Journal article

Publication year: 2018

Pages: 3234-3236

Journal: The Journal of Clinical Investigation

Volume number: 128

Issue number: 8

ISSN: 0021-9738

eISSN: 1558-8238

Open access status: Green

DOI Link: https://doi.org/10.1172/JCI122032

Publisher: American Society for Clinical Investigation

Abstract: 
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.

Harvard Citation style: Lohmeyer, J., Morty, R. and Herold, S. (2018) Antibiotic therapy-induced collateral damage: IgA takes center stage in pulmonary host defense, The Journal of Clinical Investigation, 128(8), pp. 3234-3236. https://doi.org/10.1172/JCI122032

APA Citation style: Lohmeyer, J., Morty, R., & Herold, S. (2018). Antibiotic therapy-induced collateral damage: IgA takes center stage in pulmonary host defense. The Journal of Clinical Investigation. 128(8), 3234-3236. https://doi.org/10.1172/JCI122032