Neuroimmune Crosstalk Role in Heart Tissue Repair

Researchers at the Max Delbrück Center have discovered that zebrafish regenerate heart tissue using communication signals between their nervous and immune systems. In general, myocardial infarctions happen when blood vessels supply blood and nutrients to the heart, resulting in portions of the afflicted heart tissue dying. Since humans are unable to grow new heart cells to reduce the damage, they instead form scar tissue that weakens the pumping power of the heart overtime. Unfortunately, even stem cell research has been proven to be unsuccessful here.

Interestingly enough, signals between the autonomic nervous system (ANS) and immune system were found to play pivotal roles in scarring cand tissue regeneration. To observe this communication, researchers induced an injury into the hearts and several macrophage receptors of zebrafish larvae. After noticing that ANS adrenergic signals resulted in macrophages multiply and regenerating heart muscle, the research team genetically engineered the fish larvae so that the signal couldn’t enter the macrophage cell. The research study found that interrupting the adrenergic ANS signal deactivated the macrophages and induced heart scarring. In difference, when macrophages are activated by these signals, they communicate with fibroblasts and promote regeneration at the damaged site, creating an environment conducive for the growth development and growth of blood, lymph, and heart vessels.

A rather interesting study, this research’s findings provide an insight into how the regeneration of human heart muscle tissue can be made foreseeable. By better understanding the differences in signaling between zebrafish and humans, biologists can better understand why cardiac tissue does not regenerate, find methods to navigate a path to initiating the regeneration process, and even how to better treat heart attack patients’ conditions.

For more information, the news article has been linked here and the published journal article has been linked here.

Smart Protein Molecule

To begin, I chose this article because it makes me happy that we are close to the idea that we are extremely near finding the cure to cancer. Researchers specifically, bioengineering professors at the University of California have created a "smart" protein that is able to tell white blood cells to become better cancer fighters. What the protein actually does is that it tells cells to ignore self destructing signals. Cancer cells use the mechanism in that they make the cells attack and self destruct, spreading to more of the body. They have called this smart molecule protein "iSnap." They have inserted into a macrophage which is a white blood cell. They then discovered that it made the cells react and engulf and divide cancer cells.


Personally, I really enjoyed this article because I love to hear when medicine is advancing with technology.  Perfecting this new finding will most definitely lead to immune cells being able to fight cancer cells leading to a cure to cancer. Realistically, this mechanism will also be able to fight diseases which will help the medicine field. The study was also done on rapidly dividing cancer cells and its success foreshadows a cure to even the toughest of cancers.



Reference: University of California - San Diego. (2017, September 28). Smart molecules trigger white blood cells to become better cancer-eating machines. ScienceDaily. Retrieved October 9, 2017 from www.sciencedaily.com/releases/2017/09/170928142121.htm
Picture : https://fthmb.tqn.com/5ry863qfeVyF7xsdP1u66r1muo4=/768x0/filters:no_upscale()/h20-58e655f93df78c5162ea0a1f.jpg

Curing HIV

Researchers have focused on white blood cells called T cells while looking for a cure. T cells are a part of the immune system the virus uses as a host. Recently researchers have discovered that this virus can be found not only in T cells but also in large white blood cells found in different tissues in the body called macrophages. This is a big discovery because it shows that T cells are not the only cells the virus can infect. For a cure to be found, researchers now have to look for therapeutic interventions that target two different cells. I think this is a big deal because finding a cure is now going to take longer since researches have to target multiple types of cells.

https://www.sciencedaily.com/releases/2017/04/170417114806.htm

https://www.nature.com/nm/journal/vaop/ncurrent/full/nm.4319.html

Anthrax spores use RNA coat to mislead immune system

Researchers from Harvard Medical University had initially discovered that the human body can detect anthrax spores by recognizing a specific RNA molecule found on the surface of the spore. In doing this, it hinders the bodies immune response to fight off the infection once anthrax has colonized into live bacteria. In a new study, researchers have found that anthrax stimulates it's host immune system by activating a certain set of immune sensors called macrophages, that are not able to detect its activity within the body.  In the article, the researchers also found that the spores are able to go undetected because it stimulates the immune signaling molecules and disrupts them by using Type 1 interferons, which impairs the bodies immune system to fight against it. The researchers hypothesized that this disease has evolved to use the RNA found on the spores to activate type 1 interferons and take over the bodies immune system. 

This article was an interesting read because it discusses how anthrax is evolving. It is also interesting because scientist are also beginning to look at the way how other bacterial spores are able to mislead the human immune system. By looking at the evolution of other bacteria, it can help researchers to follow its patterns of evolvement and eventually help save the lives of patients who contract these diseases. 

Article  

About Anthrax

Anthrax Spores Trick Human Immune System

Bacillus anthracis, also known as Anthrax, has many methods for replicating and living inside a host. When it enters the host it is usually in the form of a dormant spore that later germinates into the living a reproducing bacterium. The host immune system is stimulated by the spores and responses are activated but they can not identify the bacterial form. For the immune system to identify the active form, TLR2 is used which is a cell surface receptor protein that attaches to the lipoproein that is found in the cell wall of the bacteria. In this study scientists have found that the RNA from the outer layer of anthrax is recognized by human macrophages through two receptors called TLR7 and TLR8. Because the spore is recognized first and in a different way, it is more difficult for the immune system to recognized the matured bacteria.

https://www.sciencedaily.com/releases/2017/04/170411104508.htm

http://jem.rupress.org/content/early/2017/04/10/jem.20161141

The Future of the Prevention of HIV

An article in ScienceDaily says that the researchers at Albert Einstein College of Medicine have figured out how regulation occurs of the protein that blocks HIV-1 from multiplying in white blood cells. HIV-1 is the virus that causes AIDS and this discovery could serve as a potential elimination of the virus. It can eliminate the residue of the HIV-1 that remains in patients that have undergone antiretroviral therapy which reduces HIV-1 levels in the blood until it is undetectable, but it still remains in the phages. Dr. Felipe Diaz-Griffero says, “If you stop antiretroviral therapy, the virus emerges from these reservoirs and returns to the general circulation in a matter of days, as if the patient had never been treated.” Now that they have identified the protein and its regulation, they can prevent the HIV-1 from arising form reservoirs, eliminating them completely. Scientists have always known that the protein is SAMHD1 but they have never been able to figure out why it only prevents HIV-1 replication in certain cells but not other crucial ones such as macrophages. SAMHD1 exists in two forms: phosphorylated and unphosphorylated. A cell is only protected from the replication of the HIV-1 when there is unphosphorylated SAMHD1 proteins present. They are now trying to figure out a way to permanently keep SAMHD1 in its unphosphorylated state.

[caption id="attachment_8000" align="aligncenter" width="625" caption="T-cell Infected by HIV "][/caption]

I think this is a great discovery in science. It can potentially lead to a cure of a disease that people have been searching for the longest time. It would be a great success in medicine if this technique could be introduced to the public. However, I am curious to know how they will be able to account for the differences that exist from patient to patient.