Indices of inflammation in the lung and liver in the early stages of the black walnut extract model of equine laminitis

Stewart, Allison J., Pettigrew, Amanda, Cochran, Anna M. and Belknap, James K. (2009) Indices of inflammation in the lung and liver in the early stages of the black walnut extract model of equine laminitis. Veterinary Immunology and Immunopathology, 129 3-4: 254-260. doi:10.1016/j.vetimm.2008.11.001

Author Stewart, Allison J.
Pettigrew, Amanda
Cochran, Anna M.
Belknap, James K.
Title Indices of inflammation in the lung and liver in the early stages of the black walnut extract model of equine laminitis
Journal name Veterinary Immunology and Immunopathology   Check publisher's open access policy
ISSN 0165-2427
Publication date 2009-06-15
Year available 2008
Sub-type Article (original research)
DOI 10.1016/j.vetimm.2008.11.001
Open Access Status Not yet assessed
Volume 129
Issue 3-4
Start page 254
End page 260
Total pages 7
Place of publication Amsterdam, Netherlands
Publisher Elsevier BV
Language eng
Abstract The liver and lung are not only described as “target organs” in sepsis in most species, but are purported to be sources of circulating inflammatory mediators central to the systemic inflammatory response syndrome (SIRS). As we have recently reported an inflammatory response in the laminar tissue in laminitis similar to that described in “target organs” in human sepsis, we investigated the inflammatory response of the lung and liver in the black walnut extract (BWE) model of equine laminitis to determine (1) if a similar systemic inflammatory response occurs in this laminitis model as described for these organs in human sepsis, and (2) if these organs may be an important source of the inflammatory mediators leading to laminar inflammation. Real-time quantitative PCR (RT-qPCR) was used to measure hepatic and pulmonary mRNA concentrations of IL-1β, IL-4, IL-6, IL-8, IL-10, TNF-α, COX-1 and COX-2. Hepatic samples were assessed from two time points in the developmental/prodromal period: (1) 1.5 h post-BWE administration (BWE-1.5H, n = 5), and (2) the “developmental time point” (onset of leukopenia, approximately 3 h post-BWE administration, BWE-DEV, n = 5). Pulmonary samples were only assessed for the BWE-DEV group. One control group (CON-3H, n = 5) was used for both the 1.5H and DEV groups. Finally, CD13 immunohistochemistry was performed to assess leukocyte emigration into hepatic and pulmonary parenchyma. Hepatic and pulmonary mRNA concentrations of the proinflammatory cytokines IL-6, IL-8 and TNF-α were significantly increased (P < 0.05) in BWE-1.5H and BWE-DEV groups compared to the control group; IL-1β mRNA concentrations were only increased in the lung. The “anti-inflammatory” cytokines, IL-10 and IL-4, underwent transient decreases at different time points. Significant increases in parenchymal leukocyte numbers occurred in both the lung and liver at the BWE-DEV time point. Hepatic and pulmonary proinflammatory cytokine expression differ from that previously reported for the laminae in that TNF-α was increased in the hepatic and pulmonary tissues, the increases in expression of IL-6 and IL-8 are dramatically smaller for the liver and lung compared to those reported for the laminae, and the peak changes appear to occur later in the disease process in the liver than in the laminae (BWE-DEV in liver vs. 1.5H in the laminae).
Keyword Cyclooxygenase
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID 2005-35204-15316
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Veterinary Science Publications
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