“Where are they now?” Catching up with the 2017 AAAAI Faculty Development Awardees

Abstract

In 2017, an editorial in the Journal of Allergy and Clinical Immunology (JACI) introduced the 3 young investigators who received the American Academy of Allergy, Asthma & Immunology (AAAAI) Faculty Development Awards (Akdis CA and Ballas Z, 10.1016/j.jaci.2017.06.001). Fostering and promoting the development of our junior colleagues is one of JACI’s core missions. The 3 awardees (Drs Lora G. Bankova, Kirsten M. Kloepfer, and Timothy P. Moran) and their research projects were introduced to the Allergy/Immunology community so that we can all help in fostering the careers of our promising young colleagues.Academic growth does not happen in a vacuum, nor does it happen fast, and it requires constant nurturing. In that spirit, the editors thought that a 5-year period would be a good temporal milestone to check on the development of these awardees. We reached out to them, and they were gracious to write a synopsis to bring the community up to date on their progress. As one can see from the précis below, these young investigators are not only surviving but they are thriving. Seeing the amount of growth and contribution to the field in 5 short years, one can rest assured that the future of the specialty is in good hands.Lora g. bankovaMy current rank is Assistant Professor of Medicine at Harvard Medical School. As a basic science investigator, and clinician, in the Division of Allergy and Clinical Immunology, I concentrate on understanding how allergens and danger signals such as ATP are sensed by epithelial cells and how these signals are propagated in the mucosa. My goal is to improve the diagnosis and management of patients with allergic conditions associated with epithelial and mast cell activation and overproduction of cysteinyl leukotrienes. I spend most of my time in the laboratory performing and supervising experiments using mouse strains with targeted deletions or using human cells. A series of selected publications is listed later.1Ualiyeva S. Yoshimoto E. Barrett N.A. Bankova L.G. Isolation and quantitative evaluation of brush cells from mouse tracheas.J Vis Exp. 2019; : 10Google Scholar, 2Bankova L.G. Dwyer D.F. Yoshimoto E. Ualiyeva S. McGinty J.W. Raff H. et al.The cysteinyl leukotriene 3 receptor regulates expansion of IL-25-producing airway brush cells leading to type 2 inflammation.Sci Immunol. 2018; 3eaat9453Crossref PubMed Scopus (91) Google Scholar, 3Ualiyeva S. Hallen N. Kanaoka Y. Ledderose C. Matsumoto I. Junger W.G. et al.Airway brush cells generate cysteinyl leukotrienes through the ATP sensor P2Y2.Sci Immunol. 2020; 5eaax7224Crossref PubMed Scopus (44) Google Scholar, 4Ualiyeva S. Lemire E. Aviles E.C. Wong C. Boyd A.A. Lai J. et al.Tuft cell-produced cysteinyl leukotrienes and IL-25 synergistically initiate lung type 2 inflammation.Sci Immunol. 2021; 6eabj0474Crossref Scopus (15) Google Scholar, 5Ualiyeva S. Boyd A.A. Barrett N.A. Bankova L.G. Isolation of nasal brush cells for single-cell preparations.Bio Protoc. 2021; 11: e4163Crossref Scopus (2) Google ScholarWe found that the airway tuft (brush) cells, a unique population of highly innervated airway epithelial cells, are activated by the protease-containing mold aeroallergen Alternaria alternata and the house dust mite allergen Dermatophagoides pteronyssinus to generate cysteinyl leukotrienes. Furthermore, we defined a feed-forward loop of allergen (Alternaria)-triggered ATP release and ATP-mediated P2Y2 receptor activation that augments the aeroallergen-elicited generation of cysteinyl leukotrienes in tuft (brush) cells. Studies to define the receptor for allergens on tuft cells and the feed- forward loops leading to tuft cell activation are funded through a National Institute of Allergy and Infectious Diseases (NIAID) R21 mechanism.Cysteinyl leukotrienes are potent eicosanoid mediators of bronchoconstriction, vasodilatation, and type 2 inflammation classically associated with established allergic inflammation where they were classically assigned to leukocytes: sensitized mast cells, eosinophils, and macrophages. Our findings