Abstract
Background: Cockroach is one of the most important sources of indoor allergens and can lead to IgE sensitization and development of rhinitis and asthma. Objective: We sought to perform a cockroach allergen component analysis to determine the allergens and antibody levels and patterns of sensitization associated with asthma and rhinitis. Methods: Antibody (IgE, IgG, and IgG4) levels to total cockroach and 8 cockroach allergens were determined in 2 groups of cockroach-sensitized 10-year-old children with (n = 19) or without (n = 28) asthma and rhinitis. Allergen-specific antibody levels were measured in streptavidin ImmunoCAPs loaded with each of the recombinant allergens from groups 1, 2, 4, 5, 6, 7, 9, and 11, and total cockroach-specific IgE levels were measured with the i6 ImmunoCAP. Results: IgE antibody levels to cockroach allergens and extract, but not IgG or IgG4 antibody levels, differed between subjects with and without asthma and rhinitis. Specifically, recognition of more cockroach allergens with higher allergen-specific IgE levels was associated with disease. Variable patterns of sensitization with no immunodominant allergens were found in both groups. There was a good correlation between the sum of allergen-specific IgE and total cockroach IgE levels (r = 0.86, P <.001). Conclusions: Component analysis of 8 cockroach allergens revealed significant differences in IgE reactivity associated with the presence of asthma and rhinitis. Allergen-specific IgE titers and sensitization profiles were associated with asthma and rhinitis.
| Original language | English |
|---|---|
| Pages (from-to) | 935-944 |
| Number of pages | 10 |
| Journal | Journal of Allergy and Clinical Immunology |
| Volume | 144 |
| Issue number | 4 |
| DOIs | |
| State | Published - Oct 2019 |
Keywords
- Cockroach allergy
- asthma
- cockroach allergen components
- diagnosis
- immunotherapy
- rhinitis
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In: Journal of Allergy and Clinical Immunology, Vol. 144, No. 4, 10.2019, p. 935-944.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Cockroach allergen component analysis of children with or without asthma and rhinitis in an inner-city birth cohort
AU - National Institute of Allergy and Infectious Diseases–funded Inner-City Asthma Consortium
AU - Pomés, Anna
AU - Glesner, Jill
AU - Calatroni, Agustin
AU - Visness, Cindy M.
AU - Wood, Robert A.
AU - O'Connor, George T.
AU - Kattan, Meyer
AU - Bacharier, Leonard B.
AU - Wheatley, Lisa M.
AU - Gern, James E.
AU - Busse, William W.
AU - Gergen, P.
AU - Togias, A.
AU - Smartt, E.
AU - Thompson, K.
N1 - Funding Information: Supported by federal funds from the National Institute of Allergy and Infectious Diseases/National Institutes of Health (NIH) under contract numbers NO1-AI-25496, NO1-AI-25482, HHSN272200900052C, and HHSN272201000052I and cooperative agreements 1UM1AI114271-01 and UM2AI117870. Additional support was provided by the National Center for Research Resources/NIH under grants RR00052, M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, and 5UL1RR024992-02 and the National Center for the Advancement of Translational Research/NIH under grants UL1TR001079 and UL1TR000040. Research was also supported by the National Institute of Allergy and Infectious Diseases of the NIH under award number R01AI077653 (to A.P.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.Disclosure of potential conflict of interest: All authors, with the exception of L. M. Wheatley, report grants from the National Institutes of Health (NIH) during the conduct of study. A. Pomés reports personal fees for employment at Indoor Biotechnologies outside the submitted work. J. Glesner reports personal fees for employment at Indoor Biotechnologies outside the submitted work. R.A. Wood reports personal fees from the American Academy of Allergy, Asthma & Immunology (AAAAI) for board membership, Johns Hopkins University for employment, and UpToDate for royalties outside the submitted work. G. T. O'Connor reports grants from the NIH, a research grant from Janssen Pharmaceuticals, and personal fees for consulting from AstraZeneca outside the submitted work and reports money paid to his institution from HAL-Allergy, the NIH, DBV Technologies, Aimmune, and Astellas outside the submitted work. M. Kattan reports personal fees from Novartis Pharma and Regeneron for serving on advisory boards outside the submitted work. L. B. Bacharier reports personal fees from Aerocrine, GlaxoSmithKline, Genentech/Novartis, Teva, Boehringer Ingelheim, and AstraZeneca for consultancy