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

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