Researchers discover a stem cell therapy that can help heal injured heart

Researchers have discovered a stem cell therapy that might help the heart recuperate from an attack.

The study reported that injecting living or even dead heart stem cells into the injured hearts of mice triggers an acute inflammatory process, which in turn generates a wound healing-like response to enhance the mechanical properties of the injured area.

Mediated by macrophage cells of the immune system, the secondary healing process provided a modest benefit to heart function after a heart attack, according to the lead researcher.

The innate immune response acutely altered cellular activity around the injured area of the heart so that it healed with a more optimized scar and improved contractile properties, the author said.

The findings build on a 2014 study published by the same team. As in earlier study, the current paper shows that injecting c-kit positive heart stem cells into damaged heart as a strategy to regenerate cardiomyocytes doesn't work.

The findings prompted  the researchers to conclude that there is a need to re-evaluate the current planned cell therapy based clinical trials to ask how this therapy might really work.

Researchers worked with 2 types of heart stem cells currently used in the clinical trials- bone marrow mononuclear cells and cardiac progenitor cells. 

As they went through the process of testing and re-verifying their data under different conditions, they were surprised to discover that in addition to the 2 types of stem cells, injecting dead cells or even an inert chemical called zymosan also provided benefit to the heart by optimizing the healing process. Zymosan is a substance designed to induce an innate immune response.

They reported that stem cells or zymosan therapies tested in this study altered immune cell response that significantly decreased the formation of extracellular matrix connective tissue in the injury areas, while also improving the mechanical properties of the scar itself.

Researchers also found that stem cells and other therapeutic substances like zymosan have to be injected directly into the heart's surrounding area of infarction injury.

Most of the current trials  were also incorrectly designed because they infuse cells into the vasculature. Our results show that the injected material has to go directly into the heart tissue flanking the infarct region. This is  where the healing is occurring and where the macrophages can work their magic, the researcher explained.

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Here’s why belly fat increases as we age

In a bid to find a new treatment for improving metabolic health, researchers have discovered why belly fat surrounding organs increases as people age.

Led by Dr. Vishwa Deep Dixit, the Waldemar Von Zedtwitz Professor of Comparative Medicine and of Immunobiology, the study was published in 'Cell Metabolism'.

Previous work found that as people age, their body's ability to generate energy by burning the belly fat is reduced. Consequently, the fat that surrounds the internal organs increases in the elderly.

Dixit's lab had found that the immune cells necessary to the fat-burning process, called macrophages, were still active but their overall numbers declined as belly fat increased with aging.

This latest study found that something else is happening as well. Adipose B cells in belly fat unexpectedly proliferated as animals aged, contributing to increased inflammation and metabolic decline.

"These adipose B cells are a unique source of inflammation," Dixit said, "Normally the B cells produce antibodies, and defend against infection. But with aging, the increased adipose B cells become dysfunctional, contributing to metabolic disease."

When they are working correctly, Dixit said, some B cells expand as needed to protect the body from infection, and then contract to baseline. But with aging, they don't contract in belly fat.

"This predisposes an animal to diabetes and metabolic dysfunction like inability to burn fat," he said.
Dixit theorises that this ongoing expansion may be due to increased human life expectancy - a pushing of the body's cells beyond their evolutionary limits. "Several mechanisms in the body are not selected for longevity," he said.

Researchers discovered that adipose B cells expand by receiving signals from nearby macrophages. Relatedly, they found that by reducing the macrophage signal and by removing adipose B cells, they could reverse the expansion process, and protect against an age-induced decline in metabolic health.

This could lead to exciting possibilities for repurposing drugs to target these dysfunctional adipose B cells for improved health outcomes and to protect against metabolic disease, Dixit said. One drug, called cytokine IL-1B, reduces one of the small proteins driving this process and is currently used to protect against heart disease.

"It's important to study whether reducing this cytokine in the elderly can lower B cell expansion in belly fat," Dixit said.

He added that there are also immunotherapy drugs that neutralise B cells that are used in certain cancers. These, too, could be tested for their effectiveness in reducing metabolic disease in elderly people, Dixit added.

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This new method can help identify aggressive breast cancer

Aggressive forms of breast cancer often manipulate the immune response in their favour. This manipulation is revealed in humans by the same immunological ‘signature’ as in mice, as has been found by the researchers.

This method makes it possible to obtain an indication of the prognosis of the disease using patients’ tumour tissue. 

When a tumour starts to grow in the body, it usually does not go unnoticed by the immune system. Macrophages, a certain form of the body’s own defence troops, migrate to the cancer cells. They are supposed to flow around the diseased cells, digest them and thus eliminate them. But sometimes tumour cells manage to escape their adversaries. Not just that! They even use the macrophages for their own purposes and grow even faster as a result.

To do this, they reprogram the immune cells. They ensure that certain genes in the macrophages are switched off and others switched on. This changes the genetic “signature” of the macrophages.

