/mL was required.

But the team says they were surprised to find that the strongest effect against acne occurred when both resveratrol and benzoyl peroxide were combined. Not only did this combination kill bacteria at all concentrations, but the effects lasted longer.

“It was like combining the best of both worlds and offering a two-pronged attack on the bacteria,” says senior author Dr. Jenny Kim, also of the division of dermatology at the Geffen School.

Commenting on the findings, Dr. Taylor says:

“We initially thought that since actions of the two compounds are opposing, the combination should cancel the other out, but they didn’t.

This study demonstrates that combining an oxidant and an antioxidant may enhance each other and help sustain bacteria-fighting activity over a longer period of time.”

Potential for new acne treatments

From culturing human skin cells and blood cells with the compounds, the team also found that benzoyl peroxide had much higher toxicity than resveratrol, which may explain why benzoyl peroxide can cause skin irritation.

The researchers point out, however, that this toxicity reduced when both resveratrol and benzoyl peroxide were combined, indicating that both of the compounds together could treat acne more effectively but produce fewer side effects.

The findings, the researchers say, may even lead to new acne treatments. “We hope that our findings lead to a new class of acne therapies that center on antioxidants such as resveratrol,” says Dr. Taylor.

The researchers note that further research is warranted to better determine how the two compounds work together to kill acne bacteria, and their findings will need to be validated in patients with acne.

Medical News Today recently reported in a study presented at the 5th American Society for Microbiology Conference on Beneficial Microbes in Washington, DC, claiming a certain bacteria could help treat acne and other skin disorders.

A number of studies have also hailed resveratrol for other benefits. In 2012, MNT reported on a study claimingresveratrol has anti-aging properties, while researchers of a more recent study claim to have identified why resveratrol may prevent heart disease and cancer.

Written by Honor Whiteman

Copyright: Medical News Today

http://www.medicalnewstoday.com/articles/283406.php

 

 

 

Malaria severity influenced by five human genes, say researchers

A large, international multi-center study – the largest of its kind to investigate the human genetics of malaria – has uncovered some new clues about susceptibility to severe malaria.

 

Writing in the journal Nature Genetics, the team, including Dr. Sarah Dunstan of The Nossal Institute of Global Health at the University of Melbourne in Australia, reports how it found five genes that have a complex role in either protecting or making people more susceptible to severe malaria.

Even with good hospital treatment, around 20% of patients who develop severe malaria die. The researchers hope their findings will lead to new drugs and vaccines to target the disease.

Malaria is a disease that develops when a mosquito infected by the parasite Plasmodium bites a person. The parasite invades and lives in the new host’s red blood cells.

There are several species of Plasmodium, of which P. falciparum is the one that most commonly causes severe disease in patients that are not immune.

Severe malaria can develop within a few days of infection. The condition affects many vital organs. If it affects the brain it can cause coma or cerebral malaria. If it affects the kidneys it can cause renal failure; in the lungs it can cause respiratory failure. It can also make the blood very acidic and lead to severe anemia and death.

Unprecedented study used large amount of data

For their study, Dr. Dunstan and colleagues analyzed data on nearly 12,000 cases of severe malaria collected from 12 sites across Africa, Asia and islands around the Pacific Ocean where access to treatment facilities can be difficult.

She says because of the international consortium behind it, the study was able to access a large amount of data to investigate genes that influence susceptibility to malaria on an unprecedented scale:

“It involved a large number of severe malaria patients from multiple countries, which allows us to identify genes that truly have an effect on whether or not you develop severe malaria.”

Of the 27 malaria resistance genes that they analyzed, the team found five – HBB, ABO, ATP2B4, G6PD and CD40LG – that were significantly involved in determining human susceptibility to severe malaria.

Role of genes in severe malaria more complex than previously thought

The results also show the role of common human genetic disorders in severe malaria are more complex than previously thought, as Dr. Dunstan explains, in reference to one of the genes:

“Our findings revealed that deficiency in G6PD, which causes a genetic blood disorder, can both reduce risk of cerebral malaria and increase risk of severe malarial anemia, both of which are fatal complications of malaria.”

The consortium behind the study is the Malaria Genomic Epidemiology Network (MalariaGEN), a global research group that is trying to understand immunity to malaria from the point of view of genetics.

MalariaGEN is based at the Wellcome Trust Centre for Human Genetics, at the University of Oxford in the UK. Professor Dominic Kwiatkowski, senior author of the study, is the principal investigator of the MalariaGEN consortium.

One of the features of the malaria parasite that makes it difficult to study is the fact it takes less than 60 seconds to travel from one blood cell to infect another, and it quickly loses its infective ability within minutes of leaving a cell.

But the parasite’s journey from one cell to another should be much easier to study in detail, now that a group based at the Wellcome Trust Sanger Institute, near Cambridge in the UK, has developed laser optical tweezers to see how malaria invades red blood cells.

