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486 Prenatal Allergen Exposure Facilitated Airway Remodeling by Airborne Allergen Stimuli in Postnatal Life
  1. JC Chen1,
  2. ML Kuo2
  1. 1Department of Pediatric Surgery, Chang Gung Memorial Hospital
  2. 2Department of Microbiology and Immunology, College of Medicine, Chang Gung University, Taoyuan, Taiwan R.O.C.

Abstract

Background Murine asthma models are mainly created through adulthood sensitization, but lack airway remodeling hallmarks.

Aims This study aimed to examine airway remodeling in the prenatally-sensitized murine asthma model.

Methods FVB/N fetuses were exposed to aluminum-free ovalbumin (OVA) of 50 µg on gestational day 14, and subjected to aerosolized OVA challenge in their postnatal life. Lung sections were examined after hematoxylin-eosin, periodic acid-Schiff, and Masson’s trichrome stainings.

Results Following prenatal OVA sensitization, neither the neonate nor the adult showed any evidence of inflammatory cell infiltration and airway remodeling. Postnatal aerosolized OVA stress elicited extensive peribronchial and perivascular eosinophilic inflammation. The allergic airways were plugged by exfoliated epithelia and mucus. We identified two distinct patterns of epithelial desquamation: complete denudation of airway epithelia, exposing fragmented basement membrane; and peeling of columnar epithelia, leaving a single layer of basal cells adherent to basement membrane. There was subepithelial collagenosis in extrapulmonary airways and smooth muscle hyperplasia was evident in terminal airways. Prenatally OVA-primed mice had no mucin-positive goblet cells in intrapulmonary airways as normal mice, but showed goblet cell metaplasia in large intrapulmonary airways even following mechanical saline stress. However, goblet cell metaplasia spread distally towards small terminal airways after aerosolized OVA challenge. Asthma models through adulthood sensitization only exhibited peribronchial or perivascular inflammation and goblet cell metaplasia.

Conclusions Fetal OVA exposure intensified airway responsiveness to airborne OVA stimuli in postnatal life to cause pathognomonic structural alterations in the lung.

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