10 research outputs found
Unfractionated and Low-Molecular-Weight Heparin and the Phosphodiesterase Inhibitors, IBMX and Cilostazol, Block Ex Vivo Equid Herpesvirus Type-1-Induced Platelet Activation
The timeline of metalloprotease events during oligofructose induced equine laminitis development
Acute Laminitis: Medical and supportive therapy
Acute laminitis is a serious complication of many primary conditions in the horse. This article summarizes the most appropriate approach to management of the horse with acute laminitis, based on current information. © 2010 Elsevier Inc. All rights reserved
The Contribution of Specific and Nonspecific Biomarkers in Diagnosis of Equine Gastric Ulcer Syndrome (EGUS) Under Field Condition
Lamellar leukocyte infiltration and involvement of IL-6 during oligofructose-induced equine laminitis development
Laminitis is known to involve deregulation of proteases and destruction of the lamellar basement membrane with the host inflammatory response also playing a role. Leukocyte infiltration has been well characterized in the black walnut model of laminitis induction, but not in carbohydrate induced models. Increased gene expression of multiple cytokines, including IL-6, has also been implicated in laminitis development. Using real time PCR, immunohistochemistry and zymography methods, we characterize leukocyte infiltration and IL-6 gene expression in oligofructose (OF) induced laminitis. As well, we use two in vitro models to investigate a role for IL-6 in protease regulation. Laminitis was induced in normal standardbred horses (n= 5) by alimentary OF dosing and lamellar biopsies were obtained throughout the 48. h experimental period. Lamellar explants and keratinocytes were also isolated from clinically normal horses for in vitro experiments. We found infiltration of calprotectin-positive leukocytes (monocytes and neutrophils) at 18-24. h post oligofructose dosing, while IL-6 gene expression was increased as early as 12. h post dosing. Additionally, while we found that IL-6 did not cause significant BM damage in vitro, it did result in increased secreted proMMP-9 levels from lamellar explants. Thus, we find that leukocyte infiltration does occur during oligofructose-induced laminitis development, however, IL-6 gene expression in the lamellae may precede leukocyte infiltration. Additionally, we show IL-6 plays a role in increasing the level of proMMP-9 in vivo in a manner that does not involve keratinocytes
Myristoylated Alanine Rich C Kinase Substrate (MARCKS) is essential to β2-integrin dependent responses of equine neutrophils
Are There Shared Mechanisms in the Pathophysiology of Different Clinical Forms of Laminitis and What Are the Implications for Prevention and Treatment?
The role of neutrophils in equine laminitis
Equine laminitis is a devastating disease in which failure of the adhesion between the digital dermal and epidermal laminae at the basement membrane results in crippling lameness and structural damage to the foot of the horse. Laminitis occurring secondary to sepsis is known to result from a significant inflammatory response that includes leukocyte emigration into the lamellar tissue. These leukocytes, in particular the neutrophil, have been extensively evaluated in experimental models of sepsis-related laminitis in the horse. This review will discuss the relevant findings elucidated from these models and how these findings have affected the development of therapies used to treat this crippling disease