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Category: biotech/medical – Page 135

New molecular strategy achieves complete synthesis of anti-MRSA natural product

Spiroaspertrione A is a complex polycyclic compound naturally produced by the fungus Aspergillus sp. TJ23. First isolated in 2017, it quickly drew scientific attention for its promising ability to combat drug-resistant bacteria and restore their sensitivity to existing antibiotics.

Scientists have now found a way to carry out the total synthesis of the molecule in 16 steps, starting from a chiral pool building block called (+)-enoxolone that costs less than one euro per gram. The synthesis technique is presented in Science.

Staphylococcus aureus (staph) is a type of bacteria that quietly lives on our skin and in our noses. It usually does no harm, but when it turns invasive, it triggers dangerous infections like sepsis, pneumonia, and many hospital-acquired infections. What makes it truly alarming is its growing resistance to antibiotics, which can turn treatable infections into deadly threats.

Geographical Expansion of Avian Metapneumovirus Subtype B: First Detection and Molecular Characterization of Avian Metapneumovirus Subtype B in US Poultry

Avian metapneumovirus (aMPV), classified within the Pneumoviridae family, wreaks havoc on poultry health. It typically causes upper respiratory tract and reproductive tract infections, mainly in turkeys, chickens, and ducks. Four subtypes of AMPV (A, B, C, D) and two unclassified subtypes have been identified, of which subtypes A and B are widely distributed across the world. In January 2024, an outbreak of severe respiratory disease occurred on turkey and chicken farms across different states in the US. Metagenomics sequencing of selected tissue and swab samples confirmed the presence of aMPV subtype B. Subsequently, all samples were screened using an aMPV subtype A and B multiplex real-time RT-PCR kit. Of the 221 farms, 124 (56%) were found to be positive for aMPV-B. All samples were negative for subtype A.

Psoriasis-linked gene mutation also impacts gut health, scientists discover

A mutation previously linked to skin disorders like psoriasis may also play a surprising role in gut health, according to new research published by scientists at VIB-UGent and colleagues from UGent, the University of Barcelona, and University College London. This mutation activates skin immune responses but also affects the intestine.

This finding, published in EMBO Molecular Medicine, reveals a new connection between genetics, the immune system, and the gut, which may have therapeutic implications.

Scientists under the leadership of Dr. Inna Afonina and Prof. Rudi Beyaert (VIB-UGent Center for Inflammation Research) have found that a mutation in the gene CARD14, known for activating skin immune responses in psoriasis patients, also affects the intestine. This mutation reduces gut motility, promotes mild inflammation, and increases vulnerability to bacterial infections.

Anti-CD19 CAR T-Cell Therapy in Advanced Stiff-Person Syndrome and Concomitant Myasthenia Gravis

The immune system works to identify and target invading pathogens. Specifically, our bodies work to get rid of any harmful infections by employing a two-part immune response. The first wave of immunity is the innate immune system. This initial reaction is broad and non-specific with innate cells circulating throughout the body to detect foreign pathogens. These cells that are involved include neutrophils, macrophages, eosinophils, basophils, and dendritic cells. Once cells detect an issue, they alert the rest of the body to completely filter out the infection. Importantly, the second wave of immunity, or the adaptive immune system, elicits a strong, specific response that target pathogens the innate immune system cannot neutralize.

Adaptive immunity builds to generate robust protection against aggressive diseases. The cells that make up this response include B and T cells. B cells are mainly responsible for generating antibodies to neutralize and signal infections throughout the body. T cells are the drivers that get rid of disease. T cell activity destroys infected cells and other pathogens lingering throughout the body or site of infection. The adaptive immune response is also critical for immune memory. Once someone experiences a disease and recovers, adaptive immune cells will remember that pathogen next time it enters the body — this is how vaccines work. A patient is injected with a non-harmful virus to expose the immune system. Immediately, the body will respond and destroy the virus. However, a few T cells will also be generated to targeted similar viruses in the future. As a result, when a patient is exposed to the infection again, they will be protected and not experience symptoms.

T cells are critical for any disease or infection, including cancer. Many immunotherapies currently being develop involve activating and directing T cells to the site of the tumor. However, immunotherapies have limited efficacy due to various mechanisms around the tumor that suppress immunity. Scientists are working to understand T cell biology to develop better immunotherapies and more accurately predict treatment outcomes in patients.

Successful experiments reprogram rogue T cells for targeted autoimmune disease therapy

Two teams of researchers have developed a cell reprogramming technology that converts rogue disease-causing T cells from our immune system into protective Treg cells. These cells help ensure that the immune system doesn’t attack the body’s own tissues. The breakthroughs could usher in more personalized and targeted cell therapies for a host of autoimmune diseases.

In the first paper, published in the journal Science Translational Medicine, scientists developed a targeted cell therapy against pemphigus vulgaris (PV). This severe autoimmune skin disease causes blisters and sores.

They took the cells that were causing the disease (Dsg3-specific pathogenic T cells) from mouse models and and converted them into harmless Treg cells. They used specialized chemical tools to switch on a gene called Foxp3, which controls a cell’s ability to help the , and cut off a specific activation signal to prevent the cells from turning back into attackers.

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