A manuscript describing the independent roles of beta adrenergic and glucocorticoid receptors in mediating ozone-induced pulmonary and systemic effects. This dataset is associated with the following publication: Henriquez, A., S. Snow, M.C. Schladweiler, C. Miller, and U. Kodavanti. Independent roles of beta-adrenergic and glucocorticoid receptors in systemic and pulmonary effects of ozone. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 32(4): 155-169, (2020).

This data set shows high throughput gene expression assessment using RNAseq to examine how ozone-induced transcriptional changes in the lung are influenced by adrenalectomy or adrenal demedullation in rats. We have previously observed that lung injury and inflammation are diminished in adrenalectomized rats and this study was planned to understand if circulating stress hormones influence ozone transcriptional effects and what ozone-induced pathway changes might be impacted by removal of adrenal glands. This dataset is associated with the following publication: Henriquez, A., J. House, D. Miller, S. Snow, A. Fisher, H. Ren, M. Schladweiler, A. Ledbetter, F. Wright, and U. Kodavanti. Adrenal-derived stress hormones modulate ozone-induced lung injury and inflammation. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 329: 249-258, (2017).

This data set contains one Excel file. In this file are all the data pertaining to the effects of propranolol and mifepristone on ozone induced lung injury and inflammation . The different tabs of the spreadsheet pertain to each figure found in the manuscript. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, J. Richards, K. Mauge-Lewis, M. McGee, and U. Kodavanti. Adrenergic and glucocorticoid receptor antagonists reduce ozone-induced lung injury and inflammation. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 339: 161-171, (2018).

Dorsal third ventricle infusions of the alpha 2 adrenergic receptor antagonist, mianserin- which increases brain concentrations of dopamine, serotonin, and acetylcholine, or the glucocorticoid receptor antagonist, mifepristone, were performed in male WKY rats prior to acute ozone exposure at 0.8 ppm for 4 hours. This experiment was designed to target hippocampal and hypothalamic neuromodulation to determine the role of indoleamines, monoamines, and glucocorticoids in mediating the systemic and pulmonary effects to ozone exposure.

This data set pertains to the manuscript "Exacerbation of ozone-induced pulmonary and systemic effects by 2-adrenergic and/or glucocorticoid agonist/s". It shows the raw data for each figure in the manuscript that is created with these data. Basically examining the influence of beta adrenergic and glucocorticoid receptor agonists on ozone-induced lung injury and inflammation. This dataset is associated with the following publication: Henriquez, A., S. Snow, M. Schladweiler, C. Miller, J. Dye, A. Ledbetter, M. Hargrove, U. Kodavanti, and J. Richards. Exacerbation of ozone-induced pulmonary and systemic effects by beta2-adrenergic and/or glucocorticoid agonist/s. Scientific Reports. Nature Publishing Group, London, UK, 9(1): 17925, (2019).

This data set is an excel file pertaining to the study that examined ozone-induced systemic and pulmonary effects in rats that underwent SHAM surgery (control), adrenal demedullation or total bilateral adrenalectomy. Different pages of the spreadsheet shows individual animal data for markers of lung injury and inflammation, body weights, whole body plethysmography measurements, levels of circulating hormones and lipids, and circulating white blood cell count as well as platelet count. This dataset is associated with the following publication: Miller, D., S. Snow, M. Schladweiler , J. Richards , A. Ghio , A. Ledbetter , and U. Kodavanti. Acute Ozone-Induced Pulmonary and Systemic Metabolic Effects are Diminished in Adrenalectomized Rats#. TOXICOLOGICAL SCIENCES. Society of Toxicology, 150(2): 312-22, (2016).

Pulmonary gene expression related to the regulation of DNA methylation following an exposure to ozone in rats. Epigenetic regulation of a pulmonary hypertensive gene, apelin, was also quantified. This dataset is associated with the following publication: Miller, C., J. Dye, M. Schladweiler, J. Richards, A. Ledbetter, E. Stewart, and U. Kodavanti. Acute inhalation of ozone induces DNA methylation of apelin in lungs of Long-Evans rats.. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 30(4): 178-186, (2018).

