- West Virginia University School of Medicine
- Physiology, Pharmacology & Toxicology
- Adjunct Faculty
Adjunct Professor, Pulmonary & Critical Care Medicine
- BS, Chemistry, University of Pittsburgh, Pittsburgh, PA
- PhD, Pharmacology and Toxicology, West Virginia University, Morgantown, WV
Select Publications in Refereed Journals
1. Shore SA, Rivera-Sanchez YM, Schwartzman IN and Johnston RA (2003) Responses to ozone are increased in obese mice. J Appl Physiol 95:938-945.
2. Johnston RA, Theman TA and Shore SA (2006) Augmented responses to ozone in obese carboxypeptidase E-deficient mice. Am J Physiol Regul Integr Comp Physiol 290:R126-R133.
3. Johnston RA, Zhu M, Rivera-Sanchez YM, Lu FL, Theman TA, Flynt L and Shore SA (2007) Allergic airway responses in obese mice. Am J Respir Crit Care Med 176:650-658.
4. Barreno RX, Richards JB, Schneider DJ, Cromar KR, Nadas AJ, Hernandez CB, Hallberg LM, Price RE, Hashmi SS, Blackburn MR, Haque IU and Johnston RA (2013). Endogenous osteopontin promotes ozone-induced neutrophil recruitment to the lungs and airway hyperresponsiveness to methacholine. Am J Physiol Lung Cell Mol Physiol 305:L118-L129.
5. Dahm PH, Richards JB, Karmouty-Quintana H, Cromar KR, Sur S, Price RE, Malik F, Spencer CY, Barreno RX, Hashmi SS, Blackburn MR, Haque IU and Johnston RA (2014). Effect of antigen sensitization and challenge on oscillatory mechanics of the lung and pulmonary inflammation in obese carboxypeptidase E-deficient mice. Am J Physiol Regul Integr Comp Physiol 307:R621-R633.
6. Malik F, Cromar KR, Atkins CL, Price RE, Jackson WT, Siddiqui SR, Spencer CY, Mitchell NC, Haque IU and Johnston RA (2017) Chemokine (C-C motif) receptor-like 2 is not essential for lung injury, lung inflammation, or airway hyperresponsiveness induced by acute exposure to ozone. Physiol Rep 5: e13545.
7. Thompson JA, Johnston RA, Price RE, Hubbs AF, Kashon ML, McKinney W and Fedan JS (2022) High-fat Western diet consumption exacerbates silica-induced pulmonary inflammation and fibrosis. Toxicol Rep 9:1045-1053.
8. Johnston RA, Atkins CL, Siddiqui SR, Jackson WT, Mitchell NC, Spencer CY, Pilkington AW IV, Kashon ML and Haque IU (2022) Interleukin-11 receptor subunit alpha-1 is required for maximal airway responsiveness to methacholine following acute exposure to ozone. Am J Physiol Regul Integr Comp Physiol 323:R921-R934.
1. Moore BB, Ballinger MN, Bauer NN, Blackwell TS, Borok Z, Budinger GRS, Camoretti-Mercado B, Erzurum SC, Himes BE, Keshamouni VG, Kulkarni HS, Mallampalli RK, Mariani TJ, Martinez FJ, McCombs JE, Newcomb DC, Johnston RA, O’Reilly MA, Prakash YS, Ridge KM, Sime PJ, Sperling AI, Violette S, Wilkes DS, Königshoff M (2023) Building career paths for Ph.D., basic and translational scientists in clinical departments in the United States: An official American Thoracic Society workshop report. Ann Am Thorac Soc 20:1077-1087.
1. Johnston RA and Belenky P (2020) Filling a hole in ozone research: The impacts of early life microbiome alterations on pulmonary responses to a non-atopic asthma trigger. Physiol Rep 8:e14346.
1. Johnston RA and Shore SA (2019) Obesity and asthma: What have we learned from animal models?, in Mechanisms and Manifestations of Obesity in Lung Disease (Johnston RA and Suratt BT eds) pp 111-142, Academic Press/Elsevier Inc., London.
