Banana leaves as an alternative wound dressing.

BACKGROUND: There is a need for cheap and efficacious wound dressings in developing countries. Banana leaves have been described as an excellent, inexpensive, easily available dressing material in tropical countries. As a natural product, banana leaves are heavily contaminated with various pathogens that must be removed before they can be used as wound dressings, but effective sterilization methods that do not affect the beneficial wound-dressing properties of banana leaves have not been described. OBJECTIVES: To study different sterilization methods and determine which can be used on banana leaves without affecting their beneficial wound-dressing properties. MATERIALS AND METHODS: We first compared the use of different decontamination techniques to reduce the natural microflora of the leaves and then tested the wound-dressing properties of the leaves in a mouse model of skin transplantation and in postsurgical patients in Uganda, Africa. RESULTS: Steam sterilization proved to be the optimal sterilization technique. Banana leaves displayed wound-dressing properties that equaled those of petroleum jelly gauze dressings and were tested successfully in a clinical setting in postsurgical patients in Uganda, Africa. CONCLUSION: We found banana leaves to be an excellent alternative wound dressing, combining the desirable properties of modern wound-dressing material with low cost.

Interleukin 23 expression in pyoderma gangrenosum and targeted therapy with ustekinumab.

BACKGROUND: Interleukin (IL)-23 is involved in the pathogenesis of the chronic inflammatory Crohn disease. Pyoderma gangrenosum (PG) is often associated with and can even be the first manifestation of this disease and has abundant neutrophilic infiltration. Because IL-23 plays a critical role in driving inflammation associated with IL-17 production and especially neutrophil recruitment, we suspect that PG might be driven by a pathogenetic mechanism similar to that of inflammatory bowel diseases or psoriasis. OBSERVATIONS: Tissue sample analysis showed highly elevated expression of IL-23 on both transcriptional and protein level in a recalcitrant PG lesion. On the basis on these data, a treatment targeting the p40 subunit of the heterodimeric IL-23 with the monoclonal antibody ustekinumab was started. Therapy with ustekinumab resulted in a significant decrease of IL-23 expression in PG and healing after 14 weeks of treatment. No relapse occurred in a 6-month follow-up period. CONCLUSIONS: Our data provide evidence of an IL-23-dominated inflammatory infiltrate in PG. This might specify a new concept for PG pathophysiology and suggests a possibility for using ustekinumab as a therapeutic agent in this disease.

ROS-induced ATF3 causes susceptibility to secondary infections during sepsis-associated immunosuppression.

Sepsis, sepsis-induced hyperinflammation and subsequent sepsis-associated immunosuppression (SAIS) are important causes of death. Here we show in humans that the loss of the major reactive oxygen species (ROS) scavenger, glutathione (GSH), during SAIS directly correlates with an increase in the expression of activating transcription factor 3 (ATF3). In endotoxin-stimulated monocytes, ROS stress strongly superinduced NF-E2-related factor 2 (NRF2)-dependent ATF3. In vivo, this ROS-mediated superinduction of ATF3 protected against endotoxic shock by inhibiting innate cytokines, as Atf3(-/-) mice remained susceptible to endotoxic shock even under conditions of ROS stress. Although it protected against endotoxic shock, this ROS-mediated superinduction of ATF3 caused high susceptibility to bacterial and fungal infections through the suppression of interleukin 6 (IL-6). As a result, Atf3(-/-) mice were protected against bacterial and fungal infections, even under conditions of ROS stress, whereas Atf3(-/-)Il6(-/-) mice were highly susceptible to these infections. Moreover, in a model of SAIS, secondary infections caused considerably less mortality in Atf3(-/-) mice than in wild-type mice, indicating that ROS-induced ATF3 crucially determines susceptibility to secondary infections during SAIS.