A Novel Nonhuman Primate Model of Nonatopic Asthma

Royer, Christopher M.; Miller, Lisa; Haczku, Angela Franciska

doi:10.1007/978-1-0716-2364-0_6

Cited by 2 publications

(2 citation statements)

References 34 publications

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“…Experimental O 3 exposure was shown to induce significant airway inflammation and hyperreactivity in mouse models of asthma [62][63][64][65][66][67][68][69][70][71][72][73][74][75], asthmatic rhesus macaques [76][77][78][79], healthy human subjects [80][81][82][83], and patients with asthma and COPD [20,[84][85][86][87][88][89][90]. Urban O 3 concentrations steadily declined in the Eastern USA in recent decades because of effective regulations limiting the release of its chemical precursors [91].…”

Section: Ozonementioning

confidence: 99%

“Air That Once Was Breath” Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation – “Climate Change, Allergy and Immunology” Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023

Bowman,

Schmidt,

Sanghar

et al. 2024

Int Arch Allergy Immunol

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Background: Wildfires are a global concern due to their wide-ranging environmental, economic, and public health impacts. Climate change contributes to an increase in the frequency and intensity of wildfires making smoke exposure a more significant and recurring health concern for individuals with airway diseases. Some of the most prominent effects of wildfire smoke exposure are asthma exacerbations and allergic airway sensitization. Likely due to the delayed recognition of its health impacts in comparison with cigarette smoke and industrial or traffic-related air pollution, research on the composition, the mechanisms of toxicity, and the cellular/molecular pathways involved is poor or non-existent. Summary: This review discusses potential underlying pathological mechanisms of wildfire-smoke-related allergic airway disease and asthma. We focused on major gaps in understanding the role of wildfire smoke composition in the development of airway disease and the known and potential mechanisms involving cellular and molecular players of oxidative injury at the epithelial barrier in airway inflammation. We examine how PM2.5, VOCs, O3, endotoxin, microbes, and toxic gases may affect oxidative stress and inflammation in the respiratory mucosal barrier. We discuss the role of AhR in mediating smoke’s effects in alarmin release and IL-17A production and how glucocorticoid responsiveness may be impaired by IL-17A-induced signaling and epigenetic changes leading to steroid-resistant severe airway inflammation. Key Message: Effective mitigation of wildfire-smoke-related respiratory health effects would require comprehensive research efforts aimed at a better understanding of the immune regulatory effects of wildfire smoke in respiratory health and disease.

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Section: Ozonementioning

confidence: 99%

“Air That Once Was Breath” Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation – “Climate Change, Allergy and Immunology” Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023

Bowman,

Schmidt,

Sanghar

et al. 2024

Int Arch Allergy Immunol

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“…[33][34][35] The degree to which vaccines or anti-viral therapeutics might protect the lung from viral injury in an NHP model could be assessed using this pulmonary physiology testing protocol. In addition, many other fields of pulmonary research using NHP or other animal models may benefit from this protocol including research in the fields of tuberculosis, 36 asthma, 37 and inhaled pollutants. 10…”

Section: Strengths and Limitationsmentioning

confidence: 99%

Testing pulmonary physiology in ventilated non‐human primates

Cervantes,

Berg,

Kapnadak

et al. 2024

J of Medical Primatology

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BackgroundAnimal models of respiratory viral infections are essential for investigating disease pathogenesis and the efficacy of antivirals and vaccine candidates. A major limitation in the research of respiratory diseases in animal models is correlating clinically relevant changes in pulmonary physiology with cellular and molecular mechanistic studies. Few animal models have captured and correlated physiologic changes in lung function and immune response within same experiment, which is critical given the heterogeneous nature of lung disease due to viral infections. In ventilated human patients, pulmonary physiology testing can be used to not only capture oxygenation, ventilation, but also pulmonary mechanics to yield quantitative measures of lung function and scalar tracings of flow‐volume and pressure‐volume loops. Application of this protocol during mechanical ventilation in non‐human (NHP) models would represent a major advance in respiratory viral disease research.MethodsWe have applied and optimized a human pulmonary physiology testing protocol to ventilated pigtail macaques (Macaca nemestrina) at baseline and 5 days after influenza A (IAV) viral inoculation.ResultsThe NHPs manifested clinical disease with hypothermia and loss of body weight. Declines in lung function were striking with a 66%–81% decline in P/F ratio, a measure of oxygenation reflecting the ratio of partial pressure of oxygen in arterial blood (PaO2) to the fraction of inspiratory oxygen concentration (FiO2). There was also a 16%–45% decline in lung compliance.ConclusionWe describe a new approach to performing pulmonary physiology testing protocol in non‐human primates to better capture quantitative correlates of respiratory disease and demonstrate protection by therapeutics and vaccines.

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A Novel Nonhuman Primate Model of Nonatopic Asthma

Cited by 2 publications

References 34 publications

“Air That Once Was Breath” Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation – “Climate Change, Allergy and Immunology” Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023

“Air That Once Was Breath” Part 1: Wildfire-Smoke-Induced Mechanisms of Airway Inflammation – “Climate Change, Allergy and Immunology” Special IAAI Article Collection: Collegium Internationale Allergologicum Update 2023

Testing pulmonary physiology in ventilated non‐human primates

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