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Impairment of innate immune killing mechanisms by bacteriostatic antibiotics

Sascha A. Kristian^*,,, Anjuli M. Timmer^*, George Y. Liu^*, Xavier Lauth^*, Neta Sal-Man, Yosef Rosenfeld, Yechiel Shai, Richard L. Gallo^*,, and Victor Nizet^*,1

Departments of
^* Pediatrics and

Medicine, University of California, San Diego, La Jolla, California, USA;

Veterans Affairs San Diego Healthcare System, La Jolla, California, USA; and

Department of Biological Chemistry, Weizmann Institute of Science, Rehovot, Israel

¹Correspondence: Department of Pediatrics, Cellular and Molecular Medicine East, 1066, University of California, San Diego School of Medicine, 9500 Gilman Dr., La Jolla, CA, USA 92093-0687. E-mail: vnizet{at}ucsd.edu

Antibiotics are designed to support host defense in controlling infection. Here we describe a paradoxical inhibitory effect of bacteriostatic antibiotics on key mediators of mammalian innate immunity. When growth of species including Escherichia coli and Staphylococcus aureus is suppressed by chloramphenicol or erythromycin, the susceptibility of the bacteria to cathelicidin antimicrobial peptides or serum complement was markedly diminished. Survival of the bacteria in human whole blood, human wound fluid, or a mouse wound infection model was in turn increased after antibiotic-induced bacteriostasis. These findings provide a further rationale against the indiscriminate use of antibiotics.—Kristian, S. A., Timmer, A. M., Liu, G. Y., Lauth, X., Sal-Man, N., Rosenfeld, Y., Shai, Y., Gallo, R. L., Nizet, V. Impairment of innate immune killing mechanisms by bacteriostatic antibiotics.

Key Words: antimicrobial peptides • cathelicidin • complement

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