Recent Scientific Conference Abstracts
1. Pilkington A IV, Takahashi M, Takahashi Y and Johnston R (2022) Effect of chemerin deficiency on ozone-induced lung injury and lung inflammation. J Allergy Clin Immunol, 149:AB417.
2. Johnston RA, Takahashi M, Takahashi Y and Pilkington AW IV (2022) Impact of diet-induced obesity and chemerin deficiency on ozone-induced lung Injury and lung inflammation. Am J Respir Crit Care Med, 205:A3285.
3. Pilkington A IV, Takahashi M, Takahashi Y, Boots T and Johnston R (2023) Chemerin deficiency exacerbates ozone-induced increases in airway responsiveness. J Allergy Clin Immunol, 151(S):AB68.
4. Johnston RA, Sinal CJ and Pilkington AW IV (2023) Impact of diet-induced obesity and G protein-coupled receptor 1 deficiency on ozone-induced lung injury and lung inflammation. Am J Respir Crit Care Med, 207:A4036.
About Richard Johnston
Richard A. Johnston is a Research Pharmacologist at the National Institute for Occupational Safety and Health, which is part of the Centers for Disease Control and Prevention and the United States Department of Health and Human Services. In addition, he is an Adjunct Professor in the Department of Physiology, Pharmacology, and Toxicology and in the Department of Medicine in the School of Medicine at West Virginia University.
He graduated summa cum laude from the University of Pittsburgh in Pittsburgh, PA with a Bachelor of Science and Program Honors in Chemistry. Subsequently, he was bestowed with the degree of Doctor of Philosophy in Pharmacology and Toxicology from West Virginia University. Following his graduation from West Virginia University, he completed a post-doctoral fellowship in Lung Biology and Respiratory Disease at the Harvard School of Public Health in Boston, MA. As a post-doctoral fellow, he was the recipient of training fellowships from the National Institutes of Health and the American Lung Association. After his post-doctoral fellowship was complete, he was an Assistant Professor in The University of Texas System until joining the National Institute for Occupational Safety and Health as a Research Pharmacologist in 2017.
Dr. Johnston has combined careers in research and teaching. His basic science research interests include mechanisms underlying the impact of obesity on the development and progression of lung disease, specifically asthma, and mechanisms by which occupational exposure to disinfectant cleaners lead to work-related asthma. To support this research, Dr. Johnston has received funding from the National Institutes of Health and the National Institute for Occupational Safety and Health. Dr. Johnston also mentors the research activities of graduate students, medical students, and post-doctoral and clinical sub-specialty fellows and provides lectures in physiology and pharmacology to graduate and medical students.
Dr. Johnston is a member of several professional societies, including the American Academy of Allergy, Asthma & Immunology, American Physiological Society, American Society for Pharmacology and Experimental Therapeutics, and American Thoracic Society. Within the American Thoracic Society, Dr. Johnston has been a member of the Members in Transition and Training Committee, Membership Committee, Planning and Evaluation Committee, and Awards Committee and co-chaired the Ph.D. and Basic and Translational Scientist Working Group. In recognition of his contributions to the American Thoracic Society, Dr. Johnston was designated as an American Thoracic Society Fellow in 2018.
Finally, Dr. Johnston has been an ad hoc reviewer of manuscripts for a number of scientific journals (American Journal of Physiology−Lung Cellular and Molecular Physiology, American Journal of Respiratory and Critical Care Medicine, American Journal of Respiratory Cell and Molecular Biology, and Environmental Health Perspectives) and of grants for the National Institutes of Health, National Occupational Research Agenda, and Netherlands Asthma Foundation.