outside the submitted work; personal fees from DBV Technologies for service on their Data Safety Monitoring Board, as well as from Merck, Sanofi/Regeneron, Vectura, and Circassia, for service on advisory boards outside the submitted work; and personal fees from WebMD/Medscape outside the submitted work. J. E. Gern reports personal fees from PREP Biopharm, Regeneron, MedImmune, Ena Pharmaceuticals, and Meissa Vaccines, as well as stock options with Meissa Vaccines, outside the submitted work and has a patent “Methods of Propagating Rhinovirus C in Previously Unsusceptible Cell Lines” issued and a patent “Adapted Rhinovirus C” pending. W. W. Busse reports personal fees from Boston Scientific for board membership and Elsevier for editorial services outside the submitted work and reports personal fees from Novartis, GlaxoSmithKline, Genentech, Sanofi/Genzyme, AstraZeneca, Teva, and Regeneron for consultancy outside the submitted work. The rest of the authors declare that they have no relevant conflicts of interest. The URECA study is a collaboration of the following institutions, investigators, and staff (principal investigators are indicated by an asterisk and the protocol chair is indicated by double asterisks): Johns Hopkins University, Baltimore, Maryland—R. Wood,* E. Matsui, H. Lederman, F. Witter, S. Leimenstoll, D. Scott, M. Cootauco, and P. Jones; Boston University School of Medicine, Boston, Massachusetts—G. O'Connor,* W. Cruikshank, M. Sandel, A. Lee-Parritz, C. Jordan, E. Gjerasi, P. Price-Johnson, L. Gagalis, L. Wang, N. Gonzalez, and M. Tuzova; Harvard Medical School, Boston, Massachusetts—D. Gold and R. Wright; Columbia University, New York, New York—M. Kattan,* C. Lamm, N. Whitney, P. Yaniv, and M. Pierce; Mount Sinai School of Medicine, New York, New York—H. Sampson, R. Sperling, and N. Rivers; Washington University School of Medicine, St Louis, Missouri—G. Bloomberg,* L. Bacharier,* Y. Sadovsky, E. Tesson, C. Koerkenmeier, R. Sharp, K. Ray, J. Durrange, I. Bauer, A. Freie, and V. Morgan; Statistical and Clinical Coordinating Center, Rho, Inc, Chapel Hill, North Carolina—C. Visness,* P. Zook, M. Yaeger, J. Martin, A. Calatroni, K. Jaffee, W. Taylor, R. Budrevich, and H. Mitchell; Scientific Coordination and Administrative Center, University of Wisconsin, Madison, Wisconsin—W. Busse,* J. Gern,** P. Heinritz, C. Sorkness, K. Hernandez, Y. Bochkov, K. Grindle, A. Dresen, T. Pappas, M. Renneberg, and B. Stoffel; and the National Institute of Allergy and Infectious Diseases, Bethesda, Maryland—P. Gergen, A. Togias, E. Smartt, and K. Thompson. Funding Information: Supported by federal funds from the National Institute of Allergy and Infectious Diseases/National Institutes of Health (NIH) under contract numbers NO1-AI-25496, NO1-AI-25482, HHSN272200900052C, and HHSN272201000052I and cooperative agreements 1UM1AI114271-01 and UM2AI117870. Additional support was provided by the National Center for Research Resources/NIH under grants RR00052, M01RR00533, 1UL1RR025771, M01RR00071, 1UL1RR024156, and 5UL1RR024992-02 and the National Center for the Advancement of Translational Research/NIH under grants UL1TR001079 and UL1TR000040. Research was also supported by the National Institute of Allergy and Infectious Diseases of the NIH under award number R01AI077653 (to A.P.). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.Disclosure of potential conflict of interest: All authors, with the exception of L. M. Wheatley, report grants from the National Institutes of Health (NIH) during the conduct of study. A. Pom?s reports personal fees for employment at Indoor Biotechnologies outside the submitted work. J. Glesner reports personal fees for employment at Indoor Biotechnologies outside the submitted work. R.A. Wood reports personal fees from the American Academy of Allergy, Asthma & Immunology (AAAAI) for board membership, Johns Hopkins University for employment, and UpToDate for royalties outside the submitted work. G. T. O'Connor reports grants from the NIH, a research grant from Janssen Pharmaceuticals, and personal fees for consulting from AstraZeneca outside the submitted work and reports money paid to his institution from HAL-Allergy, the NIH, DBV Technologies, Aimmune, and Astellas outside the submitted work. M. Kattan reports personal fees from Novartis Pharma and Regeneron for serving on advisory boards outside the submitted work. L. B. Bacharier reports personal fees from Aerocrine, GlaxoSmithKline, Genentech/Novartis, Teva, Boehringer Ingelheim, and AstraZeneca for consultancy outside the submitted work; personal