BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Lungs

How a Unique Type of T-cell Can Protect Against Pneumonia

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On February 28, 2023

In Student Post

We’ve all probably heard of pneumonia, or even know someone who has had it. Pneumonia is a lung infection that can be caused by bacteria, viruses, or fungi. This infection causes the lungs’ air sacs to fill with fluid, making it hard to breathe. The majority of cases of community acquired pneumonia are linked to Streptococcus pneumoniae (the pneumococcus). Because there is a significant chance of developing bloodstream infection in these cases, the fatality rate is high. Even with antibiotic treatments and vaccines, the fatality rate is 20% for young adults and 60% for the elderly. Although the reason why some individuals are more susceptible to this disease and why others are not has been a mystery for decades, scientists have discovered a cell that may provide some answers.

At the University of Liverpool, the Bacterial Pathogenesis and Immunity Group has identified a subset of white blood cells in mice known as TNFR2 expressing regulatory T cells (Tregs).

In class, we learned that T cells were involved in the cell-mediated response of adaptive immunity. During the immune response, T-helper cells are activated by interleukin to recognize the antigen and trigger the cell-mediated and humoral responses. T-memory cells are created to confer future immunity while T-killer cells are created to kill infected or cancerous cells. A subset of T-cells called regulatory T cells also regulate the immune system. During pneumonia infection specifically, these cells are involved in bacteraemic pneumonia resistance through maintaining and controlling frontline immune responses during infection in the lungs. T Regulatory Cells

When these cells are not functioning correctly or are missing, there is excessive and uncontrolled inflammation that results in tissue damage. This allows the bacteria to enter the bloodstream through the disrupted lung tissue barrier and cause sepsis, which is the body’s life-threatening response to infection.

Professor Aras Kadioglu, the leader of the Bacterial Pathogenesis and Immunity Group, stated, “This is a significant finding, which opens the door to potential new therapies which may target and modulate these subset of Tregs to prevent and treat severe invasive pneumococcal diseases.”

This article caught my attention because I have never heard of this subset of T cells before. Given how severe pneumonia is, it will be interesting to see how scientists will use this information to create new life-saving treatments.

Can Your Lungs Work Against COVID-19?

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On February 28, 2023

In Student Post

Within the last two to three years there has been an immense focus in the field of science, COVID-19. This pandemic has sparked a myriad of research opportunities as well as brought up questions we didn’t even know we needed answered.

With this, recent research at the University of Sydney shows that our lungs contain a protein that blocks the COVID-19 infection and works to create a protective barrier within our body. The way it works is that a protein receptor found in our lungs sticks to the virus, and then pulls it away from the targeted cells. The protein is known as the Leucine-Rich Repeat-Containing Protein 15 or in short, LRRC15. For context, leucine is an essential amino acid for protein synthesis as well as many other biological functions. The protein is a built-in receptor inside of our bodies that binds to the COVID-19 virus and doesn’t pass on the infection.

Lungs diagram detailed

Initially, the research was published on February 9, 2023, in the PLOS Biology Journal. Led by Professor Greg Neely and his team members, the findings serve to open a new sect of immunology and COVID research, specifically around the protein, LRRC15. Moreover, it creates a path to develop new drugs and treatments to prevent infections such as COVID-19. Greely states that ” This new receptor acts by binding to the virus and sequestering it which reduces infection,” essentially the receptor is able to attach to the virus and “squish” it before it moves to infection. He also pushes the idea that the new receptor can be used to “design broad-acting drugs that can block viral infection or even suppress lung fibrosis.” Continually Dr. Lipin Loo, one of Greely’s team members, mentions, “We think it acts a bit like Velcro, molecular Velcro, in that it sticks to the spike of the virus and then pulls it away from the target cell types,” here he outlines the stickiness of both the receptor and the virus as well as the receptor’s nature to latch onto the virus and “hold” it. In addition, Loo states, “When we stain the lungs of healthy tissue, we don’t see much of LRRC15, but then in COVID-19 lungs, we see much more of the protein,” here he fronts the idea that COVID-19 lungs are far richer in the LRRC15 protein than normal lungs, this may be due to a result of the protein’s ability to immobilize the virus.

