Rachel Alford

A Texas native, Rachel Alford graduated cum laude from Baylor University in May 2021 with a bachelor’s of science in Environmental Science. She is currently a master’s of science student in the Environmental and Occupational Health Department of IU’s School of Public Health, and does her thesis research under Dr. Patricia Silveyra. Having an interest in women’s health disparities and environmental justice issues, Ms. Alford is focused on studying sex differences in the lung and gut microbiome of asthmatic models.  

Sex differences in the lung microbiome in a mouse model of allergic asthma

Asthma is a disease that leads to compromised lung function and affects millions of patients worldwide. Disparities in sensitivity between men and women to these factors have also been identified; however, it remains unclear whether mediators such as the microbiome contribute to such differences. To understand the mechanisms associated with previously observed sex disparities in allergen-induced asthma, we used a mouse model of house dust mite (HDM)-induced asthma. Preliminary findings showed sex differences in respiratory mechanics and activation of the immune response following HDM challenge. In the present study, we tested the hypothesis that the lung microbiome promotes different disease phenotypes in mice challenged with HDM. We analyzed the 16S microbiome in DNA extracted from whole lung tissue of male and female C57BL/6 mice exposed to HDM or phosphate buffered saline (PBS) for 5 weeks (n=3/group); finding that males had a higher relative abundance of Firmicutes and other bacteria than females at basal levels, but this pattern was reversed with HDM challenge. In addition, the relative ratio of Firmicutes:Bacteroidetes was similar for both sexes in PBS-treated animals, but was almost twice as high in males than in females (4.2 vs 2.24, respectively) in mice challenged with HDM for 5 weeks. Moreover, females treated with HDM displayed higher bacterial diversity and relative abundance of Proteobacteria when compared to controls, an effect that was not observed in males. We conclude that sex-specific changes in lung microbial communities contribute to the mechanisms underlying differential asthma phenotypes in males vs. females.


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