Propofol Increases..... Sites of Infection.PDF (7.46 MB)
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Propofol increases host susceptibility to microbial infection by reducing subpopulations of mature immune effector cells at sites of infection

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journal contribution
posted on 12.09.2016 by L. Visvabharathy, B. Xayarath, G. Weinberg, R. A. Shilling, N. E. Freitag
Anesthetics are known to modulate host immune responses, but separating the variables of surgery from anesthesia when analyzing hospital acquired infections is often difficult. Here, the bacterial pathogen Listeria monocytogenes (Lm) was used to assess the impact of the common anesthetic propofol on host susceptibility to infection. Brief sedation of mice with physiologically relevant concentrations of propofol increased bacterial burdens in target organs by more than 10,000-fold relative to infected control animals. The adverse effects of propofol sedation on immune clearance of Lm persisted after recovery from sedation, as animals given the drug remained susceptible to infection for days following anesthesia. In contrast to propofol, sedation with alternative anesthetics such as ketamine/xylazine or pentobarbital did not increase susceptibility to systemic Lm infection. Propofol altered systemic cytokine and chemokine expression during infection, and prevented effective bacterial clearance by inhibiting the recruitment and/or activity of immune effector cells at sites of infection. Propofol exposure induced a marked reduction in marginal zone macrophages in the spleens of Lm infected mice, resulting in bacterial dissemination into deep tissue. Propofol also significantly increased mouse kidney abscess formation following infection with the common nosocomial pathogen Staphylococcus aureus. Taken together, these data indicate that even brief exposure to propofol severely compromises host resistance to microbial infection for days after recovery from sedation.

Funding

This work was supported by Public Health Service grant AI097160 (N. E. F).

History

Publisher Statement

This is a copy of an article published in the PLoS ONE. © 2015 Visvabharathy et al.

Publisher

Public Library of Science

Language

en_US

issn

1932-6203

Issue date

18/09/2015

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