identified a role for cysteinyl leukotrienes in the innate response to aeroallergens as frontline immune response mediators. We identified 2 targets of tuft cell–derived cysteinyl leukotrienes—dendritic cells and innate type 2 lymphoid cells. We uncovered an unappreciated highly potent synergy between the 2 dominant tuft cell mediators—leukotriene C4 and IL-25—to activate these innate immune cells at subthreshold doses. Furthermore, deletion of Ltc4s, the enzyme required for cysteinyl leukotriene generation, in tuft cells leads to reduced type 2 systemic immune responses, especially when combined with antibody blockade of IL-25. These studies were funded by a National Institutes of Health (NIH) K08 award and the AAAAI Faculty Development Award.The AAAAI Faculty Development Award was essential to providing funding to set up my independent laboratory, to obtain data for the successful R21 application and a current R01 application.KIRSTEN M. kloepferThe AAAAI Foundation Faculty Development Award provided crucial financial support early in my career, allowing me to generate preliminary data, and successfully obtain a K23 Award from the NIAID to continue my project. During the past 5 years, I presented my findings at AAAAI and the American Thoracic Society and received the American Academy of Pediatrics Section of Allergy and Immunology Outstanding Abstract Award in 2018. A selection of published articles is listed later.1Kloepfer K.M. Sarsani V. Poroyko V. Lee W.M. Pappas T.E. Kang T. et al.Community acquired rhinovirus infection is associated with changes in the airway microbiome.J Allergy Clin Immunol. 2017; 140: 312-315.e8Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 2Kloepfer K.M. Deschamp A.R. Ross S.E. Peterson-Carmichael S.L. Hemmerich C.M. Rusch D.B. et al.In children, the microbiota of the nasopharynx and brochoalveolar lavage fluid are both similar and different.Pediatr Pulmonol. 2018; 53: 475-482Crossref PubMed Scopus (23) Google Scholar, 3Eapen A. Kloepfer K.M. Serum sickness-like reaction in a pediatric patient using omalizumab for chronic spontaneous urticaria.Pediatr Allergy Immunol. 2018; 29: 449-450Crossref Scopus (7) Google Scholar, 4Kloepfer K.M. Ross S.E. Hemmerich C.M. Slaven J.S. Rusch D.B. Davis S.D. Increased microbiota diversity associated with higher FEV0.5 in infants.Pediatr Pulmonol. 2020; 55: 27-29Crossref Scopus (1) Google Scholar, 5Altman M.C. Beigelman A. Ciaccio C. Gern J.E. Heymann P.W. Jackson D.J. et al.Evolving concepts in how viruses impact asthma.J Allergy Clin Immunol. 2020; 145: 1332-1344Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 6Huddleston C.M. Slaven J. Weist A.D. Krupp N.L. Kloepfer K.M. Increased healthcare use in patient with moderate-to-severe asthma due to frequent preferred medication changes.Ann Allergy Asthma Immunol. 2022; 129: 255-257Abstract Full Text Full Text PDF Scopus (1) Google Scholar These findings include changes in the oral microbiota in infants exposed to second-hand smoke; the association between decreased lung function at age 3 months and decreased microbial diversity in the upper airway; and lower lung function values during the first year of life in infants living in food deserts. In August 2021, we finished sequencing the nasal and oral samples prospectively obtained between birth and age 12 months from 180 infants. We are currently writing a manuscript that details the newborn upper airway microbiota within 48 hours of birth, its association with local cytokine production, and the differences observed between neonates with a maternal history of asthma versus neonates without a parental history of allergies, asthma, or atopic dermatitis. This will be followed by a second manuscript detailing the progression of the microbiota over the first year of life, and its association with pulmonary function at age 1, 3, and 12 months. These data will serve as preliminary data in my upcoming R21 and R01 grant submissions. On the basis of my success as a developing independent researcher, I was invited to serve as the site principal investigator for the NIH-funded Preventing Asthma in High-Risk Kids (PARK) study; and as a