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Broad-spectrum suppression of bacterial pneumonia by aminoglycoside-propagated
Acinetobacter baumannii.
Authors Hood-Pishchany MI, Pham L, Wijers CD, Burns WJ, Boyd KL, Palmer LD, Skaar EP,
Noto MJ
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal PLoS pathogens
Year 2020
Date Published 3/1/2020
Volume : Pages 16 : e1008374
PubMed Reference 32168364
Abstract Antimicrobial resistance is increasing in pathogenic bacteria. Yet, the effect
of antibiotic exposure on resistant bacteria has been underexplored and may
affect pathogenesis. Here we describe the discovery that propagation of the
human pathogen Acinetobacter baumannii in an aminoglycoside antibiotic results
in alterations to the bacterium that interact with lung innate immunity
resulting in enhanced bacterial clearance. Co-inoculation of mice with A.
baumannii grown in the presence and absence of the aminoglycoside, kanamycin,
induces enhanced clearance of a non-kanamycin-propagated strain. This finding
can be replicated when kanamycin-propagated A. baumannii is killed prior to
co-inoculation of mice, indicating the enhanced bacterial clearance results from
interactions with innate host defenses in the lung. Infection with
kanamycin-propagated A. baumannii alters the kinetics of phagocyte recruitment
to the lung and reduces pro- and anti-inflammatory cytokine and chemokine
production in the lung and blood. This culminates in reduced histopathologic
evidence of lung injury during infection despite enhanced bacterial clearance.
Further, the antibacterial response induced by killed aminoglycoside-propagated
A. baumannii enhances the clearance of multiple clinically relevant
Gram-negative pathogens from the lungs of infected mice. Together, these
findings exemplify cooperation between antibiotics and the host immune system
that affords protection against multiple antibiotic-resistant bacterial
pathogens. Further, these findings highlight the potential for the development
of a broad-spectrum therapeutic that exploits a similar mechanism to that
described here and acts as an innate immunity modulator.


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