To outline COVID-19 infects us by using a spike protein to attach to a specific receptor in our cells. It mainly uses the ACE2 receptor to enter human cells. Moreover, our lung cells have high levels of ACE2 receptors, which is why being infected can often cause severe problems in our lungs. Similar to ACE2, LRRC15 is a receptor for COVID. But, LRRC15 does not support infection, instead, it sticks to the virus and immobilizes it. This prevents other cells from becoming infected. LRRC15 attaches to the spike of the virus and pulls it away from certain target cell types. The LRRC15 protein is widely present throughout our body, it is in the: lungs, skin, tongue, fibroblasts, placenta, and lymph nodes. However, the researchers observe that the lungs “light up” with LRRC15 after infection. They think the new protein is a part of our body’s natural response to combatting the COVID-19 infection. It creates a barrier that separates the virus from our lung cells most susceptible to COVID-19 infection

SARS-COV-2

To connect to our AP Bio Class, we learned about adaptive immunity where we develop an acquired immunity after being exposed to pathogens, a specific response. I see some similarity here in that the LRRC15 protein is specific to immobilizing the COVID-19 infection. Additionally, in our Cell Signalling Chapter, we focused on signal transduction and its stages, reception, transduction, and response. Specifically in the reception stage, we focused on intracellular and transmembrane receptors. I think that LRRC15 would be transmembrane in order for it to efficiently bind to the COVID-19 Spike. With this, however, I would like to see more about the transduction component of the LRRC15 receptor. Lastly in our Enzyme Unit, we learned about how different factors can affect enzymatic activity; heat, pH, and even general surroundings. I wonder which factors work to hinder and work to stimulate the purpose of the LRRC15. I invite any and all comments with additional info relevant to the topics discussed.

The Future of Lung Health

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On October 25, 2022

In Student Post

In the 19th century, a tuberculosis outbreak killed every one in seven people worldwide. Scientists believed it to be a genetic disease that mainly children developed making it known as “the robber of youth”. It wasn’t until the year 1882 that Robert Koch’s discovery of tubercule bacillus revealed that tuberculosis was not a genetic disease but highly contagious. Although there was some hesitation in the medical community at first, Koch’s findings helped the U.S. launch massive public health campaigns to educate the public on tuberculosis prevention and treatment. Later in 1904, “William Osler and William Welch, together with Edward Livingston Trudeau, founded the forerunner of the American Thoracic Society, the National Association for the Study and Prevention of Tuberculosis”.  This sparked the beginning of pulmonary research – the conduction of clinically-oriented research into diseases and disorders affecting the lungs and respiratory tract (including molecular and cell-based investigations). With pulmonary research being around for more than 10o years, one would believe discovering something new at this point in history would be a long shot. But, recently researchers at the Perelman School of Medicine at the University of Pennsylvania found RASCs.

TB Culture

RASCs, also known as respiratory airway secretory cells, “line tiny airway branches, deep in the lungs, near the alveoli structures where oxygen is exchanged for carbon dioxide.” Scientists found that RASCs have stem-cell-like properties that allow them to regenerate other cells that are essential for normal functioning alveoli. They also discovered that smoking and the common smoking-related ailment called chronic obstructive pulmonary disease can disrupt the regenerative functions of RASCs. COPD is a chronic inflammatory lung disease that causes obstructed airflow from the lungs. Emphysema and chronic bronchitis are the two most common conditions that contribute to COPD (both bronchitis and emphysema affect the alveoli, the air sacks of the lungs).  The study’s first author Maria Basil, states “COPD is a devastating and common disease, yet we really don’t understand the cellular biology of why or how some patients develop it. Identifying new cell types, in particular new progenitor cells, that are injured in COPD could really accelerate the development of new treatments,”. COPD causes around 3 million deaths worldwide and current treatments can only slow the disease down rather than stop or reverse it. Mice being the common test subjects in lab procedures lack key features of the human lungs, which leads scientists to use healthy human donors to discover RASCs. Since RASCs are secretory cells it means that they produce proteins needed for the fluid lining of the airway. An organelle that we know produces secretory proteins is the ribosome. Ribosomes are tiny organelles that contain RNA and specific proteins within the cytoplasm. Ribosomes are directly involved in the manufacture of proteins by using RNA and amino acids. The discovery of RASCs will not only help advance future COPD treatments but can also lead to discover ways to treat other lung dieases.

