Abstract
ObjectiveAsthma is a complex pulmonary inflammatory disease characterized by the hyper-responsiveness, remodeling and inflammation of airways. Formaldehyde is a common indoor air pollutant that can cause asthma in people experiencing long-term exposure. The irritant effect and adjuvant effect are the two possible pathways of formaldehyde promoted asthma.Methodology/Principal FindingsTo explore the neural mechanisms and adjuvant effect of formaldehyde, 48 Balb/c mice in six experimental groups were exposed to (a) vehicle control; (b) ovalbumin; (c) formaldehyde (3.0 mg/m3); (d) ovalbumin+formaldehyde (3.0 mg/m3); (e) ovalbumin+formaldehyde (3.0 mg/m3)+HC-030031 (transient receptor potential ankyrin 1 antagonist); (f) ovalbumin+formaldehyde (3.0 mg/m3)+ capsazepine (transient receptor potential vanilloid 1 antagonist). Experiments were conducted after 4 weeks of combined exposure and 1-week challenge with aerosolized ovalbumin. Airway hyper-responsiveness, pulmonary tissue damage, eosinophil infiltration, and increased levels of interleukin-4, interleukin-6, interleukin-1β, immunoglobulin E, substance P and calcitonin gene-related peptide in lung tissues were found in the ovalbumin+formaldehyde (3.0 mg/m3) group compared with the values seen in ovalbumin -only immunized mice. Except for interleukin-1β levels, other changes in the levels of biomarker could be inhibited by HC-030031 and capsazepine.Conclusions/SignificanceFormaldehyde might be a key risk factor for the rise in asthma cases. Transient receptor potential ion channels and neuropeptides have important roles in formaldehyde promoted-asthma.
Highlights
Over recent decades, asthma has become an increasingly prevalent disease
OVA-sensitized groups exhibited a greater airway response to MCH compared with the vehicle control group (p,0.01) and FA exposure significantly enhanced the degree of airway reactivity in OVA-sensitized mice (p,0.01)
We reported that the TRPA1 channel antagonist HC030031 and TRPV1 channel antagonist CPZ reduced FA
Summary
Asthma has become an increasingly prevalent disease. It represents a serious public-health problem worldwide, with an estimated 300 million people of all ages affected (especially children) [1]. CD4 TH2 cells are activated, resulting in the release of TH2associated cytokines. This action leads to the synthesis of immunoglobulin (Ig) E antibody. This is followed by the degranulation of mast cells and infiltration of the airway mucosa with eosinophils, which induces tissue remodeling and AHR [4,5]
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