A 26-month-old male mixed-breed dog of Korean origin was subjected to necropsy following death after a history of decreased appetite and weight loss. Necropsy revealed generalized lymphadenopathy and splenomegaly. Histopathological examination of samples from the spleen, mandibular lymph nodes, liver, kidney, and large intestine showed granulomas with numerous macrophages containing intracytoplasmic Leishmania amastigotes. Transmission electron microscopy revealed Leishmania amastigotes in the macrophage cytoplasm. All tissues with granulomas were positive for Leishmania spp, which was confirmed to be Leishmania infantum by conventional polymerase chain reaction (PCR), real-time PCR, and in situ hybridization. To our knowledge, this is the second case of canine visceral leishmaniasis in Korea.

The use of bee venom (Apis mellifera L., BV) occasionally causes side effects such as inflammation and allergic reactions in the recipients. Several case reports also suggested the treatment of BV has some limitations in its clinical uses, due to the occurrence of dermal necrosis and anaphylatic reactions. It is generally understood that bee venom allergy is mainly the result of its allergic component, phospholipase A2 (PLA2). The present study was aimed to generate PLA2-free bee venom (PBV) and evaluate its efficacy as skin care and cosmetic preparation, comparing with original bee venom (BV). Our results showed that both BV and PBV exhibited significant protective effects in UVB-irradiated human keratinocyte (HaCaT) and human dermal fibroblast (HDF) cells and they also induced type I collagen synthesis in UVB-irradiated HDF cells except BV at 3 μg/ml. Furthermore, BV and PBV showed the inhibition of UVB-stimulated matrix metalloproteinase-1 (MMP-1), a major collagen degrading enzyme in skin. However, BV, unlike PBV, exhibited strong cytotoxicities in skin cells (both HaCaT and HDF) at its working concentrations of anti-wrinkle effect. The underlying cell signaling mechanisms of anti-wrinkle effects of BV and PBV were demonstrated by the activation of ERK1/2, and p38. Conclusively, PBV appears to be the bee venom of choice with less cytotoxicity and higher efficacy on UVB-irradiated skin cells in comparison with original bee venom (BV). Therefore, PBV can better be used as a cosmetic ingredient exhibiting excellent anti-wrinkle effect against photoaging than original BV.

Schwann cells play an important role in peripheral nerve regeneration. Upon nerve injury, Schwann cells are activated and produce various proinflammatory mediators including IL-6, LIF and MCP-1, which result in the recruitment of macrophages and phagocytosis of myelin debris. However, it is unclear how the nerve injury induces Schwann cell activation. Recently, it was reported that necrotic cells induce immune cell activation via toll-like receptors (TLRs). This suggests that the TLRs expressed on Schwann cells may recognize nerve damage by binding to the endogenous ligands secreted by the damaged nerve, thereby inducing Schwann cell activation. To explore the possibility, we stimulated iSC, a rat Schwann cell line, with damaged neuronal cell extracts (DNCE). The stimulation of iSC with DNCE induced the expression of various inflammatory mediators including IL-6, LIF, MCP-1 and iNOS. Studies on the signaling pathway indicate that NF-xB, p38 and JNK activation are required for the DNCE-induced inflammatory gene expression. Furthermore, treatment of either anti-TLR3 neutralizing antibody or ribonuclease inhibited the DNCE-induced proinflammatory gene expression in iSC. In summary, these results suggest that damaged neuronal cells induce inflammatory Schwann cell activation via TLR3, which might be involved in the Wallerian degeneration after a peripheral nerve injury.