Lungs open

Why Healthy People are Dying from Vaping

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On November 11, 2019

In Student Post

E-cigarette Related Pulmonary Disease

 

 

 

 

 

 

This article explores the new phenomenon of deaths that have arisen in relatively healthy people linked to vaping or e-cigarette use. Despite the title referring to the victims as “healthy”, there is an inherent contradiction as the people being studied in fact are using vaping as part of the daily lifestyle.  As such, they are exposing themselves to harmful contaminates and toxins including both viscous oils and chemical contaminants present in the vaping liquids that are potentially toxic to the lungs.  The vaping outbreak has led to almost 1,300 lung injuries and 26 deaths as of October 2019.

While the cause of the vaping related illnesses remains a mystery to investigators, numerous potential causes have been proposed.  Two of the major culprits, according to Dr. Michael Siegel a professor at BU School of Public Health, are thought to be either the oils or chemicals found in vaping products.  Regardless of which is the cause, both place an excessive burden on the lungs, resulting in difficulty pulping oxygen to the body tissues. As a result of the reduced oxygen, a variety of symptoms have emerged in the victims, and overall these symptoms have been coined EVALI: E-cigarette or vaping product use associated lung injury.

There are various risks associated with exposure to both the oils and the chemicals present in most vaping products. The oils, such as vitamin E Acetate are often added as thickening agents to black market vaping products which are inherently dangerous as they are not regulated by the FDA. Furthermore, the oils are thought to coat the lungs and as Dr. Siegel points out, our lungs are not designed to handle oil exposure, as the oil coats the air sacs that are needed for gas exchange and thus limit the body’s ability to acquire oxygen. The patients may experience respiratory failure, and as a result require mechanical ventilation in order to be able to breathe sufficiently. Conversely, it is also thought that chemical contaminants may be the primary problem.  Dr. Siegel draws attention to the risks associated with them including “damage to the lungs, which triggers a severe inflammatory response“.

Building on the knowledge that vaping is causing a mysterious outbreak of illnesses and deaths, researchers have taken interest in studying the problem more in depth. Samples were taken from 17 patients throughout the US who suffered from EVALI, and researchers concluded that the lung samples did not indicate that the oils were in fact the primary cause of the disease and symptoms. Instead, the samples showed evidence of injury similar to chemical pneumonitis, which results from inhalation of chemical fumes, and the authors cited in the publication in the New England Journal of Medicine that these chemicals are most likely the cause.  This information can be very promising for future research, as with this knowledge the actual cause of EVALI can be better pinpointed.

The damage found in vaping patients included very severe symptoms, with some patients even experiencing their lung cells falling off from extreme damage. The severity of this damage also led to acute respiratory distress syndrome, which allows materials such as dead cells and blood clotting proteins to enter the lung’s air sacs. The presence of these materials are quite dangerous as they prevent efficient oxygen exchange from occurring. Shockingly, this disease has an extremely high mortality rate and no known cure. This leaves people with the prospect that they may not recover, and as of right now all that can be done is temporary treatment or more importantly prevention in those portions of the population who are not vaping.  Scientists and doctors do not yet know if EVALI and associated acute respiratory distress syndrome is reversible or permanent. Thus, education is key to warn people of these risks so that they can make educated choices when being exposed to the possibility of partaking in vaping. 

 

 

 

*Sing in Rihanna’s voice* Breath out, Breathe in (mRNA)… American Oxygen!

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On January 14, 2019

In Student Post

Researches at the Massachusetts Institute of Technology (MIT) have designed a potentially groundbreaking tool for helping treat lung disease. Their design? One might find the answer rather surprising: inhalable mRNA.

What is mRNA?

Also known as messenger ribonucleic acid, mRNA is a subunit of RNA, and is responsible for carrying the genetic information copied from DNA in the form of a code. More specifically, mRNA is synthesized during transcription. As explained in the article, mRNA, “encodes genetic instructions that stimulate cells to produce specific proteins.” Click here to learn more about mRNA.

