Microbes and asthma: the missing cellular and molecular links

Curr Opin Pulm Med. 2012 Jan;18(1):14-22. doi: 10.1097/MCP.0b013e32834dccc0.


Purpose of review: In this review, we describe the 'state-of-the-art' in our knowledge of asthma and what gaps exist, which can be exploited in the future for effective translation of our knowledge from the bench or population studies to diagnosis and therapy.

Recent findings: The advent of microbiome research has expanded the potential role of microbes in asthma. There has been a significant increase in our understanding of the pathologic, genetic, cellular and molecular mechanisms of asthma. Nonetheless, the contribution of microbes to the genesis, exacerbation and treatment of asthma are poorly understood.

Summary: Asthma is a complex chronic disease of the lung whose incidence is growing at all ages despite the progress that has been made in the areas of diagnosis and treatment of asthma. The complexity is partly due to the environmental insults such as allergens and microbial infections that play differential roles in the pathogenesis of childhood vis-à-vis elderly asthma. Microbes may play important roles in the exacerbation of asthma and hence in the comorbidities due to asthma, and also in the causation of asthma.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Age Factors
  • Aged
  • Aged, 80 and over
  • Asthma / etiology
  • Asthma / immunology
  • Asthma / microbiology*
  • CD4-Positive T-Lymphocytes
  • Child
  • Child, Preschool
  • Corynebacterium Infections / complications*
  • Corynebacterium Infections / immunology
  • Female
  • Humans
  • Infant
  • Interleukin-1 / immunology
  • Interleukin-6 / immunology
  • Male
  • Metagenome
  • Respiratory Tract Infections / complications
  • Respiratory Tract Infections / immunology
  • Respiratory Tract Infections / microbiology*
  • Staphylococcal Infections / complications*
  • Staphylococcal Infections / immunology
  • Tumor Necrosis Factor-alpha / immunology


  • Interleukin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha