Gut bacteria could be good or bad

Bacteria that live in and on human body are emerging as an increasingly important player in health and wellness. Human co-existence with these organisms is complex, minor changes in this relationship can leads to adverse reaction on human health.

Researchers from the University of Rochester Medical Center found that impairing a rare group of cells in the small intestine allows gut bacteria to invade the organ and cause major inflammation. The study was conducted in mice, but has implications for the treatment of inflammatory bowel disease (IBD), a group of disorders characterized by chronic inflammation in the digestive track.

Keeping guts in good shape requires the cooperation of multiple intestinal cells with the bacteria that live around them. Though small in number, intestinal cells called Paneth cells play an important role; they make antimicrobial compounds that keep bacteria in check and help form the lining of the small intestine, a physical barrier between the organ and the resident bacteria.

Previous research shows that changes or mutations in Paneth cells are associated with increased inflammation, including in individuals with Crohn's disease, a type of IBD. But, scientists were unsure how Paneth cells opened the door to inflammatory damage.

Researchers led by Felix O. Yarovinsky, M.D. found the answer in a process called autophagy, which helps cells remove unwanted cellular material or debris. His team turned off autophagy in Paneth cells in mice and then exposed them to a stressor-a parasite called Toxoplasma gondii. Without autophagy, the barrier between the small intestine and the gut bacteria broke down; bacteria invaded the organ and caused severe infection and inflammation.

Paneth cells are like the guardians of the intestine and autophagy is like their armor, when their  armor were removed, the Paneth cells couldn't control the intestinal bacteria and it went wild, causing severe disease. The study suggests that normal autophagy in Paneth cells is required to regulate bacteria in the gut, keeping it at bay and preventing the gut bacteria from invading host tissue.

Paneth cells make up just 2 percent of the cells in the intestine, and the fact that restricting autophagy in these cells led to big problems was an unexpected result. Gut bacteria play a role in the development of IBD, which includes Crohn's disease and ulcerative colitis. But how bacteria in the gut are controlled in these conditions remains elusive. This study and others point to Paneth cells as key regulators of the interactions between host and gut bacteria, and further research could inform the design of future therapies.
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How to live longer

Many cells in human body, such as those which make up brain need to last a lifetime. To do this human cells have developed ways of protecting themselves. One way is through a process called autophagy, which literally means self-eating, where damaged components are collected together and removed from the cell.This is very important as accumulation of damage in cells has been linked to several diseases including dementia.

Lead author, Dr Viktor Korolchuk explains: "As we age, we accumulate damage in our cells and so it is thought that activating autophagy could help us treat older people suffering from dementia. In order to be able to do this we need to understand how we can induce this cell cleaning." In this study the authors were able to identify how a protein called p62 is activated to induce autophagy. They found that p62 can be activated by reactive oxygen species (ROS). ROS are by-products of our metabolism that can cause damage in the cell.

This ability of p62 to sense ROS allows the cell to remove the damage and to survive this stress. In lower organisms, such as fruit flies, p62 is not able to do this. The team identified the part of the human p62 protein which allows it to sense ROS and created genetically modified fruit flies with 'humanised' p62. These 'humanised' flies survived longer in conditions of stress. Abilities like sensing stress and activating protective processes like autophagy may have evolved to allow better stress resistance and a longer lifespan.

Specific mutations in human p62, which cause a neurodegenerative disease called amyotrophic lateral sclerosis (ALS), can prevent activation of p62 by ROS. These cells are then unable to induce protective autophagy, and the authors explain that this could underlie the premature death of neurons in patients with this devastating age-related disease. In contrast, 'humanised' p62 fruit flies did not live longer suggesting that other mechanisms may be required. The research demonstrates that a collection of small adaptations like that of human p62 could have accumulated over time and these adaptations could underlie our increased natural defences and longer lifespans. The discovery of these adaptations allows a better understanding of how to treat age-related diseases.
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Source of ageing process

Genes belong to a process called autophagy - this one of the cells most critical survival processes, it promotes health and fitness in young worms but drive the process of ageing later in life.

 Promoting longevity by closing down autophagy in old worms improves neuronal and subsequent whole body health. Getting old happens to every species, natural selection results in the fittest individuals for a given environment surviving to breed and pass on their genes to the next generation.

The more fruitful a trait is at promoting reproductive success, the stronger the selection for that trait will be. Some genes encourage ageing while still being essential for development, there are series of genes involved in regulating autophagy, which accelerate the ageing process.

The process of autophagy is a critical recycling process in the cell. Autophagy is known to become slower with age and closing it down in the initiation of the process allows the worms to live longer.

There are severe negative consequences when it breaks down and then you are better off bypassing it all together. In young worms, autophagy is working properly and is essential to reach maturity but after reproduction, it begins to malfunction causing the worms to age.

 By inactivating autophagy in the neurons of old worms they were able to prolong the worms life and increased the total health of the worms. Turning autophagy off only in one tissue and the whole animal gets a boost. The neurons are much healthier in the treated worms and keeps the muscles and the rest of the body in good shape.
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Malaria drug protects fetuses from Zika

Zika virus infection can cause brain damage and sometimes death of fetus in the womb, it infects the fetus by manipulating the normal barrier to infection in the body.

Exposure to zika virus activated genes related to autophagy, the virus multiply in the placenta, autophagy process in the placenta promotes zika's survival and it infects the placental cells.

The malaria drug, Hydroxychloroquine suppresses the autophagy response, this reduces the virus in the fetuses and placentas.
With this suppression, their is less damage and the fetuses grow normally.

The malaria drug protects the fetus from the zika virus even when the virus is still present in the mother. It effectively blocks viral transmission to the fetus by interfering with the process of zika virus infection transmission and protects fetus from viral infection.

Hydroxychloroquine suppresses the autophagy response, this reduces the virus in the fetuses and placentas.
With this suppression their is less damage and the fetuses grow normally.
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Extra-virgin olive oil prevents cognitive decline and Alzheimer's disease

Extra-virgin olive oil protects memory and learning ability and reduces the formation of amyloid-beta plaques and neurofibrillary tangles in the brain.

The oil reduces brain inflammation and activates autophagy. Autophagy is the process of cells breakdown and removing of intracellular toxins like amyloid plaques and tau tangles.

Brain cells from mice fed with diets enriched in extra-virgin olive oil had higher levels of autophagy and reduced levels of amyloid plaques and phosphorylated tau. Phosphorylated tau causes neurofibrillary tangles that leads to nerve cell dysfunction in the brain that causes Alzheimer disease.

 Transgenic mouse model was used by researchers to investigate the links between extra-virgin olive oil and dementia, Alzheimer's disease.

The researchers divided the animals into two groups, one that received a diet enriched with extra-virgin olive oil and one that received the regular diet without the oil.

The olive oil was introduced into the diet when the mice were six months old, before symptoms of Alzheimer's disease begin to emerge in the animal model.

 There was no difference between the two groups of animals. However, at age 9 months and 12 months, mice on the extra virgin olive oil diet performed significantly better on tests designed to evaluate working memory, spatial memory, and learning abilities.

Studies of brain tissue from both groups of mice showed dramatic differences in nerve cell appearance and function.
The integrity of the connections between neurons, known as synapses, were preserved in animals on the extra-virgin olive oil diet.

Brain cells from animals in the olive oil group showed a dramatic increase in nerve cell autophagy activation, which was solely responsible for the reduction in levels of amyloid plaques and phosphorylated tau.

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