subinvestigator for the National Heart, Lung, and Blood Institute’s Precision Interventions for Severe and/or Exacerbation Prone Asthma (PrecISE) Network and on 2 P01 Awards investigating novel treatment methods for severe asthma.Outside of my time in research, I provide allergy expertise in the multidisciplinary Indiana University School of Medicine Pediatric High-Risk Asthma Clinic. I actively participate in the multicenter Pediatric Severe Asthma Consortium, an American Thoracic Society Interest Section. I am the Vice-Chair of the AAAAI committee Microbes in Allergy and Asthma, and the Vice-President of the Indiana Allergy and Immunology Society. I was promoted to Associate Professor with Tenure in July 2021.Timothy p. moranI am currently an Associate Professor in the Department of Pediatrics and a member of the Center for Environmental Medicine, Asthma and Lung Biology at the University of North Carolina School of Medicine. Since receiving the AAAAI Foundation Faculty Development Award in 2017, I have authored 14 peer-reviewed publications and numerous abstracts presented at AAAAI Annual Meetings and other scientific meetings.1Immormino R.M. Jania C.M. Tilley S.L. Moran T.P. Neuropilin-2 regulates airway inflammation in a neutrophilic asthma model.Immun Inflamm Dis. 2022; 10: e575Crossref Scopus (1) Google Scholar, 2Smeekens J.M. Immormino R.M. Balogh P.A. Randell S.H. Kulis M.D. Moran T.P. Indoor dust acts as an adjuvant to promote sensitization to peanut through the airway.Clin Exp Allergy. 2019; 49: 1500-1511Crossref PubMed Scopus (13) Google Scholar, 3Smeekens J.M. Immormino R.M. Kulis M.D. Moran T.P. Timing of exposure to environmental adjuvants is critical to mitigate peanut allergy.J Allergy Clin Immunol. 2021; 147: 387-390.e4Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar Support from the Faculty Development Award resulted in a successful application for a Mentored Clinical Scientist Development Award (K08) through the National Institute of Environmental Health Sciences (NIEHS) to investigate the role of neuropilin-2 in environmental lung disease. During this project, I found that neuropilin-2 expression by lung macrophages was an important negative regulator of airway inflammation associated with neutrophilic asthma. The AAAAI Foundation Faculty Development Award also provided the opportunity to develop new research collaborations to explore the role of the indoor environment in food allergy development. My colleagues and I have found that immunogenic factors (adjuvants) in house dust are important for inducing airway sensitization to environmental peanut and the development of peanut allergy in animal models. This work has resulted in my becoming the recipient of an NIEHS Outstanding New Environmental Scientist (ONES) Award. These R01 research grants are aimed at early-stage investigators who intend to make a long-term commitment to research in the environmental health sciences and assist them in launching an innovative research program focused on understanding how environmental exposures affect people’s health. The focus of this ONES award is to investigate the mechanisms by which environmental adjuvants present within the indoor exposome promote peanut allergy development in children. In 2017, an editorial in the Journal of Allergy and Clinical Immunology (JACI) introduced the 3 young investigators who received the American Academy of Allergy, Asthma & Immunology (AAAAI) Faculty Development Awards (Akdis CA and Ballas Z, 10.1016/j.jaci.2017.06.001). Fostering and promoting the development of our junior colleagues is one of JACI’s core missions. The 3 awardees (Drs Lora G. Bankova, Kirsten M. Kloepfer, and Timothy P. Moran) and their research projects were introduced to the Allergy/Immunology community so that we can all help in fostering the careers of our promising young colleagues. Academic growth does not happen in a vacuum, nor does it happen fast, and it requires constant nurturing. In that spirit, the editors thought that a 5-year period would be a good temporal milestone to check on the development of these awardees. We reached out to them, and they were gracious to