Jocelyn M Biagini1, John W Kroner2, Asel Baatyrbek Kyzy2, Alexandra Gonzales2, Hua He3, Mariana Stevens2, Brittany Grashel2, Daniel Spagna2, Samuel Paul2, Rahul Patel2, Angelo Bucci2, Michael G Sherenian1, Liza Bronner Murrison1, Lisa J Martin4, Gurjit K Khurana Hershey5. 1. Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio. 2. Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 3. Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. 4. Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio. 5. Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: gurjit.hershey@cchmc.org.
Abstract
BACKGROUND: The atopic march has been studied mostly in White populations, biasing our current paradigms. OBJECTIVE: We sought to define the atopic march in Black and White children and explore mechanisms for racial differences. METHODS: Utilizing the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort (n = 601), we assessed longitudinal sensitization, food allergy (FA), allergic rhinitis, risk of asthma development (through the Pediatric Asthma Risk Score), Scoring for Atopic Dermatitis (SCORAD), transepidermal water loss, skin filaggrin (FLG) expression, exposures, and genetic heritability to define AD progression endotypes in Black and White children. RESULTS: White MPAACH children were more likely to be sensitized to aero and food allergens (P = .0001) and over 3 times more likely to develop FA and/or allergic rhinitis (AR) without asthma risk (P < .0001). In contrast, Black children were over 6 times more likely to proceed to high asthma risk without FA, sensitization, or AR (P < .0001). White children had higher lesional and nonlesional transepidermal water loss (both P < .001) as well as decreased nonlesional keratinocyte FLG expression (P = .02). Black children had increased genetic heritability for asthma risk and higher rates of exposures to secondhand smoke and traffic-related air pollution. CONCLUSIONS: Black and White children with AD have distinct allergic trajectories defined by different longitudinal endotypes. Black children exhibit higher asthma risk despite a more intact skin barrier and less sensitization, FA, and AR. White children have less asthma risk, despite a more dysfunctional skin barrier, and more FA, AR, and sensitization. The observed racial differences are likely due in part to increased genetic heritability for asthma risk and harmful environmental exposures in Black children. Collectively, our findings provide a new paradigm for an atopic march that is inclusive of Black children.
BACKGROUND: The atopic march has been studied mostly in White populations, biasing our current paradigms. OBJECTIVE: We sought to define the atopic march in Black and White children and explore mechanisms for racial differences. METHODS: Utilizing the Mechanisms of Progression of Atopic Dermatitis to Asthma in Children (MPAACH) cohort (n = 601), we assessed longitudinal sensitization, food allergy (FA), allergic rhinitis, risk of asthma development (through the Pediatric Asthma Risk Score), Scoring for Atopic Dermatitis (SCORAD), transepidermal water loss, skin filaggrin (FLG) expression, exposures, and genetic heritability to define AD progression endotypes in Black and White children. RESULTS: White MPAACH children were more likely to be sensitized to aero and food allergens (P = .0001) and over 3 times more likely to develop FA and/or allergic rhinitis (AR) without asthma risk (P < .0001). In contrast, Black children were over 6 times more likely to proceed to high asthma risk without FA, sensitization, or AR (P < .0001). White children had higher lesional and nonlesional transepidermal water loss (both P < .001) as well as decreased nonlesional keratinocyte FLG expression (P = .02). Black children had increased genetic heritability for asthma risk and higher rates of exposures to secondhand smoke and traffic-related air pollution. CONCLUSIONS: Black and White children with AD have distinct allergic trajectories defined by different longitudinal endotypes. Black children exhibit higher asthma risk despite a more intact skin barrier and less sensitization, FA, and AR. White children have less asthma risk, despite a more dysfunctional skin barrier, and more FA, AR, and sensitization. The observed racial differences are likely due in part to increased genetic heritability for asthma risk and harmful environmental exposures in Black children. Collectively, our findings provide a new paradigm for an atopic march that is inclusive of Black children.
Authors: A R Sitarik; S Havstad; A M Levin; S V Lynch; K E Fujimura; D R Ownby; C C Johnson; G Wegienka Journal: Indoor Air Date: 2018-03-13 Impact factor: 5.770
Authors: Wendy F Davidson; Donald Y M Leung; Lisa A Beck; Cecilia M Berin; Mark Boguniewicz; William W Busse; Talal A Chatila; Raif S Geha; James E Gern; Emma Guttman-Yassky; Alan D Irvine; Brian S Kim; Heidi H Kong; Gideon Lack; Kari C Nadeau; Julie Schwaninger; Angela Simpson; Eric L Simpson; Jonathan M Spergel; Alkis Togias; Ulrich Wahn; Robert A Wood; Judith A Woodfolk; Steven F Ziegler; Marshall Plaut Journal: J Allergy Clin Immunol Date: 2019-01-09 Impact factor: 10.793
Authors: Jocelyn M Biagini Myers; Michael G Sherenian; Asel Baatyrbek Kyzy; Rosario Alarcon; Amen An; Zachary Flege; David Morgan; Tammy Gonzalez; Mariana L Stevens; Hua He; John W Kroner; Daniel Spagna; Brittany Grashel; Lisa J Martin; Andrew B Herr; Gurjit K Khurana Hershey Journal: J Allergy Clin Immunol Pract Date: 2020-04-14
Authors: Maxwell M Tran; Diana L Lefebvre; Christoffer Dharma; David Dai; Wendy Y W Lou; Padmaja Subbarao; Allan B Becker; Piush J Mandhane; Stuart E Turvey; Malcolm R Sears Journal: J Allergy Clin Immunol Date: 2017-11-15 Impact factor: 10.793
Authors: Vincent Ojwang; Bright I Nwaru; Hanna-Mari Takkinen; Minna Kaila; Onni Niemelä; Anna-Maija Haapala; Jorma Ilonen; Jorma Toppari; Heikki Hyöty; Riitta Veijola; Mikael Knip; Suvi M Virtanen Journal: Pediatr Allergy Immunol Date: 2020-01-11 Impact factor: 6.377
Authors: Danielle C M Belgrave; Raquel Granell; Angela Simpson; John Guiver; Christopher Bishop; Iain Buchan; A John Henderson; Adnan Custovic Journal: PLoS Med Date: 2014-10-21 Impact factor: 11.069
Authors: Elisabet Johansson; Jocelyn M Biagini; Lisa J Martin; Hua He; John W Kroner; Cassandra Almasri; Veronica Velasquez; Maud Sonzogni; Stanley B DeVore; Daniel Spagna; Brittany Grashel; Gurjit K Khurana Hershey Journal: Ann Allergy Asthma Immunol Date: 2022-01-23 Impact factor: 6.248