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369 results on '"Schladweiler, Mette C."'

5. Ozone Reacts With Carbon Black to Produce a Fulvic Acid-Like Substance and Increase an Inflammatory Effect

Author

Ghio, Andrew J, Gonzalez, David H, Paulson, Suzanne E, Soukup, Joleen M, Dailey, Lisa A, Madden, Michael C, Mahler, Beth, Elmore, Susan A, Schladweiler, Mette C, and Kodavanti, Urmila P

Subjects
Medical Biotechnology, Biomedical and Clinical Sciences, Climate-Related Exposures and Conditions, Lung, Good Health and Well Being, Air Pollutants, Animals, Benzopyrans, Humans, Male, Ozone, Particulate Matter, Rats, Soot, ozone, fulvic acid, air pollution, iron, lung diseases, carbon black, fulvic acid-like substance, inflammation, rats, Clinical Sciences, Toxicology, Clinical sciences
Abstract

Exposure to ambient ozone has been associated with increased human mortality. Ozone exposure can introduce oxygen-containing functional groups in particulate matter (PM) effecting a greater capacity of the particle for metal complexation and inflammatory effect. We tested the postulate that (1) a fulvic acid-like substance can be produced through a reaction of a carbonaceous particle with high concentrations of ozone and (2) such a fulvic acid-like substance included in the PM can initiate inflammatory effects following exposure of respiratory epithelial (BEAS-2B) cells and an animal model (male Wistar Kyoto rats). Carbon black (CB) was exposed for 72 hours to either filtered air (CB-Air) or approximately 100 ppm ozone (CB-O3). Carbon black exposure to high levels of ozone produced water-soluble, fluorescent organic material. Iron import by BEAS-2B cells at 4 and 24 hours was not induced by incubations with CB-Air but was increased following coexposures of CB-O3 with ferric ammonium citrate. In contrast to CB-Air, exposure of BEAS-2B cells and rats to CB-O3 for 24 hours increased expression of pro-inflammatory cytokines and lung injury, respectively. It is concluded that inflammatory effects of carbonaceous particles on cells can potentially result from (1) an inclusion of a fulvic acid-like substance after reaction with ozone and (2) changes in iron homeostasis following such exposure.

Published
2020

15. Repeated exposure to eucalyptus wood smoke alters pulmonary gene and metabolic profiles in male Long-Evans rats

Author

Cochran, Samuel J, primary, Dunigan-Russell, Katelyn, additional, Hutton, Grace M, additional, Nguyen, Helen, additional, Schladweiler, Mette C, additional, Jones, Dean P, additional, Williams, Wanda C, additional, Fisher, Anna A, additional, Gilmour, M Ian, additional, Dye, Janice A, additional, Smith, M Ryan, additional, Miller, Colette N, additional, and Gowdy, Kymberly M, additional

Published
2024
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22. Multi-tissue transcriptomic and serum metabolomic assessment reveals systemic implications of acute ozone-induced stress response in male Wistar Kyoto rats

Author

Jackson, Thomas W., primary, House, John S., additional, Henriquez, Andres R., additional, Schladweiler, Mette C., additional, Jackson, Kimberly MP, additional, Fisher, Anna A., additional, Snow, Sam J., additional, Alewel, Devin I., additional, Motsinger-Reif, Allison, additional, and Kodavanti, Urmila P., additional

Published
2023
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30. Stress Drivers of Glucose Dynamics during Ozone Exposure Measured Using Radiotelemetry in Rats

Author

Henriquez, Andres R., primary, Snow, Samantha J., additional, Jackson, Thomas W., additional, House, John S., additional, Motsinger-Reif, Alison A., additional, Ward-Caviness, Cavin K., additional, Schladweiler, Mette C., additional, Alewel, Devin I., additional, Miller, Colette N., additional, Farraj, Aimen K., additional, Hazari, Mehdi S., additional, Grindstaff, Rachel, additional, Diaz-Sanchez, David, additional, Ghio, Andrew J., additional, and Kodavanti, Urmila P., additional

Published
2022
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31. Prenatal ozone exposure programs a sexually dimorphic susceptibility to high‐fat diet in adolescent Long Evans rats

