Abstract
The leishmanin skin test (LST) is an in vivo technique commonly used to evaluate the Leishmania-specific cellular immune response in dogs. However, information regarding the local immune response in LST-positive reactions is scarce. We examined the pattern of toll-like receptor 2 (TLR2), TLR4, TLR7, interleukin- (IL-) 10, interferon gamma (IFN-γ), and (program death ligand) PD-L1 gene expression in LST-positive reactions and paired normal-looking skin of nine infected Ibizan hound dogs. Healthy skin from ten seronegative dogs from a nonendemic area was analysed as a negative control. Immune gene expressions were examined by quantitative PCR (qPCR) analysis. LST-positive reactions presented significant upregulation of TLR2, TLR4, IL-10, IFN-γ, and PD-L1 and downregulation of TLR7 when compared with healthy skin of seronegative control dogs from a nonendemic area. All transcripts but TLR7 were significantly higher in LST-positive reaction than in paired normal-looking skin of Ibizan hound. The expression profile of immune genes in LST-positive reactions was similar to that previously observed in clinically lesioned skin of mildly diseased dogs with papular dermatitis due to Leishmania infantum infection. This data provide additional support for the important role of TLRs in canine leishmaniosis.
Highlights
Canine leishmaniosis (CanL) caused by Leishmania infantum is a vector borne zoonotic disease endemic in many areas around the world, including many parts of the Mediterranean basin [1]
toll-like receptor 2 (TLR2) (p = 0:002), TLR4 (p = 0:04), IL-10 (p < 0:0001), IFN-γ (p < 0:0001), and PD-L1 (p < 0:0001) transcripts were significantly higher in leishmanin skin test (LST)-positive reaction skin samples than in healthy skin from control dogs from a nonendemic area
Relative quantification of TLR7 was significantly lower in LST-positive skin than in healthy skin from seronegative control dogs from a nonendemic area (p = 0:002)
Summary
Canine leishmaniosis (CanL) caused by Leishmania infantum is a vector borne zoonotic disease endemic in many areas around the world, including many parts of the Mediterranean basin [1]. Many investigations on immune response in CanL have been focused on adaptive immune response, and the data on the importance of the innate immune responses are scarce [4]. Much of the work in CanL has focused on adaptive immune response, there is a great interest in the involvement of tolllike receptors (TLRs) in the innate immune response against Leishmania infection and how their expression could modulate adaptive immune response [4,5,6,7]. Numerous studies have demonstrated that engagement of individual TLR, mainly on dendritic cells, can influence CD4+ T cell priming and effector differentiation by skewing the Th1Th2 balance, the role of different TLRs on adaptive immune response in Leishmania infection remains an unresolved issue [7]. TLR2 is one of the TLRs more frequently
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