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A better understanding of inflammation and lung immunity over the past two decades has led to new, innovative treatments for asthma, including biologic therapies.<\/p>\n
This is especially true for a subtype known as eosinophilic asthma — asthma that’s related to the recruitment and overactivation of white blood cells in the lungs called eosinophils.<\/p>\n
However, a different type of asthma called neutrophilic asthma has fewer treatment options and doesn’t respond as well to first line asthma therapy.<\/p>\n
As a result, people with this type of asthma, which is usually diagnosed in adults, often experience more serious disease and a poorer quality of life.<\/p>\n
A team of researchers led by Anukul Shenoy, Ph.D., of the Department of Microbiology and Immunology and the Division of Pulmonary and Critical Care Medicine at U-M and Joseph Mizgerd, Ph.D., of Boston University Chobanian & Avedisian School of Medicine are trying to address a lack of knowledge around neutrophilic asthma and have developed one of the first mouse models for the condition.<\/p>\n
By repeatedly, but briefly, exposing mice to an inhaled allergen over time, they were able to mimic the exposure and immune activity within the airways of adult humans.<\/p>\n
This type of allergen exposure resulted in an increase in accumulation of different types of T cells called CD4+TRM<\/sub> cells — memory cells that are present in adult lungs and responsible for a rapid response to a previously encountered allergen.<\/p>\n When activated, one subset of CD4+TRM<\/sub> cells lining the airways produces a cytokine IL-17A which then persuades the epithelial cells of the lung to recruit neutrophils, a type of white blood cell that causes inflammation.<\/p>\n While neutrophils are important for protection against pathogens their activation in response to a harmless allergen in asthmatics leads to severe lung damage.<\/p>\n Interestingly, the team also discovered that the epithelial cells try and control this inflammation by using a specialized immune-facing molecule called MHC-II.<\/p>\n They do so by using MHC-II to instruct a different subset of CD4+TRM<\/sub> cells in the airways to produce a cytokine IFN-gamma, which then potently suppressed inflammation in this mouse model of neutrophilic asthma.<\/p>\n<\/div>\n