Polymorphonuclear neutrophils (PMN) are potent inflammatory effector cells essential to host defense, but at the same time they may cause significant tissue damage. Thus, timely induction of neutrophil apoptosis is crucial to avoid tissue damage and induce resolution of inflammation. NK cells have been reported to influence innate and adaptive immune responses by multiple mechanisms including cytotoxicity against other immune cells. In this study, we analyzed the effect of the interaction between NK cells and neutrophils. Coculture experiments revealed that human NK cells could trigger caspase-dependent neutrophil apoptosis in vitro. This event was dependent on cell–cell contact, and experiments using blocking Abs indicated that the effect was mediated by the activating NK cell receptor NKp46 and the Fas pathway. CD56-depleted lymphocytes had minimal effects on neutrophil survival, suggesting that the ability to induce neutrophil apoptosis is specific to NK cells. Our findings provide evidence that NK cells may accelerate neutrophil apoptosis, and that this interaction may be involved in the resolution of acute inflammation.

The aim of this study was to investigate the antimicrobial activity of currently available topical skin pharmaceuticals against Candida albicans, Escherichia coli, Staphylococcus aureus, Staphylococcus epidermidis and Streptococcus pyogenes. The agar dilution assay was used to determine the minimal inhibitory concentration for cream formulations and their active substances. Corticosteroid formulations with the antiseptics clioquinol or halquinol were active against all microbes. The hydrogen peroxide formulation was primarily active against staphylococci. Clotrimazole, miconazole and econazole showed an effect against staphylococci in addition to their effect on C. albicans. In contrast, terbinafine had no antibacterial effect. Fusidic acid was active against staphylococci, with slightly weaker activity against S. pyogenes and no activity against C. albicans or E. coli. In summary, some topical skin pharmaceuticals have broad antimicrobial activity in vitro, clioquinol and halquinol being the most diverse. In limited superficial skin infection topical treatment can be an alternative to systemic antibiotics and should be considered. With the global threat of multi-resistant bacteria there is a need for new, topical, non-resistance-promoting, antimicrobial preparations for the treatment of skin infections.

The aim of this study was to monitor Staphylococcus aureus colonization and disease severity in adults with atopic dermatitis (AD) during 5 months. Twenty-one patients attended 3 visits each for severity SCORing of Atopic Dermatitis (SCORAD) assessment, quantitative cultures from the skin and conventional cultures from the anterior nares, tonsils and perineum. S. aureus isolates were typed for strain identity with pulsed-field gel electrophoresis (PFGE). Seventy-one percent of patients were colonized with S. aureus on lesional skin at least once. Density (colony-forming units (CFU)/cm2) was higher on lesional skin than on non-lesional skin (p < 0.05). Density on lesional skin and number of colonized body sites were positively correlated with SCORAD (p = 0.0003 and p = 0.007, respectively). Persistent carriers of the same strain on lesional skin had higher mean SCORAD index than intermittent/non-carriers (36.3 and 17.1, respectively, p = 0.002). The results show a temporal correlation between several aspects of S. aureus colonization and disease severity in AD raising the question of the importance of this in pathogenesis and treatment.

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Fusidic acid-resistant Staphylococcus aureus (FRSA) has been identified as a causative agent in outbreaks of impetigo and its emergence has been associated with increased use of topical fusidic acid. The frequency of FRSA in atopic dermatitis (AD) has been less extensively investigated. The aim of this study was to investigate the bacterial spectrum and frequency of FRSA in patients with impetigo or secondarily infected AD. A prospective study in our clinic in 2004 to 2008 included 38 patients with impetigo and 37 with secondarily infected AD. S. aureus was the predominant finding in all groups (bullous impetigo 92% (12/13), impetigo 76% (19/25) and secondarily infected AD 89% (33/37)). Seventy-five percent of S. aureus were fusidic acid resistant in bullous impetigo, 32% in impetigo and 6.1% in secondarily infected AD (bullous impetigo vs. AD p < 0.0001, impetigo vs. AD p < 0.05). We then performed a retrospective patient record review including all patients with impetigo or secondarily infected AD seen at the clinic during the first and last year of the prospective study. In the first year 33% (19/58) of the S. aureus isolates were fusidic acid-resistant in impetigo and 12% (5/43) in secondarily infected AD (p < 0.05). In the last year corresponding values were 24% (6/25) for impetigo and 2.2% (1/45) for AD (p < 0.01). In summary, the prospective study and the patient record review both showed higher FRSA levels in impetigo than in AD. FRSA levels were persistently low in AD. Continued restrictive use of topical fusidic acid is advised to limit an increase in FRSA levels in dermatology patients.