write a synopsis to bring the community up to date on their progress. As one can see from the précis below, these young investigators are not only surviving but they are thriving. Seeing the amount of growth and contribution to the field in 5 short years, one can rest assured that the future of the specialty is in good hands. Lora g. bankovaMy current rank is Assistant Professor of Medicine at Harvard Medical School. As a basic science investigator, and clinician, in the Division of Allergy and Clinical Immunology, I concentrate on understanding how allergens and danger signals such as ATP are sensed by epithelial cells and how these signals are propagated in the mucosa. My goal is to improve the diagnosis and management of patients with allergic conditions associated with epithelial and mast cell activation and overproduction of cysteinyl leukotrienes. I spend most of my time in the laboratory performing and supervising experiments using mouse strains with targeted deletions or using human cells. A series of selected publications is listed later.1Ualiyeva S. Yoshimoto E. Barrett N.A. Bankova L.G. Isolation and quantitative evaluation of brush cells from mouse tracheas.J Vis Exp. 2019; : 10Google Scholar, 2Bankova L.G. Dwyer D.F. Yoshimoto E. Ualiyeva S. McGinty J.W. Raff H. et al.The cysteinyl leukotriene 3 receptor regulates expansion of IL-25-producing airway brush cells leading to type 2 inflammation.Sci Immunol. 2018; 3eaat9453Crossref PubMed Scopus (91) Google Scholar, 3Ualiyeva S. Hallen N. Kanaoka Y. Ledderose C. Matsumoto I. Junger W.G. et al.Airway brush cells generate cysteinyl leukotrienes through the ATP sensor P2Y2.Sci Immunol. 2020; 5eaax7224Crossref PubMed Scopus (44) Google Scholar, 4Ualiyeva S. Lemire E. Aviles E.C. Wong C. Boyd A.A. Lai J. et al.Tuft cell-produced cysteinyl leukotrienes and IL-25 synergistically initiate lung type 2 inflammation.Sci Immunol. 2021; 6eabj0474Crossref Scopus (15) Google Scholar, 5Ualiyeva S. Boyd A.A. Barrett N.A. Bankova L.G. Isolation of nasal brush cells for single-cell preparations.Bio Protoc. 2021; 11: e4163Crossref Scopus (2) Google ScholarWe found that the airway tuft (brush) cells, a unique population of highly innervated airway epithelial cells, are activated by the protease-containing mold aeroallergen Alternaria alternata and the house dust mite allergen Dermatophagoides pteronyssinus to generate cysteinyl leukotrienes. Furthermore, we defined a feed-forward loop of allergen (Alternaria)-triggered ATP release and ATP-mediated P2Y2 receptor activation that augments the aeroallergen-elicited generation of cysteinyl leukotrienes in tuft (brush) cells. Studies to define the receptor for allergens on tuft cells and the feed- forward loops leading to tuft cell activation are funded through a National Institute of Allergy and Infectious Diseases (NIAID) R21 mechanism.Cysteinyl leukotrienes are potent eicosanoid mediators of bronchoconstriction, vasodilatation, and type 2 inflammation classically associated with established allergic inflammation where they were classically assigned to leukocytes: sensitized mast cells, eosinophils, and macrophages. Our findings identified a role for cysteinyl leukotrienes in the innate response to aeroallergens as frontline immune response mediators. We identified 2 targets of tuft cell–derived cysteinyl leukotrienes—dendritic cells and innate type 2 lymphoid cells. We uncovered an unappreciated highly potent synergy between the 2 dominant tuft cell mediators—leukotriene C4 and IL-25—to activate these innate immune cells at subthreshold doses. Furthermore, deletion of Ltc4s, the enzyme required for cysteinyl leukotriene generation, in tuft cells leads to reduced type 2 systemic immune responses, especially when combined with antibody blockade of IL-25. These studies were funded by a National Institutes of Health (NIH) K08 award and the AAAAI Faculty Development Award.The AAAAI Faculty Development Award was essential to providing funding to set up my independent laboratory, to obtain data for the successful R21 application and a current R01 application. My current rank is Assistant Professor of Medicine at Harvard