fees from DBV Technologies for service on their Data Safety Monitoring Board, as well as from Merck, Sanofi/Regeneron, Vectura, and Circassia, for service on advisory boards outside the submitted work; and personal fees from WebMD/Medscape outside the submitted work. J. E. Gern reports personal fees from PREP Biopharm, Regeneron, MedImmune, Ena Pharmaceuticals, and Meissa Vaccines, as well as stock options with Meissa Vaccines, outside the submitted work and has a patent ?Methods of Propagating Rhinovirus C in Previously Unsusceptible Cell Lines? issued and a patent ?Adapted Rhinovirus C? pending. W. W. Busse reports personal fees from Boston Scientific for board membership and Elsevier for editorial services outside the submitted work and reports personal fees from Novartis, GlaxoSmithKline, Genentech, Sanofi/Genzyme, AstraZeneca, Teva, and Regeneron for consultancy outside the submitted work. The rest of the authors declare that they have no relevant conflicts of interest. Publisher Copyright: © 2019
PY - 2019/10
Y1 - 2019/10
N2 - Background: Cockroach is one of the most important sources of indoor allergens and can lead to IgE sensitization and development of rhinitis and asthma. Objective: We sought to perform a cockroach allergen component analysis to determine the allergens and antibody levels and patterns of sensitization associated with asthma and rhinitis. Methods: Antibody (IgE, IgG, and IgG4) levels to total cockroach and 8 cockroach allergens were determined in 2 groups of cockroach-sensitized 10-year-old children with (n = 19) or without (n = 28) asthma and rhinitis. Allergen-specific antibody levels were measured in streptavidin ImmunoCAPs loaded with each of the recombinant allergens from groups 1, 2, 4, 5, 6, 7, 9, and 11, and total cockroach-specific IgE levels were measured with the i6 ImmunoCAP. Results: IgE antibody levels to cockroach allergens and extract, but not IgG or IgG4 antibody levels, differed between subjects with and without asthma and rhinitis. Specifically, recognition of more cockroach allergens with higher allergen-specific IgE levels was associated with disease. Variable patterns of sensitization with no immunodominant allergens were found in both groups. There was a good correlation between the sum of allergen-specific IgE and total cockroach IgE levels (r = 0.86, P <.001). Conclusions: Component analysis of 8 cockroach allergens revealed significant differences in IgE reactivity associated with the presence of asthma and rhinitis. Allergen-specific IgE titers and sensitization profiles were associated with asthma and rhinitis.
AB - Background: Cockroach is one of the most important sources of indoor allergens and can lead to IgE sensitization and development of rhinitis and asthma. Objective: We sought to perform a cockroach allergen component analysis to determine the allergens and antibody levels and patterns of sensitization associated with asthma and rhinitis. Methods: Antibody (IgE, IgG, and IgG4) levels to total cockroach and 8 cockroach allergens were determined in 2 groups of cockroach-sensitized 10-year-old children with (n = 19) or without (n = 28) asthma and rhinitis. Allergen-specific antibody levels were measured in streptavidin ImmunoCAPs loaded with each of the recombinant allergens from groups 1, 2, 4, 5, 6, 7, 9, and 11, and total cockroach-specific IgE levels were measured with the i6 ImmunoCAP. Results: IgE antibody levels to cockroach allergens and extract, but not IgG or IgG4 antibody levels, differed between subjects with and without asthma and rhinitis. Specifically, recognition of more cockroach allergens with higher allergen-specific IgE levels was associated with disease. Variable patterns of sensitization with no immunodominant allergens were found in both groups. There was a good correlation between the sum of allergen-specific IgE and total cockroach IgE levels (r = 0.86, P <.001). Conclusions: Component analysis of 8 cockroach allergens revealed significant differences in IgE reactivity associated with the presence of asthma and rhinitis. Allergen-specific IgE titers and sensitization profiles were associated with asthma and rhinitis.
KW - Cockroach allergy
KW - asthma
KW - cockroach allergen components
KW - diagnosis
KW - immunotherapy
KW - rhinitis
UR - http://www.scopus.com/inward/record.url?scp=85068866594&partnerID=8YFLogxK
U2 - 10.1016/j.jaci.2019.05.036
DO - 10.1016/j.jaci.2019.05.036
M3 - Article
C2 - 31201891
AN - SCOPUS:85068866594
SN - 0091-6749
VL - 144
SP - 935
EP - 944
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 4
ER -