“This changed signature, in turn, reveals whether the tumour has a good or bad prognosis,” explains  a Dr.  from the LIMES Institute (the acronym stands for ‘Life and Medical Sciences’) at the University of Bonn.

In order to identify the changes caused by the tumour, it is necessary to know which genes are normally active in the macrophages. However, this varies considerably, depending on the organ in which the scavenger cells perform their service.

In addition, tumour-induced changes are not always identical but differ from one patient to another. “Depending on which mutation is responsible for breast cancer, other functions are switched on or off in the macrophages,” stresses the Dr.

“We have now searched these animals for the signature of the scavenger cells in the tumours,” says the Dr. To this end, the bioinformatics expert and his colleagues isolated macrophages from mice affected by breast cancer and compared them with those from healthy breast tissue.

Researchers have also found almost identical signatures in the scavenger cells of many breast cancer patients. “In this case, it was possible to transfer the mouse results directly to humans,” explains  a Prof., head of the Genomics and Immunoregulation team at the LIMES Institute.

“However, the prerequisite was that the patients suffered from the same form of breast cancer as the animals.” The results also demonstrate how important it is to develop specific mouse models depending on the type of cancer.

The results can be used not just to predict tumour aggressiveness. After all, the signature also provides information on the cancer cells’ survival strategies. This may eventually lead to the development of new countermeasures. “However, it will certainly take many years for new treatment options to emerge if any,” adds the Dr.

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Indian scientists claim to have found 100% cure for tuberculosis

Infecting about nine million people worldwide every year, Tuberculosis is a deadly disease. Out of the nine million people infected from the disease, 32 per cent are from India. Many people don’t even realise that they have the infection as it remains dormant for years before becoming infectious.

What causes Tuberculosis?
The tuberculosis bacterium is hunted by the white blood cells called macrophages. A macrophage is an important part of our immune system. The term literally means big eaters. A macrophage is an amoeba-like organism and it’s work is to clean the body of microscopic invaders and debris. The macrophage has the innate ability to consume all the invaders including fungi, viruses, bacteria and parasites. But instead of killing the bacteria, it forms a sac-like body called granuloma around it, which keeps the bacteria dormant for as long as it’s present.

But this sac can get ruptured when your immunity is lowered due to weakness or any other illness like HIV. TB is a leading killer among people who are infected with HIV.

The new cure for tuberculosis
A team of scientists found how tuberculosis is released from the sacs granuloma formed by the macrophages around them. The granuloma keeps the TB bacteria under control. The topic has been researched and studied for years with no positive result.

ResultsScientists found that these TB bacteria secrete a protein called MPT63, which might be the reason behind the sac break. When there is acidity, these protein structures change their formation and suddenly become toxic to the host cells (macrophages). This ends up killing the cell and releasing the bacteria.

The Head of Structural Biology and Bioinformatics Division said, “Our team would now try to validate these findings in field strains of TB bacillus and see whether they can be used to develop new therapeutic interventions”.

Now with this discovery, scientists will begin looking for methods to negate the effect of the MPT63 protein. Keeping the TB locked-in permanently and saving millions of patients every year.

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‘Secret handshake’ detected between sperm and uterus

A team of researchers has discovered the making of a “secret handshake” between sperm and the cells lining the uterus that finally let one sperm out of nearly 200 million to make it through and fertilise a single egg, say researchers.

Uterine cells express a receptor that recognizes a glycan molecule on the surface of sperm cells.

It’s possible that this interaction may adjust the female’s immune response and help sperm make it through the leukocytic reaction, said the researchers. The leukocytic reaction is not well understood.

What we do know, explained molecular anthropologist  is that “after crossing the cervix, millions of sperm that arrive in the uterus are faced by a barrage of macrophages and neutrophils”.

This attack by the innate immune system kills a majority of the sperm cells in semen, winnowing hundreds of millions of sperm down to just a few hundred that enter the fallopian tubes.

The defensive response may be beneficial in preventing polyspermy, when an egg is fertilized by more than one sperm and cannot develop.

“It’s somewhat embarrassing how little we can say about what this [interaction] means,” said  a researcher.

Reproduction, he said, “is a very, very delicate tug-of-war at many levels. The fact that there is (also) this immune game going on is completely fascinating.”

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IIT Kanpur identifies novel molecule to control hyper inflammation

Researchers at the Indian Institute of Technology (IIT) Kanpur have identified and characterised a novel small protein molecule that can effectively control inflammation leading to better treatment outcomes. In contrast, inflammation control by molecules that are undergoing clinical trials may not be optimal due to inherent drawbacks. The work was done in collaboration with the University of Queensland.

Hyper inflammation

While some amount of inflammation at the site of infection is required for effective clearance of pathogens, too much inflammation compromises pathogen-clearing ability. Hyper inflammation also destroys the tissues surrounding the inflamed area leading to inflammation disorders such as sepsis, inflammatory bowel syndrome, rheumatoid arthritis and psoriasis. 