Written by Catharine Paddock PhD

http://www.medicalnewstoday.com/articles/283154.php

 

Leaky gut – a source of non-AIDS complications in HIV-positive patients

Human immunodeficiency virus (HIV) infection is no longer a fatal condition, thanks to newer medications inhibiting the retrovirus, but a puzzling phenomenon has surfaced among these patients – non-AIDS complications. Scientists at Case Western Reserve University School of Medicine have resolved the mystery with their discovery of the leaky gut as the offender. Bacterial products seep out of the colon, trigger inflammation throughout the body and set into motion the processes of cardiovascular, neurodegenerative, chronic kidney and metabolic diseases, and cancer. Their findings appear in PLOS Pathogens.

“Because the space inside the colon (the lumen) contains the highest concentration of bacteria in the body, we provide evidence that bacterial products are leaking out of the colon into the bloodstream of these patients,” said senior author, Alan D. Levine, PhD, professor of medicine, pharmacology, pathology, molecular biology and microbiology, and pediatrics, Case Western Reserve University School of Medicine. “The immune system responds by launching an attack on these bacterial products, activating inflammation throughout the body that never stops.”

Bacteria can induce serious illness, but bacterial products are harmless remnants of dead bacteria. However, the immune system does not easily distinguish between live bacteria and bacterial products. Therefore, an immune attack is launched when bacterial products enter the bloodstream. In an HIV infection, tight junctions within the colon become the weak link providing an entryway for bacterial products to leak out.

Tight junctions are small, indented areas along the epithelial surface of the colon, something like the interior folds of a partially inflated accordion. Tight junctions form a barrier within the colon by sealing adjacent epithelial cells, and each tight junction seals the gut lumen (colon interior) from the colon exterior. Epithelial (or surface) cells are compacted against each other, but a miniscule opening (the intercellular space) allows ultra fine molecules to pass through. The tight junction complex forms tiny strands to seal that intercellular space.

Levine and colleagues demonstrated in their investigation that patients whose HIV was well controlled with antiretroviral medications still had weakened intestinal tight junctions. They came to this conclusion by comparing biopsies from 31 virally suppressed HIV-positive patients and from 35 healthy patients who had no HIV infection. (Virally suppressed means the level of circulating virus in the bloodstream is extremely low or undetectable.) The biopsies were obtained from patients at University Hospitals Case Medical Center during routine colonoscopies, a procedure to inspect visually the health of the colon. During the procedure, biopsies were collected from three places in patients’ intestines: the end of the small intestine (terminal ileum), the beginning and middle portions of the colon (ascending and transverse) and toward the end of the colon (descending).

“Not only did we find evidence of less tight junctions in the virally suppressed HIV-positive patients, we found that the reduction in tight junctions increased the farther down we went into the colon,” Levine said. “So essentially, these patients had the weakest tight junctions where the most bacteria are located. Additionally, we correlated the reduced tight junctions with increased inflammation.”

Investigators examined the biopsy tissue that sealed the spaces between epithelial cells and formed a barrier against luminal bacteria. They found that the number of cells and their density (or packing) was unchanged, meaning the leaks are not caused by cell death or pronounced changes in tissue structure or epithelial surface. However, the RNA and proteins that contribute to the organization of the tight junctions in the colon were decreased.

“The decline of the tight junctions correlated with increased microbial translocation and a greater level of inflammation throughout the body,” Levine said. “This finding provides evidence that a defect in the gut wall allowing bacterial products to leak out is the likely source of immune activation and subsequent inflammation. Basically, we found with this group of HIV-positive patients that the gut is leaky and why.”

These findings provide a clear target for clinical intervention – repair the molecular and structural epithelial leakiness in the tight junctions of the colon. However, critical questions must be resolved: Is the disruption caused by an HIV infection, the remaining HIV virus itself, antiretroviral drugs or all three combined to play a role in weakened tight junctions? What changes in epithelial cells might cause decreased activity of the tight junctions? Will repairs to the tight junction lead to stronger barrier function and reduced gut leakiness? Will reduced gut leakiness result in less systemic inflammation and therefore cause less cardiovascular, neurodegenerative, chronic kidney and metabolic diseases, and cancer in the virally suppressed HIV-positive patient?

“The key observation here is that virally suppressed HIV-positive patients have an important molecular and tissue defect – a leaky gut,” Levine said. “Thus, the clinical implication is quite clear. We will need additional supplemental therapeutic approaches to repair this damaged epithelium in the colon.”

This work was supported by grants from the National Institutes of Health (AI 076174, T32 GM007250, TL1 TR000441 and T32 GM-008803), the Case Western Reserve University Center for AIDS Research (AI 036219), Skin Diseases Research Center (P30 AR-039750), Visual Sciences Research Center Core (P30-EY11373) and School of Dental Medicine (P01 DE-019759).

http://www.medicalnewstoday.com/releases/282082.php