A better undersrstanding of inflammation and lung immunity over the past two decades has lad to new, innovative trees for Asthma, Including Biologic Therapies. This is especially true for a subtype knowledge as eosinophilic asthma – sevenma That’s related to the recruitment and overactiveation of white blood cells in the lungs called eosinophils.

However, a different type of asthma called Neutrophilic Asthma has fewer treatment options and doesn Bollywood as well to first-Line ashma therapy. As a result, people with this type of asthma, which is usually diagnosed in adults, often experience more serial disease and a poorer quality of life.

A Team of Researchers LED by Anukul Shenoy, Ph.D., of the Department of Microbiology and Immunology and the Division of Pulmonary and Critical Critical Care Medicine at Um and Joseph Mizgard, PH.D. University Chobanian & Avedisian School of Medicine, is Trying to Address a Lack of Knowledge Around Neutrophilic Asthma and have developed one of the first models models for the condition.

The paper is Published in the journey Cell reports,

By repeated but briefly exposing mice to an inhaled allergen over time, the researchrs was able the exposure and immune activity with the airways of adult humans.

This type of allergen exposure resulted in an increase in account of different types of t cells called CD4^,T_Rm Cells – Memory cells that are present in adult lungs and responsible for a rapid response to a previous encounters allergen.

When Activated, One Subset of CD4^,T_Rm Cells lining the airways produces a cytokine called IL-17A, which then persuades the epithelial cells of the lung to recruit neutrophils, a type of white blood cells inflammation.

While Neutrophils are important for Protection Against Pathogens, their activation in response to a harmless allergen in As Asthmatics Leads to Severe Lung Damage.

Interestingly, the team also discovered that the epithelial cells try and control this inflammation by using a specialized immune-facing molecule called mhc -i.

They do so by using MHC-II to Instruct a different Subset of CD4^,T_Rm Cells in the airways to produces a cytokine ifn-gamma, which then potentially suppressed inflammation in this mouse model of neutrophilic asthma.