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Title: Inactivation of common airborne antigens by perfluoroalkyl chemicals modulates early life allergic asthma
Authors: Wang, Mengjing
Li, Qianqian
Hou, Meifang
Chan, Louisa L. Y.
Liu, Meng
Ter, Soo Kai
Dong, Ting
Xia, Yun
Chotirmall, Sanjay Haresh
Fang, Mingliang
Keywords: Science::Medicine
Issue Date: 2021
Source: Wang, M., Li, Q., Hou, M., Chan, L. L. Y., Liu, M., Ter, S. K., Dong, T., Xia, Y., Chotirmall, S. H. & Fang, M. (2021). Inactivation of common airborne antigens by perfluoroalkyl chemicals modulates early life allergic asthma. Proceedings of the National Academy of Sciences of the United States of America, 118(24), e2011957118-.
Project: 04MNP000567C120
Journal: Proceedings of the National Academy of Sciences of the United States of America 
Abstract: Allergic asthma, driven by T helper 2 cell-mediated immune responses to common environmental antigens, remains the most common respiratory disease in children. Perfluorinated chemicals (PFCs) are environmental contaminants of great concern, because of their wide application, persistence in the environment, and bioaccumulation. PFCs associate with immunological disorders including asthma and attenuate immune responses to vaccines. The influence of PFCs on the immunological response to allergens during childhood is unknown. We report here that a major PFC, perfluorooctane sulfonate (PFOS), inactivates house dust mite (HDM) to dampen 5-wk-old, early weaned mice from developing HDM-induced allergic asthma. PFOS further attenuates the asthma protective effect of the microbial product lipopolysaccharide (LPS). We demonstrate that PFOS prevents desensitization of lung epithelia by LPS, thus abolishing the latter's protective effect. A close mechanistic study reveals that PFOS specifically binds the major HDM allergen Der p1 with high affinity as well as the lipid A moiety of LPS, leading to the inactivation of both antigens. Moreover, PFOS at physiological human (nanomolar) concentrations inactivates Der p1 from HDM and LPS in vitro, although higher doses did not cause further inactivation because of possible formation of PFOS aggregates. This PFOS-induced neutralization of LPS has been further validated in primary human cell models and extended to an in vivo bacterial infection mouse model. This study demonstrates that early life exposure of mice to a PFC blunts airway antigen bioactivity to modulate pulmonary inflammatory responses, which may adversely affect early pulmonary health.
ISSN: 0027-8424
DOI: 10.1073/pnas.2011957118
Schools: Lee Kong Chian School of Medicine (LKCMedicine) 
School of Civil and Environmental Engineering 
Rights: © 2021 The Authors. All rights reserved.
Fulltext Permission: none
Fulltext Availability: No Fulltext
Appears in Collections:CEE Journal Articles
LKCMedicine Journal Articles

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