Author

Stewart, Erica J., primary, Dye, Janice A., additional, Schladweiler, Mette C., additional, Phillips, Pamela M., additional, McDaniel, Katherine L., additional, Richards, Judy H., additional, Grindstaff, Rachel D., additional, Padgett, William T., additional, Moore, Makala L., additional, Hill, Donna, additional, Gordon, Christopher J., additional, Kodavanti, Urmila P., additional, and Miller, Colette N., additional

Published
2022
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32. Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats

Author

Farraj, Aimen K, primary, Martin, Brandi L, additional, Schladweiler, Mette C, additional, Miller, Colette N, additional, Smoot, Jacob, additional, Williams, Wanda, additional, Fisher, Anna, additional, Oshiro, Wendy, additional, Tennant, Alan, additional, Martin, W Kyle, additional, Henriquez, Andres R, additional, Grindstaff, Rachel, additional, Gavett, Stephen H, additional, Gilmour, M Ian, additional, Kodavanti, Urmila P, additional, Hazari, Mehdi S, additional, and Dye, Janice A, additional

Published
2022
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38. Vascular and Cardiac Impairments in Rats Inhaling Ozone and Diesel Exhaust Particles

Author

Kodavanti, Urmila P., Thomas, Ronald, Ledbetter, Allen D., Schladweiler, Mette C., Shannahan, Jonathan H., Wallenborn, J. Grace, Lund, Amie K., Campen, Matthew J., Butler, Elizabeth O., Gottipolu, Reddy R., Nyska, Abraham, Richards, Judy E., Andrews, Deborah, Jaskot, Richard H., McKee, John, Kotha, Sainath R., Patel, Rishi B., and Parinandi, Narasimham L.

Published
2011

41. Intratracheal instillation of respirable particulate matter elicits neuroendocrine activation.

Author

Alewel, Devin I., Henriquez, Andres R., Schladweiler, Mette C., Grindstaff, Rachel, Fisher, Anna A., Snow, Samantha J., Jackson, Thomas W., and Kodavanti, Urmila P.

Subjects
PARTICULATE matter, FLY ash, ADRENAL glands, LUNGS, GLUCOSE intolerance, LUNG injuries, GENE expression, THYROTROPIN receptors
Abstract

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. 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. 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. 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. [ABSTRACT FROM AUTHOR]

Published
2023
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42. Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats.

Author

Farraj, Aimen K, Martin, Brandi L, Schladweiler, Mette C, Miller, Colette N, Smoot, Jacob, Williams, Wanda, Fisher, Anna, Oshiro, Wendy, Tennant, Alan, Martin, W Kyle, Henriquez, Andres R, Grindstaff, Rachel, Gavett, Stephen H, Gilmour, M Ian, Kodavanti, Urmila P, Hazari, Mehdi S, and Dye, Janice A

Subjects
CARDIOVASCULAR diseases risk factors, HOUSE dust mites, PLETHYSMOGRAPHY, NEUTROPHILS, ALLERGIES, ARRHYTHMIA, AIRWAY resistance (Respiration)
Abstract

Recent epidemiological findings link asthma to adverse cardiovascular responses. Yet, the precise cardiovascular impacts of asthma have been challenging to disentangle from the potential cardiovascular effects caused by asthma medication. The purpose of this study was to determine the impacts of allergic airways disease alone on cardiovascular function in an experimental model. Female Wistar rats were intranasally sensitized and then challenged once per week for 5 weeks with saline vehicle or a mixture of environmental allergens (ragweed, house dust mite, and Aspergillus fumigatus). Ventilatory and cardiovascular function, measured using double-chamber plethysmography and implantable blood pressure (BP) telemetry and cardiovascular ultrasound, respectively, were assessed before sensitization and after single and final allergen challenge. Responses to a single 0.5 ppm ozone exposure and to the cardiac arrhythmogenic agent aconitine were also assessed after final challenge. A single allergen challenge in sensitized rats increased tidal volume and specific airways resistance in response to provocation with methacholine and increased bronchoalveolar lavage fluid (BALF) eosinophils, neutrophils, lymphocytes, cytokines interleukin (IL)-4, IL-5, IL-10, IL-1β, tumor necrosis factor-α, and keratinocyte chemoattract-growth-related oncogene characteristic of allergic airways responses. Lung responses after final allergen challenge in sensitized rats were diminished, although ozone exposure increased BALF IL-6, IL-13, IL-1 β, and interferon-γ and modified ventilatory responses only in the allergen group. Final allergen challenge also increased systolic and mean arterial BP, stroke volume, cardiac output, end-diastolic volume, sensitivity to aconitine-induced cardiac arrhythmia, and cardiac gene expression with lesser effects after a single challenge. These findings demonstrate that allergic airways responses may increase cardiovascular risk in part by altering BP and myocardial function and by causing cardiac electrical instability. [ABSTRACT FROM AUTHOR]

