Autophagy and role in asthma

Soma Jyothula, N. Tony Eissa

Research output: Contribution to journalReview articlepeer-review

41 Scopus citations


PURPOSE OF REVIEW: Asthma is a common worldwide respiratory illness with significant morbidity and mortality. The disease is characterized by airway inflammation with involvement of multiple biological pathways. Genetic predisposition and increased susceptibility to severe respiratory viral infections are well known clinical features of asthma. Autophagy is an evolutionarily conserved cellular degradation process with significant impact on immunity and antiviral response. In this review we have described the role of autophagy in immune cell survival, proliferation and function. Autophagy has complex effects on immune response involved in inflammation, specifically Th2 immune response. Common respiratory viruses are associated with increased morbidity and mortality in asthmatic patients. RECENT FINDINGS: We describe recent studies showing the effect of autophagy on replication and immune response to common respiratory viruses. The role of autophagy in asthma has recently been investigated. Two studies have been published describing the association of autophagy with asthma. Genetic polymorphism in specific autophagy genes is associated with asthma and influences gene expression in an experimental in-vivo model. SUMMARY: These studies provide us with a window into the possible role of autophagy in asthma and offer new clues to pathogenesis. Modulation of autophagy has the potential to develop into a new therapeutic avenue to treat this common respiratory ailment.

Original languageEnglish (US)
Pages (from-to)30-35
Number of pages6
JournalCurrent Opinion in Pulmonary Medicine
Issue number1
StatePublished - Jan 2013


  • asthma
  • autophagy
  • common respiratory viruses
  • genetic polymorphism

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


Dive into the research topics of 'Autophagy and role in asthma'. Together they form a unique fingerprint.

Cite this