The Benefits:

Inhalable mRNA? Yes, you read that correctly. Essentially, patients would inhale the mRNA in an aerosol form. By doing such, the mRNA would come into direct contact with the patient’s lung’s cells, which would then trigger the production of “therapeutic” proteins. As stated in the article, such mRNA molecules, “[turn] the patients’ own cells into drug factories.” If done successfully, mRNA has the potential to treat a myriad of lung-related illnesses, cystic fibrosis among them. Daniel Anderson, an associate professor in MIT’s Department of Chemical Engineering, expresses confidence regarding the findings, stating, “We think the ability to deliver mRNA via inhalation could allow us to treat a range of different disease of the lung.”

Obstacles:

Presently, scientists face the challenge of targeting cells with the mRNA aerosol molecules by using methods which are both safe and efficient. Additionally, scientists are tasked with the challenge of transporting these mRNA molecules in protective carriers, as the body’s natural reaction is to break mRNA down.

The Experiment:

In order to determine the impact of inhalable mRNA, Dr. Daniel Anderson has successfully manipulated a mice’s lung cells to produce a target protein. Dr. Anderson and his lab have begun designing materials which can transport mRNA to organs such as the liver. In particular, he and his lab utilized polyethylenimine (PEI), as it doesn’t break down easily. However, this very aspect of the polymer has the potential to cause side effects. In an effort to avoid these unwanted symptoms, the team moved on to a biodegradable material called “hyperbranched poly”. To test this material, the scientists converted the material into a droplet form, using a nebulizer to deliver the inhalable mist to a group of mice. Twenty four hours later, the team found that the mice were indeed producing the sought-after bioluminescent protein. Moreover, with the decrease in mRNA dosage came the decrease in protein production.

Pictured above is polyethylenimine (PEI), the initial polymer used in Dr. Anderson’s experiment.

The Future of Inhalable mRNA:

Such developments, such as those performed by Dr. Anderson and his team, increase the potential reality of testing on patients. To read the full findings of the aforementioned experiment, click here.

Advanced new understanding of lung abnormality… thank you turtles!

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On December 10, 2017

In Student Post

A recent study of an unusual snapping turtle with one lung was found to share similar characteristics to humans born with one lung who survive infancy. “These shared traits include an enlarged single lung with a more homogenous distribution of respiratory parenchyma(the gas exchanging tissues), an opposing bronchus that ends where the opposite lung should be and malformations of the spine (such as scoliosis),” said Dr. Schnacher an Assistant Professor of cell biology at Louisiana State University. This study is important because there is very little known about lung morphogenesis.But we do knowthat mutations in genes cause severe, even lethal, lung malformations and lung formation. It is possible that similar genetic mutations are at play in both the turtle and in humans! What an interesting parallel!

 

 

 

 

 

The snapping turtle was found in Minnesota and brought to a wildlife rehabilitation center because of a deformity on its shell. However, it wasn’t long until the turtle’s second abnormality was discovered, its singular lung. The turtle was passed down to the hands of Dr. Schnacherand it went through computed tomography(CT) and microCT imaging. The images created 3D models of the area. For comparison, images of a normal turtle specimen were also taken. The comparison was conducted to observe the negative spaces within the lungs– the bronchial tree, lung skeleton, and lung surface. The architecture of the spaces and the patterns inside the lung were compared to the “normal” turtle. In addition, these models also facilitate a visual of specific structures that are very difficult to see in living animals, such as blood vessels and air spaces. What is so innovative about this technology is that qualitative and quantitative comparisons can be made between organisms with absolutely no harm to the specimens! For animal lovers like me this is a huge breakthrough.

So, what was the big reveal? The primary difference between the turtle with one lung and the normal turtle was that the normal turtle had an larger surface area and density value in regard to its gas exchanging tissue. The tissue originates from the secondary airways, thus the 14.3% increase is very signifigant. However, this abnormality had no effect on the turtles survival rate, it only effected aquatic locomotion and buoyancy control. How does this relate to humans now? The turtle represents an example of a non-fatal congenital defect and a clear pathway of how the turtle adapted to compensate for it. This increased understanding of soft tissue structures reveals key breakthroughs to one day understand and improve diagnoses in humans! I think the future holds big answers, what do you think?

 

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