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Exposure to allergen and diesel exhaust particles potentiates secondary allergen-specific memory responses, promoting asthma susceptibility.
J Allergy Clin Immunol 2015; 136(2):295-303.e7JA

Abstract

BACKGROUND

Exposure to traffic pollution particulate matter, predominantly diesel exhaust particles (DEPs), increases the risk of asthma and asthma exacerbation; however, the underlying mechanisms remain poorly understood.

OBJECTIVE

We sought to examine the effect of DEP exposure on the generation and persistence of allergen-specific memory T cells in asthmatic patients and translate these findings by determining the effect of early DEP exposure on the prevalence of allergic asthma in children.

METHODS

The effect of DEPs on house dust mite (HDM)-specific memory responses was determined by using an asthma model. Data from children enrolled in the Cincinnati Childhood Allergy and Air Pollution Study birth cohort were analyzed to determine the effect of DEP exposure on asthma outcomes.

RESULTS

DEP coexposure with HDM resulted in persistent TH2/TH17 CD127(+) effector/memory cells in the lungs, spleen, and lymph nodes of adult and neonatal mice. After 7 weeks of rest, a single exposure to HDM resulted in airway hyperresponsiveness and increased TH2 cytokine levels in mice that had been previously exposed to both HDM and DEPs versus those exposed to HDM alone. On the basis of these data, we examined whether DEP exposure was similarly associated with increased asthma prevalence in children in the presence or absence of allergen exposure/sensitization in the Cincinnati Childhood Allergy and Air Pollution Study birth cohort. Early-life exposure to high DEP levels was associated with significantly increased asthma prevalence among allergic children but not among nonallergic children.

CONCLUSION

These findings suggest that DEP exposure results in accumulation of allergen-specific TH2/TH17 cells in the lungs, potentiating secondary allergen recall responses and promoting the development of allergic asthma.

Authors+Show Affiliations

Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Epidemiology and Biostatistics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio; Department of Environmental Health, University of Cincinnati, Cincinnati, Ohio.Department of Internal Medicine, University of Cincinnati, Cincinnati, Ohio.Department of Environmental Health, University of Cincinnati, Cincinnati, Ohio.Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio.Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, Cincinnati, Ohio. Electronic address: Gurjit.Hershey@cchmc.org.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

25748065

Citation

Brandt, Eric B., et al. "Exposure to Allergen and Diesel Exhaust Particles Potentiates Secondary Allergen-specific Memory Responses, Promoting Asthma Susceptibility." The Journal of Allergy and Clinical Immunology, vol. 136, no. 2, 2015, pp. 295-303.e7.
Brandt EB, Biagini Myers JM, Acciani TH, et al. Exposure to allergen and diesel exhaust particles potentiates secondary allergen-specific memory responses, promoting asthma susceptibility. J Allergy Clin Immunol. 2015;136(2):295-303.e7.
Brandt, E. B., Biagini Myers, J. M., Acciani, T. H., Ryan, P. H., Sivaprasad, U., Ruff, B., ... Khurana Hershey, G. K. (2015). Exposure to allergen and diesel exhaust particles potentiates secondary allergen-specific memory responses, promoting asthma susceptibility. The Journal of Allergy and Clinical Immunology, 136(2), pp. 295-303.e7. doi:10.1016/j.jaci.2014.11.043.
Brandt EB, et al. Exposure to Allergen and Diesel Exhaust Particles Potentiates Secondary Allergen-specific Memory Responses, Promoting Asthma Susceptibility. J Allergy Clin Immunol. 2015;136(2):295-303.e7. PubMed PMID: 25748065.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exposure to allergen and diesel exhaust particles potentiates secondary allergen-specific memory responses, promoting asthma susceptibility. AU - Brandt,Eric B, AU - Biagini Myers,Jocelyn M, AU - Acciani,Thomas H, AU - Ryan,Patrick H, AU - Sivaprasad,Umasundari, AU - Ruff,Brandy, AU - LeMasters,Grace K, AU - Bernstein,David I, AU - Lockey,James E, AU - LeCras,Timothy D, AU - Khurana Hershey,Gurjit K, Y1 - 2015/03/04/ PY - 2014/08/25/received PY - 2014/10/24/revised PY - 2014/11/04/accepted PY - 2015/3/10/entrez PY - 2015/3/10/pubmed PY - 2015/10/23/medline KW - Allergic asthma KW - children KW - diesel exhaust particle KW - house dust mite KW - memory KW - recall KW - traffic pollution SP - 295 EP - 303.e7 JF - The Journal of allergy and clinical immunology JO - J. Allergy Clin. Immunol. VL - 136 IS - 2 N2 - BACKGROUND: Exposure to traffic pollution particulate matter, predominantly diesel exhaust particles (DEPs), increases the risk of asthma and asthma exacerbation; however, the underlying mechanisms remain poorly understood. OBJECTIVE: We sought to examine the effect of DEP exposure on the generation and persistence of allergen-specific memory T cells in asthmatic patients and translate these findings by determining the effect of early DEP exposure on the prevalence of allergic asthma in children. METHODS: The effect of DEPs on house dust mite (HDM)-specific memory responses was determined by using an asthma model. Data from children enrolled in the Cincinnati Childhood Allergy and Air Pollution Study birth cohort were analyzed to determine the effect of DEP exposure on asthma outcomes. RESULTS: DEP coexposure with HDM resulted in persistent TH2/TH17 CD127(+) effector/memory cells in the lungs, spleen, and lymph nodes of adult and neonatal mice. After 7 weeks of rest, a single exposure to HDM resulted in airway hyperresponsiveness and increased TH2 cytokine levels in mice that had been previously exposed to both HDM and DEPs versus those exposed to HDM alone. On the basis of these data, we examined whether DEP exposure was similarly associated with increased asthma prevalence in children in the presence or absence of allergen exposure/sensitization in the Cincinnati Childhood Allergy and Air Pollution Study birth cohort. Early-life exposure to high DEP levels was associated with significantly increased asthma prevalence among allergic children but not among nonallergic children. CONCLUSION: These findings suggest that DEP exposure results in accumulation of allergen-specific TH2/TH17 cells in the lungs, potentiating secondary allergen recall responses and promoting the development of allergic asthma. SN - 1097-6825 UR - https://www.unboundmedicine.com/medline/citation/25748065/Exposure_to_allergen_and_diesel_exhaust_particles_potentiates_secondary_allergen_specific_memory_responses_promoting_asthma_susceptibility_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-6749(15)00094-9 DB - PRIME DP - Unbound Medicine ER -