Published
2023
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43. Glucose dynamics during ozone exposure measured using radiotelemetry: Stress drivers and human concordance

Author

Henriquez, Andres R, primary, Snow, Samantha J, additional, House, John S, additional, Motsinger-Reif, Alison A, additional, Ward-Caviness, Cavin, additional, Schladweiler, Mette C, additional, Alewel, Devin I, additional, Miller, Colette N, additional, Farraj, Aimen K, additional, Hazari, Mehdi S, additional, Grindstaff, Rachel, additional, Diaz-Sanchez, David, additional, Ghio, Andrew J, additional, and Kodavanti, Urmila, additional

Published
2021
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45. Inhaled Diesel Emissions Generated with Cerium Oxide Nanoparticle Fuel Additive Induce Adverse Pulmonary and Systemic Effects

Author

Snow, Samantha J., McGee, John, Miller, Desinia B., Bass, Virginia, Schladweiler, Mette C., Thomas, Ronald F., Krantz, Todd, King, Charly, Ledbetter, Allen D., Richards, Judy, Weinstein, Jason P., Conner, Teri, Willis, Robert, Linak, William P., Nash, David, Wood, Charles E., Elmore, Susan A., Morrison, James P., Johnson, Crystal L., Gilmour, Matthew Ian, and Kodavanti, Urmila P.

Published
2014
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46. A single exposure to eucalyptus smoke sensitizes rats to the postprandial cardiovascular effects of a high carbohydrate oral load

Author

Martin, Brandi L., Thompson, Leslie C., Kim, Yong Ho, Snow, Samantha J., Schladweiler, Mette C., Phillips, Pamela, Harmon, Molly, King, Charly, Richards, Judy, George, Ingrid, W. Kyle Martin, Haykal-Coates, Najwa, M. Ian Gilmour, Kodavanti, Urmila P., Hazari, Mehdi S., and Aimen K. Farraj

Abstract

Previous studies have shown that air pollution exposure primes the body to heightened responses to everyday stressors of the cardiovascular system. The purpose of this study was to examine the utility of postprandial responses to a high carbohydrate oral load, a cardiometabolic stressor long used to predict cardiovascular risk, in assessing the impacts of exposure to eucalyptus smoke (ES), a contributor to wildland fire air pollution in the Western coast of the United States. Three-month-old male Sprague Dawley rats were exposed once (1 h) to filtered air (FA) or ES (700 µg/m3 fine particulate matter), generated by burning eucalyptus in a tube furnace. Rats were then fasted for six hours the following morning, and subsequently administered an oral gavage of either water or a HC suspension (70 kcal% from carbohydrate), mimicking a HC meal. Two hours post gavage, cardiovascular ultrasound, cardiac pressure–volume (PV), and baroreceptor sensitivity assessments were made, and pulmonary and systemic markers assessed. ES inhalation alone increased serum interleukin (IL)-4 and nasal airway levels of gamma glutamyl transferase. HC gavage alone increased blood glucose, blood pressure, and serum IL-6 and IL-13 compared to water vehicle. By contrast, only ES-exposed and HC-challenged animals had increased PV loop measures of cardiac output, ejection fraction %, dP/dtmax, dP/dtmin, and stroke work compared to ES exposure alone and/or HC challenge alone. Exposure to a model wildfire air pollution source modifies cardiovascular responses to HC challenge, suggesting air pollution sensitizes the body to systemic triggers.

Published
2020
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47. The Role of Hepatic Vagal Tone in Ozone-Induced Metabolic Dysfunction in the Liver

Author

Colonna, Catherine H, primary, Henriquez, Andres R, additional, House, John S, additional, Motsinger-Reif, Alison A, additional, Alewel, Devin I, additional, Fisher, Anna, additional, Ren, Hongzu, additional, Snow, Samantha J, additional, Schladweiler, Mette C, additional, Miller, Desinia B, additional, Miller, Colette N, additional, Kodavanti, Prasada Rao S, additional, and Kodavanti, Urmila P, additional

Published
2021
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