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  • Immunologic effects of forest fire exposure show increases in IL-1β and CRP. Allergy Prunicki, M. M., Dant, C. C., Cao, S., Maecker, H., Haddad, F., Kim, J. B., Snyder, M., Wu, J., Nadeau, K. 2020

    View details for DOI 10.1111/all.14251

    View details for PubMedID 32112439

  • Immunology of COVID-19: mechanisms, clinical outcome, diagnostics and perspectives - a report of the European Academy of Allergy and Clinical Immunology (EAACI). Allergy Sokolowska, M., Lukasik, Z., Agache, I., Akdis, C. A., Akdis, D., Akdis, M., Barcik, W., Brough, H., Eiwegger, T., Eliaszewicz, A., Eyerich, S., Feleszko, W., Gomez Casado, C., Hoffmann-Sommergruber, K., Janda, J., Jiménez-Saiz, R., Jutel, M., Knol, E., Kortekaas Krohn, I., Kothari, A., Makowska, J., Moniuszko, M., Morita, H., O'Mahony, L., Nadeau, K., Ozdemir, C., Pali-Schöll, I., Palomares, O., Papaleo, F., Prunicki, M., Schmidt-Weber, C. B., Sediva, A., Schwarze, J., Shamji, M. H., Tramper-Stranders, G., van, W., Untersmayr, E. 2020

    Abstract

    With the worldwide spread of the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) resulting in declaration of a pandemic by the World Health Organization (WHO) on March 11, 2020, the SARS-CoV-2-induced Coronavirus disease-19 (COVID-19) has become one of the main challenges of our times. The high infection rate and the severe disease course led to major safety and social restriction measures worldwide. There is an urgent need of unbiased expert knowledge guiding the development of efficient treatment and prevention strategies. This report summarizes current immunological data on mechanisms associated with the SARS-CoV-2 infection and COVID-19 development and progression to the most severe forms. We characterize the differences between adequate innate and adaptive immune response in mild disease and the deep immune dysfunction in the severe multi-organ disease. The similarities of the human immune response to SARS-CoV-2 and the SARS-CoV and MERS-CoV are underlined. We also summarize known and potential SARS-CoV-2 receptors on epithelial barriers, immune cells, endothelium and clinically involved organs such as lung, gut, kidney, cardiovascular and neuronal system. Finally, we discuss the known and potential mechanisms underlying the involvement of comorbidities, gender and age in development of COVID-19. Consequently, we highlight the knowledge gaps and urgent research requirements to provide a quick roadmap for ongoing and needed COVID-19 studies.

    View details for DOI 10.1111/all.14462

    View details for PubMedID 32584441

  • The impact of prescribed fire versus wildfire on the immune and cardiovascular systems of children ALLERGY Prunicki, M., Kelsey, R., Lee, J., Zhou, X., Smith, E., Haddad, F., Wu, J., Nadeau, K. 2019; 74 (10): 1989–91

    View details for DOI 10.1111/all.13825

    View details for Web of Science ID 000493013400015

  • Pollution-Associated Exposure Signature in Teenagers Haddad, F., Cauwenberghs, N., Movassagh, H., Maecker, H., Arthur, J., Wu, J., Nadeau, K., Prunicki, M. MOSBY-ELSEVIER. 2020: AB82
  • Mass Cytometry Reveals Monocytes are Associated with Air Pollution and Blood Pressure in Minority Children Prunicki, M., Nadeau, K., Lee, J., Zhou, X., Movassagh, H., Wu, J. MOSBY-ELSEVIER. 2020: AB128
  • Cumulative Lifetime Burden of Cardiovascular Disease From Early Exposure to Air Pollution. Journal of the American Heart Association Kim, J. B., Prunicki, M., Haddad, F., Dant, C., Sampath, V., Patel, R., Smith, E., Akdis, C., Balmes, J., Snyder, M. P., Wu, J. C., Nadeau, K. C. 2020; 9 (6): e014944

