Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure

Background: Given the increasing prevalence of wildfires worldwide, understanding the effects of wildfire air pollutants on human health—particularly in specific immunologic pathways—is crucial. Exposure to air pollutants is associated with cardiorespiratory disease; however, immune and epithelial b...

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Main Authors: Juan Aguilera, MD, PhD, Abhinav Kaushik, PhD, Nicholas Cauwenberghs, PhD, Anja Heider, PhD, Ismail Ogulur, PhD, Duygu Yazici, PhD, Eric Smith, BS, Shifaa Alkotob, MD, Mary Prunicki, MD, PhD, Cezmi A. Akdis, MD, PhD, Kari C. Nadeau, MD, PhD
Format: Article
Language:English
Published: Elsevier 2023-05-01
Series:Journal of Allergy and Clinical Immunology: Global
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2772829323000188
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author Juan Aguilera, MD, PhD
Abhinav Kaushik, PhD
Nicholas Cauwenberghs, PhD
Anja Heider, PhD
Ismail Ogulur, PhD
Duygu Yazici, PhD
Eric Smith, BS
Shifaa Alkotob, MD
Mary Prunicki, MD, PhD
Cezmi A. Akdis, MD, PhD
Kari C. Nadeau, MD, PhD
author_facet Juan Aguilera, MD, PhD
Abhinav Kaushik, PhD
Nicholas Cauwenberghs, PhD
Anja Heider, PhD
Ismail Ogulur, PhD
Duygu Yazici, PhD
Eric Smith, BS
Shifaa Alkotob, MD
Mary Prunicki, MD, PhD
Cezmi A. Akdis, MD, PhD
Kari C. Nadeau, MD, PhD
author_sort Juan Aguilera, MD, PhD
collection DOAJ
description Background: Given the increasing prevalence of wildfires worldwide, understanding the effects of wildfire air pollutants on human health—particularly in specific immunologic pathways—is crucial. Exposure to air pollutants is associated with cardiorespiratory disease; however, immune and epithelial barrier alterations require further investigation. Objective: We sought to determine the impact of wildfire smoke exposure on the immune system and epithelial barriers by using proteomics and immune cell phenotyping. Methods: A San Francisco Bay area cohort (n = 15; age 30 ± 10 years) provided blood samples before (October 2019 to March 2020; air quality index = 37) and during (August 2020; air quality index = 80) a major wildfire. Exposure samples were collected 11 days (range, 10-12 days) after continuous exposure to wildfire smoke. We determined alterations in 506 proteins, including zonulin family peptide (ZFP); immune cell phenotypes by cytometry by time of flight (CyTOF); and their interrelationship using a correlation matrix. Results: Targeted proteomic analyses (n = 15) revealed a decrease of spondin-2 and an increase of granzymes A, B, and H, killer cell immunoglobulin-like receptor 3DL1, IL-16, nibrin, poly(ADP-ribose) polymerase 1, C1q TNF-related protein, fibroblast growth factor 19, and von Willebrand factor after 11 days’ average continuous exposure to smoke from a large wildfire (P < .05). We also observed a large correlation cluster between immune regulation pathways (IL-16, granzymes A, B, and H, and killer cell immunoglobulin-like receptor 3DL1), DNA repair [poly(ADP-ribose) 1, nibrin], and natural killer cells. We did not observe changes in ZFP levels suggesting a change in epithelial barriers. However, ZFP was associated with immune cell phenotypes (naive CD4+, TH2 cells). Conclusion: We observed functional changes in critical immune cells and their proteins during wildfire smoke exposure. Future studies in larger cohorts or in firefighters exposed to wildfire smoke should further assess immune changes and intervention targets.
