Interleukin-17A pathway target genes are upregulated in Equus caballus supporting limb laminitis.

摘要: Supporting Limb Laminitis (SLL) is a painful and crippling secondary complication of orthopedic injuries infections in horses, often resulting euthanasia. SLL causes structural alterations inflammation the interdigitating layers specialized epidermal dermal tissues, lamellae, which suspend equine distal phalanx from hoof capsule. Activation interleukin-17A (IL-17A)-dependent inflammatory pathway an stress response that contributes to physiologic cutaneous wound healing as well pathological skin conditions. As first test hypothesis lamellae horses diagnosed with also respond by activating IL-17A pathway, expression IL-17A, IL-17 receptor subunit A 11 effector genes was measured RT-PCR or qPCR. Lamellar tissue isolated Thoroughbreds euthanized due naturally occurring age breed matched non-laminitic controls. By RT-PCR, Receptor expressed both laminitic while primarily detectable tissues. target gene undetectable samples exception weak detection DEFB4B, S100A9 PTSG2. In contrast, all examined, except CCL20, were some samples. qPCR, severe acute (n = 7) ~15-100 fold higher levels DEFB4B compared controls 8). upregulated developmental/subclinical 8) moderate ~ 5-fold, chronic 5) ~15-200 fold. situ hybridization (DEFB4) immunofluorescence (calprotectin, dimer S100A9/S100A8 proteins) demonstrated keratinocytes, suprabasal cell layers, These data demonstrate upregulation cohort support similarities stresses damage exist between human