This dataset includes data for the manuscript in progress, Intracerebroventricular kynurenic acid modulation differentially regulates the immune and neuroendocrine stress response to acute ozone exposure. This study employed the use of kynurenic acid or the kynurenic acid synthesis inhibitor, PF-04859989 infused into the dorsal third ventricle of the brain in male WKY rats, prior to acute ozone exposure at 0.8 ppm, to evaluate the role of kynurenic acid in modulating the neuroendocrine stress response to ozone. Our results indicate that kynurenic acid may have a protective role in the brain, in attenuating the pulmonary and systemic effects of ozone exposure, perhaps through multiple mechanisms. This dataset is associated with the following publication: Rentschler, K., M.C. Schladweiler, R. Grindstaff, W. Williams, P.R. Kodavanti, D. Freeborn, L. Klein, G. Jung, D. Herr, P. Evansky, J. McKee, S. Gavett, and U. Kodavanti. Differential Effects of Intracerebroventricular Kynurenic Acid Regulation on the Inflammatory and Neuroendocrine Response to Acute Ozone Exposure. Presented at Society of Toxicology, Orlando, FL, USA, 03/16/2025 - 03/20/2025.

Objective: Inhalation of ozone activates central sympathetic-adrenal-medullary and hypothalamic-pituitary-adrenal stress axes. While airway neural networks are known to communicate noxious stimuli to higher brain centers, it is not known to what extent responses generated from pulmonary airways contribute to neuroendocrine activation. Materials and methods: Unlike inhalational exposures that involve the entire respiratory tract, we employed intratracheal (IT) instillations to expose only pulmonary airways to either soluble metal-rich residual oil fly ash (ROFA) or compressor-generated diesel exhaust particles (C-DEP). Male Wistar-Kyoto rats (12-13 weeks) were IT instilled with either saline, C-DEP or ROFA (5 mg/kg) and necropsied at 4 or 24 hr to assess temporal effects. Results: IT-instillation of particulate matter (PM) induced hyperglycemia as early as 30-min and glucose intolerance when measured at 2 hr post-exposure. We observed PM- and time-specific effects on markers of pulmonary injury/inflammation (ROFA>C-DEP; 24 hr>4hr) as corroborated by increases in lavage fluid injury markers, neutrophils (ROFA>C-DEP), and lymphocytes (ROFA). Increases in lavage fluid pro-inflammatory cytokines differed between C-DEP and ROFA in that C-DEP caused larger increases in TNF-α whereas ROFA caused larger increases in IL-6. No increases in circulating cytokines occurred. At 4 hr, PM impacts on neuroendocrine activation were observed through depletion of circulating leukocytes, increases in adrenaline (ROFA), and decreases in thyroid-stimulating-hormone, T3, prolactin, luteinizing-hormone, and testosterone. C-DEP and ROFA both increased lung expression of genes involved in acute stress and inflammatory processes. Moreover, small increases occurred in hypothalamic Fkbp5, a glucocorticoid-sensitive gene. Conclusion: Respiratory alterations differed between C-DEP and ROFA, with ROFA inducing greater overall lung injury/inflammation; however, both PM induced a similar degree of neuroendocrine activation. These findings demonstrate neuroendocrine activation after pulmonary-only PM exposure, and suggest the involvement of pituitary- and adrenal-derived hormones. This dataset is associated with the following publication: Alewel, D., A. Henriquez, M. Schladweiler, R. Grindstaff, A. Astriab Fisher, S. Snow , T. Jackson, and U. Kodavanti. Intratracheal instillation of respirable particulate matter elicits neuroendocrine activation. INHALATION TOXICOLOGY. Taylor & Francis, Inc., Philadelphia, PA, USA, 35(3-4): 59-75, (2023).

Ozone exposure induces neuroendocrine stress response, which causes lymphopenia. We hypothesized that ozone-induced increases in stress hormones will temporally follow changes in circulating granulocytes, monocytes and lymphocyte subpopulations. The goal of this study was to chronicle the changes in circulating stress hormones, cytokines, and leukocyte trafficking during 4-hour exposure to ozone. Male Wistar Kyoto rats were exposed to air or ozone (0.4 or 0.8 ppm) for 0.5, 1, 2, or 4 hours. After each time point, we assessed, circulating stress hormones and cytokines, lung gene expression, and live and apoptotic granulocytes, monocytes (classical and non-classical), and lymphocytes (B, Th and Tc) in blood, thymus and spleen using flow cytometry. This dataset is associated with the following publication: Henriquez, A., W. Williams, S. Snow, M.C. Schladweiler, C. Fisher, M. Hargrove, D. Alewel, C. Colonna, S. Gavett, C. Miller, and U. Kodavanti. The Dynamicity of Acute Ozone-Induced Systemic Leukocyte Trafficking and Adrenal-Derived Stress Hormones. TOXICOLOGY. Elsevier Science Ltd, New York, NY, USA, 458(152823): 1, (2021).