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BackgroundLidocaine (LD) is one of the most commonly used local anesthetics for performing arthroscopic surgery and managing of osteoarthritic pain in both human and veterinary medicine. However, over the last years, several studies have focused on the chondrotoxic effects of LD. In order to ensure that intra-articular lidocaine is safe to use, treatments aimed at mitigating chondrocyte death have recently been investigated. The aim of this study is to evaluate the possible protective effects of platelet-rich plasma (PRP) against LD cytotoxicity on canine articular chondrocytes.ResultsArticular canine chondrocytes, were exposed to 1% or 1.8% LD alone or in co-presence with 10% PRP for 30 min. In order to evaluate the effects of PRP pre-treatments, experiments were carried out on cells cultured in serum-free medium-or in medium supplemented with 10% PRP or 10% fetal bovine serum. Cell viability was evaluated by methyl thiazolyl tetrazolium assay and cell apoptosis was analyzed by flow cytometry using annexin V-fluorescein isothiocyanate/propidium iodide. The results showed that LD significantly reduced canine chondrocytes viability, probably due to apoptosis induction. Pre-treatment or the co-presence of PRP in the media restored the number of viable chondrocytes. The PRP also seemed to protect the cells from LD-induced apoptosis.ConclusionsPre-treatments and/or the simultaneous administration of PRP reduced LD-induced cytotoxicity in canine chondrocytes. Further in vivo studies are required to determine whether PRP can be used as a save protective treatment for dogs receiving intra-articular LD injections.

The first perspective: The host geneticsThe outcome of fungal disease is determined by complex interactions between fungal pathogens, human hosts and their environment including the host microbiome (1-4). Morbidity and mortality in fungal disease remain very high despite recent advances in the diagnostic and treatment of these conditions (5-7). There are only three classes of antifungal drugs available to treat these disease and, antifungal resistance linked to the use of agricultural use of triazole fungicides is on the rise (8). The development of new antifungal drugs to treat human fungal disease is challenging as both, host and pathogen are eukaryotes and, there are different potential druggable targets exposed at different points of fungal morphogenesis.So far, the identification of high-risk patients for fungal disease has relied on the use of clinical scores that combine the use of clinical and host factors to predict the risk of subsequent disease (9-11). However, the prevalence of opportunistic fungal diseases within at-risk population, ranges from 0.1 -20% (12). In the last decades, individual genetic variation has been recognised as a major contribution of functional immune responses against fungal pathogens. Several monogenic defects and polymorphisms in genes regulating antifungal immunity or pathogen sensing have been associated with susceptibility to aspergillosis, cryptococcosis and candidiasis (13) (Figure 1).Sensing of human fungal pathogens by the host immune system requires the interplay between pathogen-associated molecular patterns (PAMPs), mostly located in the cell wall of fungal pathogens, and pattern recognition receptors (PRRs) (14-17). The interaction between PRRs and PAMPs, leads to the regulation of uptake of fungal pathogens by immune cells. In addition to membrane receptors, soluble PRRs such as pentraxins or mannose binding lectins (MBLs) are also critical for pathogen sensing and efficient phagocytosis (18, 19).To date, polymorphisms in PTX3 have been reported in different clinical settings as a risk factor for invasive pulmonary aspergillosis in haematopoietic stem cell transplant recipients (20), solid organ transplants (21) and chronic obstructive pulmonary disease (22). Using ex Frontiers in Immunology frontiersin.org 01