Neural integration and allergic disease

Bradley J. Undem, Radhika Kajekar, Dawn D. Hunter, Allen C. Myers

Research output: Contribution to journalArticlepeer-review

96 Scopus citations


Changes in neural activity play a key role in many symptoms of allergic disease, including sneezing, coughing, itching, and ocular irritation, among others. The mechanisms underlying allergen-induced changes in neural activity (reflexes) are largely unknown and under active investigation. Allergic inflammation can affect neural activity on a variety of levels, including at the primary afferent sensory nerve, integrative centers of the central nervous system, autonomic ganglia, and autonomic neuroeffector junction. At the level of the afferent sensory nerve, mediators released after allergen exposure either directly or indirectly increase neuronal firing. At the level of sensory ganglia, which contain cell bodies that innervate a variety of organs, changes in neuronal excitability may lead to a generalization of allergic symptoms. In the central nervous system, where afferent inputs from throughout the body converge, allergic inflammation may be associated with central sensitization, leading to the modulation of the neural reflexes. Finally, at the autonomic ganglia and neuroeffector junction, allergic inflammation appears to be associated with enhanced ganglionic transmission and neurotransmitter release, respectively. Mechanisms by which allergen challenge affects neuronal activity at various levels of the nervous system are reviewed, with a primary emphasis on studies of airway physiologic factors.

Original languageEnglish (US)
Pages (from-to)S213-S220
JournalJournal of Allergy and Clinical Immunology
Issue number5 SUPPL.
StatePublished - 2000


  • Allergic inflammation
  • Central nervous system
  • Excitatory postsynaptic potential
  • Neuroeffector junction
  • Neurogenic inflammation
  • Upper airway

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


Dive into the research topics of 'Neural integration and allergic disease'. Together they form a unique fingerprint.

Cite this