A small protein (C5a) that is a part of the innate immunity (immediate defence against pathogens that have never been encountered before) gets activated when a pathogen enters the body. The C5a protein then binds to a particular receptor (C5aR1) found on the surface of certain cells such as macrophages and neutrophils to begin the process of inflammation and pathogen clearance.

Neutrophiles are already present in the body and circulate in the blood. Once the small protein binds to the C5aR1 receptor found on neutrophils, there is increased migration towards the site of infection leading to hyper inflammation. At the same time, binding of the small protein to the receptor on macrophages reduces the amount of a pro-inflammatory cytokine called interleukin-6 (IL-6) that is released, which is desirable to overcome inflammatory symptoms. 

Therapeutic agents now undergoing clinical testing prevent the C5a protein from binding to the receptor found on neutrophils leading to reduced migration of neutrophils to the site of infection. Hyper inflammation is thus prevented. However, it has the opposite effect on interleukin-6 release. Unlike the C5a protein, the drug candidate molecules do not reduce the amount of IL-6 being released thereby causing more inflammation.

Role of IL-6

“There is more inflammation when the amount of IL-6 at the site of infection is more. So it is desirable to reduce the amount of IL-6 being released to overcome the inflammatory symptoms,” says a researcher.

The small protein molecule identified by IIT Kanpur researchers addresses the shortcomings seen with the drug molecules now undergoing clinical testing. The drug molecule that IIT Kanpur team used for this study is already known to bind to the C5aR1 receptor. But its effects were not characterised in term of IL-6 release and neutrophil migration.

“Our peptide molecule binds to the C5aR1 receptor found on neutrophils and reduces their migration to the site of infection. And unlike the molecules now being tested, our peptide molecule also reduces the amount of IL-6 being released,” says a Prof. Under in vitro conditions, the combined effect may lead to reduced inflammation.

“The molecule only reduces and not blocks neutrophil migration. There should be sufficient inflammation at the infection site to clear the pathogens,” says the first author of the paper.

The peptide molecule identified by the team is smaller than the C5a protein so the binding to the receptor is weak. “So we have to use higher concentration of our synthetic peptide to achieve better results. Future work would be to increase the strength of binding by improving the molecule so that less concentration is needed,” the Prof. says. The team plans to carry out animal studies in future to measure the therapeutic potential of the molecule.

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Energizing the immune system to eat cancer

Macrophages are immune cells just like T and B cells, but differ in that they can eat cells that are not supposed to be in the body. 

Immune cells called macrophages are supposed to serve and protect, but cancer has found ways to put them to sleep. Now researchers  say they've identified how to fuel macrophages with the energy needed to attack and eat cancer cells. It is well established that macrophages can either support cancer cell growth and spread or hinder it. But most tumors also express a signal called CD47, which can lull macrophages into a deep sleep and prevent them from eating. Researchers have found that rewiring macrophage metabolism can overcome this signal and act like an alarm clock to rouse and prepare macrophages to go to work.

Macrophages are immune cells just like T and B cells, but differ in that they can eat cells that are not supposed to be in the body. In fact, they are the most prominent immune cell found in cancer, but unfortunately, most are often convinced to help cancer grow and spread. Cancer cells frequently stop macrophages from attacking them by expressing CD47, a "don't eat me" signal. Researchers now say that merely blocking inhibitory signals like CD47 is not always sufficient to convince macrophages to attack cancer. Instead, two signals are required. First, they need a signal to activate them—such as a toll-like receptor agonist. After that, a second signal—such as a CD47 inhibitor—can lower the threshold needed to wage battle on the cancer.

"It turns out macrophages need to be primed before they can go to work, which explains why solid tumours may resist treatment with CD47 inhibitors alone," said the study's senior author.

The team used this approach by activating macrophages with CpG, a toll-like receptor agonist that sends the first signal, and found that it rapidly induced shrinkage of tumors and prolonged survival of mice even without the requirement of T cells. Unexpectedly, they also found that the activated macrophages were able to eat cancer cells even in the presence of high levels of CD47.

To understand the molecular basis of this phenomenon, the team traced the metabolic activity of macrophages and determined that activated macrophages began to utilize both glutamine and glucose as fuel to support the energy requirements needed for them to eat cancer cells. This rewiring of the macrophages metabolism was necessary for CpG to be effective, and the researchers say these findings point to the importance of macrophage metabolism in determining the outcome of an immune response.

"Cancer does not shrink without the help of macrophages and macrophages need the right fuel to eat cancer cells and shrink tumors," the author said. "To do this, a shift in metabolism is needed to steer the energy in the right direction. It is the metabolism that ultimately allows macrophages to override signals telling them not to do their job."

The researcher points out that patients with diabetes, cardiovascular disease, and other conditions are routinely treated with drugs that could affect macrophage metabolism, but virtually nothing is known about how these drugs might impact immunotherapy responses in cancer, meaning the team's discovery has implications even for existing treatments. 

Provided by: Perelman School of Medicine at the University of Pennsylvania

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