Abstract
Neutrophils are important assets in defense against invading bacteria like staphylococci. However, (dysfunctioning) neutrophils can also serve as reservoir for pathogens that are able to survive inside the cellular environment. Staphylococcus aureus is a notorious facultative intracellular pathogen. Most vulnerable for neutrophil dysfunction and intracellular infection are immune-deficient patients or, as has recently been described, severely injured patients. These dysfunctional neutrophils can become hide-out spots or “Trojan horses” for S. aureus. This location offers protection to bacteria from most antibiotics and allows transportation of bacteria throughout the body inside moving neutrophils. When neutrophils die, these bacteria are released at different locations. In this review, we therefore focus on the capacity of several groups of antibiotics to enter human neutrophils, kill intracellular S. aureus and affect neutrophil function. We provide an overview of intracellular capacity of available antibiotics to aid in clinical decision making. In conclusion, quinolones, rifamycins and sulfamethoxazole-trimethoprim seem very effective against intracellular S. aureus in human neutrophils. Oxazolidinones, macrolides and lincosamides also exert intracellular antibiotic activity. Despite that the reviewed data are predominantly of in vitro origin, these findings should be taken into account when intracellular infection is suspected, as can be the case in severely injured patients.
Highlights
Neutrophils are the first line of defense against invading bacteria, preventing and clearing infection continuously [1]
The gross majority of the articles only provided in vitro data (n = 98), but some showed in vivo/ex vivo data (n = 12)
The data discussed in this review are of in vitro origin, unless stated otherwise
Summary
Neutrophils are the first line of defense against invading bacteria, preventing and clearing infection continuously [1]. Neutrophils are recruited to the site of infection where they recognize bacteria using. After which the cell membrane remodels around the receptor-ligand complex to form a phagosome [2,3]. The phagosome fuses with secretory vesicles and granules to form the phagolysosome, which include bactericidal enzymes, vacuolar ATPases and the NADPH oxidase complex. The acidic milieu, caused by proteases, reactive oxygen species (ROS), antimicrobial peptides and other processes cause intraluminal degradation of the bacteria [4]. Neutrophils play an important role in the salvage of tissue damage and tissue repair after infection or in case of trauma [5,6,7]. Dysfunctional neutrophils are prominent in patients with congenital neutrophil dysfunction but are seen in several acute inflammatory conditions and severely injured patients [8,9]
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