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.

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).

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).

we hypothesized that ozone-adaptation is linked to diminution of neuroendocrine stress-axes activation and glucocorticoid levels. Male Wistar-Kyoto-rats (12-week-old) were injected with vehicle or a therapeutically-relevant dexamethasone dose (0.01-mg/kg/day; intraperitoneal) for 1-month to determine if suppression of glucocorticoid signaling was linked to adaptation. Vehicle- and dexamethasone-treated rats were exposed to air or 0.8-ppm ozone, 4 hours/dayx2 or 4 days to assess the impacts of acute exposure and adaptation, respectively. This dataset is associated with the following publication: Heinriquez, A., S. Snow, J. Dye, M.C. Schladweiler, D. Alewel, C. Miller, and U. Kodavanti. The contribution of the neuroendocrine system to adaption after repeated daily ozone exposure in rats. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 447(116085): 1, (2022).

we hypothesized that ozone-adaptation is linked to diminution of neuroendocrine stress-axes activation and glucocorticoid levels. Male Wistar-Kyoto-rats (12-week-old) were injected with vehicle or a therapeutically-relevant dexamethasone dose (0.01-mg/kg/day; intraperitoneal) for 1-month to determine if suppression of glucocorticoid signaling was linked to adaptation. Vehicle- and dexamethasone-treated rats were exposed to air or 0.8-ppm ozone, 4 hours/dayx2 or 4 days to assess the impacts of acute exposure and adaptation, respectively. This dataset is associated with the following publication: Heinriquez, A., S. Snow, J. Dye, M.C. Schladweiler, D. Alewel, C. Miller, and U. Kodavanti. The contribution of the neuroendocrine system to adaption after repeated daily ozone exposure in rats. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 447(116085): 1, (2022).

Individuals with psychosocial stress often experience an exaggerated response to air pollutants. Ozone (O3) exposure has been associated with the activation of the neuroendocrine stress-response system. We hypothesized that preexistent mild chronic stress plus social isolation (CS), or social isolation (SI) alone, would exacerbate the acute effects of O3 exposure on the circulating adrenal-derived stress hormones, and the expression of the genes regulating glucocorticoid stress signaling via an altered stress adaptation in a brain-region-specific manner. Male Wistar–Kyoto rats (5 weeks old) were socially isolated, plus were subjected to either CS (noise, confinement, fear, uncomfortable living, hectic activity, and single housing), SI (single housing only, restricted handling and no enrichment) or no stress (NS; double housing, frequent handling and enrichment provided) for 8 weeks. The rats were then exposed to either air or O3 (0.8 ppm for 4 h), and the samples were collected immediately after. The indicators of sympathetic and hypothalamic–pituitary axis (HPA) activation (i.e., epinephrine, corticosterone, and lymphopenia) increased with O3 exposure, but there were no effects from CS or SI, except for the depletion of serum BDNF. CS and SI revealed small changes in brain-region-specific glucocorticoid-signaling-associated markers of gene expression in the air-exposed rats (hypothalamic Nr3c1, Nr3c2 Hsp90aa1, Hspa4 and Cnr1 inhibition in SI; hippocampal HSP90aa1 increase in SI; and inhibition of the bed nucleus of the stria terminalis (BNST) Cnr1 in CS). Gene expression across all brain regions was altered by O3, reflective of glucocorticoid signaling effects, such as Fkbp5 in NS, CS and SI. The SI effects on Fkbp5 were greatest for SI in BNST. O3 increased Cnr2 expression in the hypothalamus and olfactory bulbs of the NS and SI groups. O3, in all stress conditions, generally inhibited the expression of Nr3c1 in all brain regions, Nr3c2 in the hippocampus and hypothalamus and Bdnf in the hippocampus. SI, in general, showed slightly greater O3-induced changes when compared to NS and CS. Serum metabolomics revealed increased sphingomyelins in the air-exposed SI and O3-exposed NS, with underlying SI dampening some of the O3-induced changes. These results suggest a potential link between preexistent SI and acute O3-induced increases in the circulating adrenal-derived stress hormones and brain-region-specific gene expression changes in glucocorticoid signaling, which may partly underlie the stress dynamic in those with long-term SI. This dataset is associated with the following publication: Valdez, M., D. Freeborn, A. Henriquez, S. Snow , J.M. Valdez, T. Jackson, P. Kodavanti, and U. Kodavanti. Influence of Mild Chronic Stress and Social Isolation on Acute Ozone-Induced Alterations in Stress Biomarkers and Brain-Region-Specific Gene Expression in Male Wistar–Kyoto Rats. Antioxidants. MDPI, Basel, SWITZERLAND, 12(11): 1964, (2023).

The dataset is comprised of multiple data-frames. Our focus is on sex and brain region specific responses to ozone in a rat model. The PCR data describes the gene expression from listed brain regions resulting from ozone exposure. Complex enzymes were also assayed due to their sensitivity to oxidative stress using biochemical colorimetric assays. And finally, we collected data for oxidative stress artifacts such as protein carbonyl productions, total antioxidants, and enzyme activity. This dataset is associated with the following publication: Valdez, M., D. Freeborn, P. Vulimiri, J. Valdez, U. Kodavanti, and P. Kodavanti. Acute Ozone-Induced Transcriptional Changes in Markers of Oxidative Stress and Glucocorticoid Signaling in the Rat Hippocampus and Hypothalamus are Sex-Specific.. International Journal of Molecular Sciences. MDPI, Basel, SWITZERLAND, 24(7): 1, (2023).

The dataset is comprised of multiple data-frames. Our focus is on sex and brain region specific responses to ozone in a rat model. The PCR data describes the gene expression from listed brain regions resulting from ozone exposure. Complex enzymes were also assayed due to their sensitivity to oxidative stress using biochemical colorimetric assays. And finally, we collected data for oxidative stress artifacts such as protein carbonyl productions, total antioxidants, and enzyme activity. This dataset is associated with the following publication: Valdez, M., D. Freeborn, P. Vulimiri, J. Valdez, U. Kodavanti, and P. Kodavanti. Acute Ozone-Induced Transcriptional Changes in Markers of Oxidative Stress and Glucocorticoid Signaling in the Rat Hippocampus and Hypothalamus are Sex-Specific.. International Journal of Molecular Sciences. MDPI, Basel, SWITZERLAND, 24(7): 1, (2023).

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 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).