Medical School. As a basic science investigator, and clinician, in the Division of Allergy and Clinical Immunology, I concentrate on understanding how allergens and danger signals such as ATP are sensed by epithelial cells and how these signals are propagated in the mucosa. My goal is to improve the diagnosis and management of patients with allergic conditions associated with epithelial and mast cell activation and overproduction of cysteinyl leukotrienes. I spend most of my time in the laboratory performing and supervising experiments using mouse strains with targeted deletions or using human cells. A series of selected publications is listed later.1Ualiyeva S. Yoshimoto E. Barrett N.A. Bankova L.G. Isolation and quantitative evaluation of brush cells from mouse tracheas.J Vis Exp. 2019; : 10Google Scholar, 2Bankova L.G. Dwyer D.F. Yoshimoto E. Ualiyeva S. McGinty J.W. Raff H. et al.The cysteinyl leukotriene 3 receptor regulates expansion of IL-25-producing airway brush cells leading to type 2 inflammation.Sci Immunol. 2018; 3eaat9453Crossref PubMed Scopus (91) Google Scholar, 3Ualiyeva S. Hallen N. Kanaoka Y. Ledderose C. Matsumoto I. Junger W.G. et al.Airway brush cells generate cysteinyl leukotrienes through the ATP sensor P2Y2.Sci Immunol. 2020; 5eaax7224Crossref PubMed Scopus (44) Google Scholar, 4Ualiyeva S. Lemire E. Aviles E.C. Wong C. Boyd A.A. Lai J. et al.Tuft cell-produced cysteinyl leukotrienes and IL-25 synergistically initiate lung type 2 inflammation.Sci Immunol. 2021; 6eabj0474Crossref Scopus (15) Google Scholar, 5Ualiyeva S. Boyd A.A. Barrett N.A. Bankova L.G. Isolation of nasal brush cells for single-cell preparations.Bio Protoc. 2021; 11: e4163Crossref Scopus (2) Google Scholar We found that the airway tuft (brush) cells, a unique population of highly innervated airway epithelial cells, are activated by the protease-containing mold aeroallergen Alternaria alternata and the house dust mite allergen Dermatophagoides pteronyssinus to generate cysteinyl leukotrienes. Furthermore, we defined a feed-forward loop of allergen (Alternaria)-triggered ATP release and ATP-mediated P2Y2 receptor activation that augments the aeroallergen-elicited generation of cysteinyl leukotrienes in tuft (brush) cells. Studies to define the receptor for allergens on tuft cells and the feed- forward loops leading to tuft cell activation are funded through a National Institute of Allergy and Infectious Diseases (NIAID) R21 mechanism. Cysteinyl leukotrienes are potent eicosanoid mediators of bronchoconstriction, vasodilatation, and type 2 inflammation classically associated with established allergic inflammation where they were classically assigned to leukocytes: sensitized mast cells, eosinophils, and macrophages. Our findings identified a role for cysteinyl leukotrienes in the innate response to aeroallergens as frontline immune response mediators. We identified 2 targets of tuft cell–derived cysteinyl leukotrienes—dendritic cells and innate type 2 lymphoid cells. We uncovered an unappreciated highly potent synergy between the 2 dominant tuft cell mediators—leukotriene C4 and IL-25—to activate these innate immune cells at subthreshold doses. Furthermore, deletion of Ltc4s, the enzyme required for cysteinyl leukotriene generation, in tuft cells leads to reduced type 2 systemic immune responses, especially when combined with antibody blockade of IL-25. These studies were funded by a National Institutes of Health (NIH) K08 award and the AAAAI Faculty Development Award. The AAAAI Faculty Development Award was essential to providing funding to set up my independent laboratory, to obtain data for the successful R21 application and a current R01 application. KIRSTEN M. kloepferThe AAAAI Foundation Faculty Development Award provided crucial financial support early in my career, allowing me to generate preliminary data, and successfully obtain a K23 Award from the NIAID to continue my project. During the past 5 years, I presented my findings at AAAAI and the American Thoracic Society and received the American Academy of Pediatrics Section of Allergy and Immunology Outstanding Abstract Award in 2018. A selection of published articles is listed later.1Kloepfer K.M. Sarsani V. Poroyko V. Lee W.M. Pappas T.E. Kang T. et al.Community acquired rhinovirus infection is associated with changes in the airway microbiome.J Allergy Clin Immunol. 