title: Lamellar pro-inflammatory cytokine expression patterns in laminitis at the developmental stage and at the onset of lameness: innate vs. adaptive immune response.
abstract: BACKGROUND
  Recent research has indicated that inflammation plays a role in the early stages of laminitis and that, similar to organ failure in human sepsis, early inflammatory mechanisms may lead to downstream events resulting in lamellar failure. Characterisation of the type of immune response (i.e. innate vs. adaptive) is essential in order to develop therapeutic strategies to counteract these deleterious events.
  
  
  OBJECTIVE
  To quantitate gene expression of pro-inflammatory cytokines known to be important in the innate and adaptive immune response during the early stages of laminitis, using both the black walnut extract (BWE) and oligofructose (OF) models of laminitis.
  
  
  METHODS
  Real-time qPCR was used to assess lamellar mRNA expression of interleukins-1beta, 2, 4, 6, 8, 10, 12 and 18, and tumour necrosis factor alpha and interferon gamma at the developmental stage and at the onset of lameness.
  
  
  RESULTS
  Significantly increased lamellar mRNA expression of cytokines important in the innate immune response were present at the developmental stage of the BWE model, and at the onset of acute lameness in both the BWE model and OF model. Of the cytokines characteristic of the Th1 and Th2 arms of the adaptive immune response, a mixed response was noted at the onset of acute lameness in the BWE model, whereas the response was skewed towards a Th1 response at the onset of lameness in the OF model.
  
  
  CONCLUSIONS
  Lamellar inflammation is characterised by strong innate immune response in the developmental stages of laminitis; and a mixture of innate and adaptive immune responses at the onset of lameness.
  
  
  CONCLUSIONS
  These results indicate that anti-inflammatory treatment of early stage laminitis (and the horse at risk of laminitis) should include not only therapeutic drugs that address prostanoid activity, but should also address the marked increases in lamellar cytokine expression.
authors.affiliation: Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Ohio State University, Columbus, Ohio 43210, USA.
authors.forename: J K
authors.initials: JK
authors.lastname: Belknap
authors.forename: S
authors.initials: S
authors.lastname: Giguère
authors.forename: A
authors.initials: A
authors.lastname: Pettigrew
authors.forename: A M
authors.initials: AM
authors.lastname: Cochran
authors.forename: A W
authors.initials: AW
authors.lastname: Van Eps
authors.forename: C C
authors.initials: CC
authors.lastname: Pollitt
mesh_terms: D000818:Animals; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D005260:Female; D005534:Foot Diseases / Q000276:immunology / Q000662:veterinary*; D005786:Gene Expression Regulation; D006734:Horse Diseases / Q000276:immunology*; D006736:Horses; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism; D031324:Juglans / Q000737:chemistry; D007794:Lameness, Animal / Q000276:immunology*; D008297:Male; D009844:Oligosaccharides / Q000009:adverse effects; D010936:Plant Extracts / Q000009:adverse effects; D016133:Polymerase Chain Reaction / Q000662:veterinary; D012333:RNA, Messenger / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines; D009844:Oligosaccharides; D010936:Plant Extracts; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C120489:oligofructose; D007371:Interferon-gamma