    Abstract

    The disease burden associated with air pollution continues to grow. The World Health Organization (WHO) estimates ≈7 million people worldwide die yearly from exposure to polluted air, half of which-3.3 million-are attributable to cardiovascular disease (CVD), greater than from major modifiable CVD risks including smoking, hypertension, hyperlipidemia, and diabetes mellitus. This serious and growing health threat is attributed to increasing urbanization of the world's populations with consequent exposure to polluted air. Especially vulnerable are the elderly, patients with pre-existing CVD, and children. The cumulative lifetime burden in children is particularly of concern because their rapidly developing cardiopulmonary systems are more susceptible to damage and they spend more time outdoors and therefore inhale more pollutants. World Health Organization estimates that 93% of the world's children aged <15 years-1.8 billion children-breathe air that puts their health and development at risk. Here, we present growing scientific evidence, including from our own group, that chronic exposure to air pollution early in life is directly linked to development of major CVD risks, including obesity, hypertension, and metabolic disorders. In this review, we surveyed the literature for current knowledge of how pollution exposure early in life adversely impacts cardiovascular phenotypes, and lay the foundation for early intervention and other strategies that can help prevent this damage. We also discuss the need for better guidelines and additional research to validate exposure metrics and interventions that will ultimately help healthcare providers reduce the growing burden of CVD from pollution.

    View details for DOI 10.1161/JAHA.119.014944

    View details for PubMedID 32174249

  • High dimensional immune biomarkers demonstrate differences in phenotypes and endotypes in food allergy and asthma. Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology Chinthrajah, R. S., Purington, N., Sampath, V., Andorf, S., Manohar, M., Prunicki, M., Zhou, X., Tupa, D., Nadeau, K. C. 2018

    View details for PubMedID 29705381

  • Exposure to NO2, CO, and PM2.5 is linked to regional DNA methylation differences in asthma CLINICAL EPIGENETICS Prunicki, M., Stell, L., Dinakarpandian, D., de Planell-Saguer, M., Lucas, R. W., Hammond, S., Balmes, J. R., Zhou, X., Paglino, T., Sabatti, C., Miller, R. L., Nadeau, K. C. 2018; 10: 2

    Abstract

    DNA methylation of CpG sites on genetic loci has been linked to increased risk of asthma in children exposed to elevated ambient air pollutants (AAPs). Further identification of specific CpG sites and the pollutants that are associated with methylation of these CpG sites in immune cells could impact our understanding of asthma pathophysiology. In this study, we sought to identify some CpG sites in specific genes that could be associated with asthma regulation (Foxp3 and IL10) and to identify the different AAPs for which exposure prior to the blood draw is linked to methylation levels at these sites. We recruited subjects from Fresno, California, an area known for high levels of AAPs. Blood samples and responses to questionnaires were obtained (n = 188), and in a subset of subjects (n = 33), repeat samples were collected 2 years later. Average measures of AAPs were obtained for 1, 15, 30, 90, 180, and 365 days prior to each blood draw to estimate the short-term vs. long-term effects of the AAP exposures.Asthma was significantly associated with higher differentially methylated regions (DMRs) of the Foxp3 promoter region (p = 0.030) and the IL10 intronic region (p = 0.026). Additionally, at the 90-day time period (90 days prior to the blood draw), Foxp3 methylation was positively associated with NO2, CO, and PM2.5 exposures (p = 0.001, p = 0.001, and p = 0.012, respectively). In the subset of subjects retested 2 years later (n = 33), a positive association between AAP exposure and methylation was sustained. There was also a negative correlation between the average Foxp3 methylation of the promoter region and activated Treg levels (p = 0.039) and a positive correlation between the average IL10 methylation of region 3 of intron 4 and IL10 cytokine expression (p = 0.030).Short-term and long-term exposures to high levels of CO, NO2, and PM2.5 were associated with alterations in differentially methylated regions of Foxp3. IL10 methylation showed a similar trend. For any given individual, these changes tend to be sustained over time. In addition, asthma was associated with higher differentially methylated regions of Foxp3 and IL10.

    View details for PubMedID 29317916

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