2017; 140: 312-315.e8Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 2Kloepfer K.M. Deschamp A.R. Ross S.E. Peterson-Carmichael S.L. Hemmerich C.M. Rusch D.B. et al.In children, the microbiota of the nasopharynx and brochoalveolar lavage fluid are both similar and different.Pediatr Pulmonol. 2018; 53: 475-482Crossref PubMed Scopus (23) Google Scholar, 3Eapen A. Kloepfer K.M. Serum sickness-like reaction in a pediatric patient using omalizumab for chronic spontaneous urticaria.Pediatr Allergy Immunol. 2018; 29: 449-450Crossref Scopus (7) Google Scholar, 4Kloepfer K.M. Ross S.E. Hemmerich C.M. Slaven J.S. Rusch D.B. Davis S.D. Increased microbiota diversity associated with higher FEV0.5 in infants.Pediatr Pulmonol. 2020; 55: 27-29Crossref Scopus (1) Google Scholar, 5Altman M.C. Beigelman A. Ciaccio C. Gern J.E. Heymann P.W. Jackson D.J. et al.Evolving concepts in how viruses impact asthma.J Allergy Clin Immunol. 2020; 145: 1332-1344Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 6Huddleston C.M. Slaven J. Weist A.D. Krupp N.L. Kloepfer K.M. Increased healthcare use in patient with moderate-to-severe asthma due to frequent preferred medication changes.Ann Allergy Asthma Immunol. 2022; 129: 255-257Abstract Full Text Full Text PDF Scopus (1) Google Scholar These findings include changes in the oral microbiota in infants exposed to second-hand smoke; the association between decreased lung function at age 3 months and decreased microbial diversity in the upper airway; and lower lung function values during the first year of life in infants living in food deserts. In August 2021, we finished sequencing the nasal and oral samples prospectively obtained between birth and age 12 months from 180 infants. We are currently writing a manuscript that details the newborn upper airway microbiota within 48 hours of birth, its association with local cytokine production, and the differences observed between neonates with a maternal history of asthma versus neonates without a parental history of allergies, asthma, or atopic dermatitis. This will be followed by a second manuscript detailing the progression of the microbiota over the first year of life, and its association with pulmonary function at age 1, 3, and 12 months. These data will serve as preliminary data in my upcoming R21 and R01 grant submissions. On the basis of my success as a developing independent researcher, I was invited to serve as the site principal investigator for the NIH-funded Preventing Asthma in High-Risk Kids (PARK) study; and as a subinvestigator for the National Heart, Lung, and Blood Institute’s Precision Interventions for Severe and/or Exacerbation Prone Asthma (PrecISE) Network and on 2 P01 Awards investigating novel treatment methods for severe asthma.Outside of my time in research, I provide allergy expertise in the multidisciplinary Indiana University School of Medicine Pediatric High-Risk Asthma Clinic. I actively participate in the multicenter Pediatric Severe Asthma Consortium, an American Thoracic Society Interest Section. I am the Vice-Chair of the AAAAI committee Microbes in Allergy and Asthma, and the Vice-President of the Indiana Allergy and Immunology Society. I was promoted to Associate Professor with Tenure in July 2021. The AAAAI Foundation Faculty Development Award provided crucial financial support early in my career, allowing me to generate preliminary data, and successfully obtain a K23 Award from the NIAID to continue my project. During the past 5 years, I presented my findings at AAAAI and the American Thoracic Society and received the American Academy of Pediatrics Section of Allergy and Immunology Outstanding Abstract Award in 2018. A selection of published articles is listed later.1Kloepfer K.M. Sarsani V. Poroyko V. Lee W.M. Pappas T.E. Kang T. et al.Community acquired rhinovirus infection is associated with changes in the airway microbiome.J Allergy Clin Immunol. 