Immune responses in the lung and local lymph node of A/J mice to intranasal sensitization and challenge with adjuvant-free ovalbumin
Resource
Toxicol Pathol,31(4),432-447.
Journal
Toxicol Pathol
Journal Volume
31
Journal Issue
4
Pages
432-447
Date Issued
2003-07
Date
2003-07
Author(s)
Abstract
Pathologic features of IgE-mediated allergic airway diseases include airway infiltration of inflammatory cells (eg, lymphocytes, plasma cells, and eosinophils) and mucous cell metaplasia (MCM) in airway epithelium. CD4+ T lymphocytes, specifically those producing a type 2 (Th2) cytokine profile, are necessary for the induction of IgE-mediated allergic airway responses. Most experimental models of IgE-mediated allergic airway disease use systemic (eg, intraperitoneal) administration of an allergen coupled with an adjuvant to sensitize animals. Cytokine changes are measured in a number of ways including in bronchoalveolar lavage fluid (BALF) or lymph node cells stimulated ex vivo. The primary objective of this study was to test the hypothesis that intranasal sensitization and challenge of mice with ovalbumin in the absence of an adjuvant will induce the pathologic features that are characteristic of IgE-mediated allergic airway disease. Another objective was to determine if intranasal delivery of this allergen will result in the induction of a profile of cytokine gene expression in the lung and tracheobronchial (TB) lymph node, that is typical of immunologic changes associated with IgE-mediated allergic airway disease. Only mice that were intranasally sensitized and challenged with ovalbumin exhibited pulmonary lesions that included marked MCM in the respiratory epithelium lining the nasal and pulmonary airways, and an associated mixed inflammatory cell influx consisting of lymphocytes, plasma cells and eosinophils. Ovalbumin-treated mice also exhibited enhanced expression of the Th2 cytokine mRNAs IL-4, IL-5, IL-10, and IL-13 in the lung and IL-4 in the TB lymph node, and concurrent increases in ovalbumin-specific IgE in the serum. The results of this study indicate that A/J mice intranasally instilled with ovalbumin without adjuvant have the hallmark histopathologic and immunologic features of IgE-mediated allergic airway disease of humans.
Other Subjects
adjuvant; cytokine; immunoglobulin E; interleukin 10; interleukin 13; interleukin 4; interleukin 5; messenger RNA; ovalbumin; animal experiment; animal model; animal tissue; article; controlled study; cytokine production; eosinophil; experimental model; helper cell; immune response; inflammatory infiltrate; lung alveolus epithelium; lung lavage; lymph node cell; lymphocytic infiltration; male; mouse; mucous cell; nonhuman; nose mucosa; plasma cell; priority journal; respiratory epithelium; respiratory tract allergy; sensitization; Th2 cell; tracheobronchial tree; Adjuvants, Immunologic; Administration, Intranasal; Animals; Bronchial Provocation Tests; Cytokines; Enzyme-Linked Immunosorbent Assay; Gene Expression Profiling; Hypersensitivity, Immediate; Immunoglobulin E; Immunohistochemistry; Lung; Lymph Nodes; Male; Mice; Nasal Mucosa; Ovalbumin; Respiratory Mucosa; Reverse Transcriptase Polymerase Chain Reaction; Animalia
Type
journal article