Antibiotic therapy-induced collateral damage: IgA takes center stage in pulmonary host defense

J Clin Invest. 2018 Aug 1;128(8):3234-3236. doi: 10.1172/JCI122032. Epub 2018 Jul 16.


The use of broad-spectrum antibiotics in empirical antimicrobial therapy is a lifesaving strategy for patients in intensive care. At the same time, antibiotics dramatically increase the risk for nosocomial infections, such as hospital‑acquired pneumonia caused by Pseudomonas aeruginosa, and other antibiotic-resistant bacteria. In this issue of the JCI, Robak and colleagues identified a mechanism by which depletion of resident gut and lung microbiota by antibiotic treatment results in secondary IgA deficiency and impaired anti-P. aeruginosa host defense. Impaired defenses could be improved by substitution of polyclonal IgA via the intranasal route in a mouse model of pneumonia. Importantly, antibiotic treatment caused lung IgA deficiency that involved reduced TLR-dependent production of a proliferation-inducing ligand (APRIL) and B cell-activating factor (BAFF) in intensive care unit patients. These patients might therefore benefit from future strategies to increase pulmonary IgA levels.

Publication types

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Animals
  • Anti-Bacterial Agents
  • Anti-Infective Agents*
  • Humans
  • IgA Deficiency*
  • Immunoglobulin A
  • Mice
  • Pneumonia*
  • Pseudomonas aeruginosa


  • Anti-Bacterial Agents
  • Anti-Infective Agents
  • Immunoglobulin A