2017; 140: 312-315.e8Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 2Kloepfer K.M. Deschamp A.R. Ross S.E. Peterson-Carmichael S.L. Hemmerich C.M. Rusch D.B. et al.In children, the microbiota of the nasopharynx and brochoalveolar lavage fluid are both similar and different.Pediatr Pulmonol. 2018; 53: 475-482Crossref PubMed Scopus (23) Google Scholar, 3Eapen A. Kloepfer K.M. Serum sickness-like reaction in a pediatric patient using omalizumab for chronic spontaneous urticaria.Pediatr Allergy Immunol. 2018; 29: 449-450Crossref Scopus (7) Google Scholar, 4Kloepfer K.M. Ross S.E. Hemmerich C.M. Slaven J.S. Rusch D.B. Davis S.D. Increased microbiota diversity associated with higher FEV0.5 in infants.Pediatr Pulmonol. 2020; 55: 27-29Crossref Scopus (1) Google Scholar, 5Altman M.C. Beigelman A. Ciaccio C. Gern J.E. Heymann P.W. Jackson D.J. et al.Evolving concepts in how viruses impact asthma.J Allergy Clin Immunol. 2020; 145: 1332-1344Abstract Full Text Full Text PDF PubMed Scopus (21) Google Scholar, 6Huddleston C.M. Slaven J. Weist A.D. Krupp N.L. Kloepfer K.M. Increased healthcare use in patient with moderate-to-severe asthma due to frequent preferred medication changes.Ann Allergy Asthma Immunol. 2022; 129: 255-257Abstract Full Text Full Text PDF Scopus (1) Google Scholar These findings include changes in the oral microbiota in infants exposed to second-hand smoke; the association between decreased lung function at age 3 months and decreased microbial diversity in the upper airway; and lower lung function values during the first year of life in infants living in food deserts. In August 2021, we finished sequencing the nasal and oral samples prospectively obtained between birth and age 12 months from 180 infants. We are currently writing a manuscript that details the newborn upper airway microbiota within 48 hours of birth, its association with local cytokine production, and the differences observed between neonates with a maternal history of asthma versus neonates without a parental history of allergies, asthma, or atopic dermatitis. This will be followed by a second manuscript detailing the progression of the microbiota over the first year of life, and its association with pulmonary function at age 1, 3, and 12 months. These data will serve as preliminary data in my upcoming R21 and R01 grant submissions. On the basis of my success as a developing independent researcher, I was invited to serve as the site principal investigator for the NIH-funded Preventing Asthma in High-Risk Kids (PARK) study; and as a subinvestigator for the National Heart, Lung, and Blood Institute’s Precision Interventions for Severe and/or Exacerbation Prone Asthma (PrecISE) Network and on 2 P01 Awards investigating novel treatment methods for severe asthma. Outside of my time in research, I provide allergy expertise in the multidisciplinary Indiana University School of Medicine Pediatric High-Risk Asthma Clinic. I actively participate in the multicenter Pediatric Severe Asthma Consortium, an American Thoracic Society Interest Section. I am the Vice-Chair of the AAAAI committee Microbes in Allergy and Asthma, and the Vice-President of the Indiana Allergy and Immunology Society. I was promoted to Associate Professor with Tenure in July 2021. Timothy p. moranI am currently an Associate Professor in the Department of Pediatrics and a member of the Center for Environmental Medicine, Asthma and Lung Biology at the University of North Carolina School of Medicine. Since receiving the AAAAI Foundation Faculty Development Award in 2017, I have authored 14 peer-reviewed publications and numerous abstracts presented at AAAAI Annual Meetings and other scientific meetings.1Immormino R.M. Jania C.M. Tilley S.L. Moran T.P. Neuropilin-2 regulates airway inflammation in a neutrophilic asthma model.Immun Inflamm Dis. 2022; 10: e575Crossref Scopus (1) Google Scholar, 2Smeekens J.M. Immormino R.M. Balogh P.A. Randell S.H. Kulis M.D. Moran T.P. Indoor dust acts as an adjuvant to promote sensitization to peanut through the airway.Clin Exp Allergy. 2019; 49: 1500-1511Crossref PubMed Scopus (13) Google Scholar, 3Smeekens J.M. Immormino R.M. Kulis M.D. Moran T.P. Timing of exposure to environmental adjuvants is critical to mitigate peanut allergy.J Allergy Clin Immunol. 2021; 147: 387-390.e4Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar Support from the Faculty Development Award resulted in a successful application for a Mentored Clinical Scientist Development Award (K08) through the National Institute of Environmental Health Sciences (NIEHS) to investigate the role of neuropilin-2 in environmental lung disease. During this project, I found that neuropilin-2 expression by lung macrophages was an important negative regulator of airway inflammation associated with neutrophilic asthma. The AAAAI Foundation Faculty Development Award also provided the opportunity to develop new research collaborations to explore the role of the indoor environment in food allergy development. My colleagues and I have found that immunogenic factors (adjuvants) in house dust are important for inducing airway sensitization to environmental peanut and the development of peanut allergy in animal models. This work has resulted in my becoming the recipient of an NIEHS Outstanding New Environmental Scientist (ONES) Award. These R01 research grants are aimed at early-stage investigators who intend to make a long-term commitment to research in the environmental health sciences and assist them in launching an innovative research program focused on understanding how environmental exposures affect people’s health. The focus of this ONES award is to investigate the mechanisms by which environmental adjuvants present within the indoor exposome promote peanut allergy development in children. I am currently an Associate Professor in the Department of Pediatrics and a member of the Center for Environmental Medicine, Asthma and Lung Biology at the University of North Carolina School of Medicine. Since receiving the AAAAI Foundation Faculty Development Award in 2017, I have authored 14 peer-reviewed publications and numerous abstracts presented at AAAAI Annual Meetings and other scientific meetings.1Immormino R.M. Jania C.M. Tilley S.L. Moran T.P. Neuropilin-2 regulates airway inflammation in a neutrophilic asthma model.Immun Inflamm Dis. 2022; 10: e575Crossref Scopus (1) Google Scholar, 2Smeekens J.M. Immormino R.M. Balogh P.A. Randell S.H. Kulis M.D. Moran T.P. Indoor dust acts as an adjuvant to promote sensitization to peanut through the airway.Clin Exp Allergy. 2019; 49: 1500-1511Crossref PubMed Scopus (13) Google Scholar, 3Smeekens J.M. Immormino R.M. Kulis M.D. Moran T.P. Timing of exposure to environmental adjuvants is critical to mitigate peanut allergy.J Allergy Clin Immunol. 2021; 147: 387-390.e4Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar Support from the Faculty Development Award resulted in a successful application for a Mentored Clinical Scientist Development Award (K08) through the National Institute of Environmental Health Sciences (NIEHS) to investigate the role of neuropilin-2 in environmental lung disease. During this project, I found that neuropilin-2 expression by lung macrophages was an important negative regulator of airway inflammation associated with neutrophilic asthma. The AAAAI Foundation Faculty Development Award also provided the opportunity to develop new research collaborations to explore the role of the indoor environment in food allergy development. My colleagues and I have found that immunogenic factors (adjuvants) in house dust are important for inducing airway sensitization to environmental peanut and the development of peanut allergy in animal models. This work has resulted in my becoming the recipient of an NIEHS Outstanding New Environmental Scientist (ONES) Award. These R01 research grants are aimed at early-stage investigators who intend to make a long-term commitment to research in the environmental health sciences and assist them in launching an innovative research program focused on understanding how environmental exposures affect people’s health. The focus of this ONES award is to investigate the mechanisms by which environmental adjuvants present within the indoor exposome promote peanut allergy development in children.