Graduate Program Affiliation: Cellular and Integrative Physiology
Obesity and Asthma
Obesity and asthma are monumental public health concerns in the United States (U.S.). Presently, over 40% of the U.S. population is obese. Asthma, a chronic lung disease characterized, in part, by cough, dyspnea, wheeze, persistent lung inflammation, and airway hyperresponsiveness, afflicts 25.1 million U.S. residents. Obesity is a major risk factor for the development of asthma. In addition, obesity worsens the severity of pre-existing asthma since obese asthmatics are less responsive to standard asthma medications (i.e., inhaled β2-agonists and corticosteroids). However, the mechanistic bases by which obesity increases the risk and severity of asthma are not well-understood, and understanding the molecular bases for these phenomena is a major focus of our laboratory’s research.
Regardless of the modality of obesity induction, we previously demonstrated that obese mice exhibit innate airway hyperresponsiveness. Furthermore, increases in airway responsiveness and lung inflammation are exacerbated in obese as compared to lean mice following exposure to atopic and non-atopic asthma stimuli. Thus, obese mice are useful tools to enhance our understanding of the mechanistic bases by which obesity increases the risk and severity of asthma.
Chronic systemic inflammation is a common sequela of obesity and is characterized by increases in circulating leukocytes and elevated serum levels of pro-inflammatory adipocytokines [acute-phase proteins (α1-antitrypsin, C-reactive protein, and plasminogen activator inhibitor-1), cytokines (IL-6, IL-8, MCP-1, and TNF-α), and hormones (leptin and resistin)]. We hypothesize that increases in circulating levels of pro-inflammatory adipocytokines in obesity prime the lung to be more susceptible to injury from atopic and non-atopic asthma stimuli. To that end, our laboratory uses neutralizing antibodies, recombinant proteins, genetically-altered mice, and mice with diet-induced obesity to identify adipocytokines that exacerbate increases in airway responsiveness and lung inflammation in obese mice. Identifying specific adipocytokines that enhance the aforementioned phenotypic features of asthma could lead to the development of new therapeutics to treat obese asthmatics who are often unresponsive to standard asthma therapies.
Occupational Exposure to Disinfectant Cleaners and Work-Related Asthma
Solutions of peracetic acid, an organic oxidant, are commonly used as disinfectant cleaners in healthcare facilities because they efficaciously inactivate fungi, gram-positive and gram-negative bacteria, and viruses. Phenotypic features of asthma, including airway hyperresponsiveness, dyspnea, and wheeze are associated with occupational exposure to disinfectant cleaning solutions containing peracetic acid. Incident cases of work-related asthma or exacerbations of pre-existing asthma are also commonly observed in healthcare workers who use disinfectants and sanitizers, including those containing peracetic acid.
Currently, no animal model of disinfectant cleaner-induced work-related asthma exists to unearth host factors (genetics and sex), dose- and time-response relationships, or biological mechanisms contributing to this form of work-related asthma. Therefore, the second major focus of our research is to develop and characterize an occupationally-relevant mouse model of work-related asthma induced by acute or subchronic inhalation exposure to vapor arising from a solution of peracetic acid. The data gathered from this research could be used in epidemiological or risk assessment studies in human cohorts, and, thus, would aid in the establishment of exposure limits for peracetic acid and the identification of workers particularly susceptible to the toxic effects of peracetic acid.
Animal Models and Experimental Techniques
By utilizing the subsequent animal models and experimental techniques, our laboratory is capable of integrating data from the level of a single molecule to that of an entire organism. However, this list is not exhaustive and new animal models and experimental techniques are added as the need arises.
Mouse Models of Obesity
a. Db/db mice
b. Cpefat mice
c. Ob/ob mice
d. Mice with diet-induced obesity
Mouse Models of Asthma
a. Atopic asthma (antigen sensitization and challenge)
b. Non-atopic asthma (acute inhalation exposure to ozone)
c. Work-related asthma (acute or subchronic inhalation exposure to peracetic acid)
a. Enzyme-linked immunosorbent assays
b. Western immunoblotting
a. Immunohistochemical staining
b. Confocal, electron, fluorescence, and light microscopy
a. Flow cytometry
a. Reverse transcription-quantitative real-time polymerase chain reactions
b. RNA sequencing
a. In vivo assessment of lung mechanics and airway responsiveness using the forced oscillation technique
b. In vivo assessment of breathing patterns using plethysmography