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spelling doaj.art-5903970b643c49eb95590d1e220bede52023-05-13T04:26:10ZengElsevierJournal of Allergy and Clinical Immunology: Global2772-82932023-05-0122100093Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposureJuan Aguilera, MD, PhD0Abhinav Kaushik, PhD1Nicholas Cauwenberghs, PhD2Anja Heider, PhD3Ismail Ogulur, PhD4Duygu Yazici, PhD5Eric Smith, BS6Shifaa Alkotob, MD7Mary Prunicki, MD, PhD8Cezmi A. Akdis, MD, PhD9Kari C. Nadeau, MD, PhD10Center for Community Health Impact, University of Texas Health Science Center School of Public Health, El Paso, TexDepartment of Medicine, Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, CalifDepartment of Cardiovascular Sciences, Hypertension and Cardiovascular Epidemiology Research Unit, KU Leuven, Leuven, BelgiumSwiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, SwitzerlandSwiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, SwitzerlandSwiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, SwitzerlandDavid Geffen School of Medicine at University of California, Los Angeles, CalifIndiana University School of Medicine, Indianapolis, IndDepartment of Medicine, Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, CalifSwiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, Switzerland; Christine Kühne-Center for Allergy Research and Education (CK-CARE), Davos, SwitzerlandDepartment of Medicine, Sean N. Parker Center for Allergy and Asthma Research, Stanford University School of Medicine, Stanford, Calif; Department of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, Mass; Corresponding author: Kari C. Nadeau, MD, PhD, Department of Environmental Health, Harvard T. H. Chan School of Public Health, 655 Huntington Ave, Boston, MA 02115.Background: Given the increasing prevalence of wildfires worldwide, understanding the effects of wildfire air pollutants on human health—particularly in specific immunologic pathways—is crucial. Exposure to air pollutants is associated with cardiorespiratory disease; however, immune and epithelial barrier alterations require further investigation. Objective: We sought to determine the impact of wildfire smoke exposure on the immune system and epithelial barriers by using proteomics and immune cell phenotyping. Methods: A San Francisco Bay area cohort (n = 15; age 30 ± 10 years) provided blood samples before (October 2019 to March 2020; air quality index = 37) and during (August 2020; air quality index = 80) a major wildfire. Exposure samples were collected 11 days (range, 10-12 days) after continuous exposure to wildfire smoke. We determined alterations in 506 proteins, including zonulin family peptide (ZFP); immune cell phenotypes by cytometry by time of flight (CyTOF); and their interrelationship using a correlation matrix. Results: Targeted proteomic analyses (n = 15) revealed a decrease of spondin-2 and an increase of granzymes A, B, and H, killer cell immunoglobulin-like receptor 3DL1, IL-16, nibrin, poly(ADP-ribose) polymerase 1, C1q TNF-related protein, fibroblast growth factor 19, and von Willebrand factor after 11 days’ average continuous exposure to smoke from a large wildfire (P < .05). We also observed a large correlation cluster between immune regulation pathways (IL-16, granzymes A, B, and H, and killer cell immunoglobulin-like receptor 3DL1), DNA repair [poly(ADP-ribose) 1, nibrin], and natural killer cells. We did not observe changes in ZFP levels suggesting a change in epithelial barriers. However, ZFP was associated with immune cell phenotypes (naive CD4+, TH2 cells). Conclusion: We observed functional changes in critical immune cells and their proteins during wildfire smoke exposure. Future studies in larger cohorts or in firefighters exposed to wildfire smoke should further assess immune changes and intervention targets.http://www.sciencedirect.com/science/article/pii/S2772829323000188Wildfire exposureair pollutionproteomicsimmune cellsmass cytometryzonulin
spellingShingle Juan Aguilera, MD, PhD
Abhinav Kaushik, PhD
Nicholas Cauwenberghs, PhD
Anja Heider, PhD
Ismail Ogulur, PhD
Duygu Yazici, PhD
Eric Smith, BS
Shifaa Alkotob, MD
Mary Prunicki, MD, PhD
Cezmi A. Akdis, MD, PhD
Kari C. Nadeau, MD, PhD
Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure
Journal of Allergy and Clinical Immunology: Global
Wildfire exposure
air pollution
proteomics
immune cells
mass cytometry
zonulin
title Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure
title_full Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure
title_fullStr Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure
title_full_unstemmed Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure
title_short Granzymes, IL-16, and poly(ADP-ribose) polymerase 1 increase during wildfire smoke exposure
title_sort granzymes il 16 and poly adp ribose polymerase 1 increase during wildfire smoke exposure
topic Wildfire exposure
air pollution
proteomics
immune cells
mass cytometry
zonulin
url http://www.sciencedirect.com/science/article/pii/S2772829323000188
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