Manuscript Featured in Toxicological Sciences!

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A recently published manuscript from the Smith Lab for Pulmonary Immunotoxicology titled “Transcriptional profiling of lung macrophages following ozone exposure in mice identifies signaling pathways regulating immunometabolic activation” was featured in the latest issue of Toxicological Sciences! Learn more here: https://doi.org/10.1093/toxsci/kfae081.

Jordan Candelario completes CAPS summer program

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Undergraduate researcher and Center for Access and Postsecondary Success (CAPS) Scholar, Jordan Candelario, completed the CAPS summer research program and presented the results of her studies at the CAPS Research Summer Poster Exhibition! Follow the link below to learn more about Jordan’s research and the CAPS program. We are very proud of her!

Recognizing Three Faculty Research Mentors Following Annual Scholar Summer Poster Exhibition

Suheera Haq receives 2024 SURF award

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Undergraduate researcher, Suheera Haq, has received a 2024 Summer Undergraduate Research Fellowship award from the UConn Office of Undergraduate Research to support her summer research project focused on investigating the role of an epigenetic reader protein, Bromodomain-containing protein 4 (BRD4), in lung injury and inflammation caused by exposure to chlorine gas. Congratulations, Suheera!!

Dr. Smith’s Manuscript Featured in Toxicological Sciences

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Dr. Smith's recently published manuscript titled, "Role of PPARγ in dyslipidemia and altered pulmonary functioning in mice following ozone exposure" was highlighted as a featured article in the July issue of Toxicological Sciences. In this manuscript, Dr. Smith and his co-authors found that administration of a PPARγ agonist (rosiglitazone) restored normal pulmonary function and decreased pulmonary lipids (PL) in ozone-exposed mice. These results highlight the importance of alveolar lipids and point to a critical role for alveolar macrophages (AM) in regulating surfactant activity and lung function after ozone.

Hypothetical Model

Inhalation of ozone disrupts lung lipid homeostasis by increasing surfactant production by alveolar epithelial type II (ATII) cells and reducing lipid uptake by alveolar macrophages (AM); this leads to an imbalance in the levels of surfactant protein B (SP-B) and phospholipids (PL) which results in decrements in lung function. Administration of the PPARγ agonist, rosiglitazone, increases expression of the lipid scavenger receptor, Cd36, which enhances clearance of excess lipids; this normalizes relative SP-B to phospholipid levels and pulmonary function. Created with Biorender.