The impact of bovine respiratory disease: the current feedlot experience.

Mortality during the finishing phase in beef steers has increased over the last 13 years at a rate of 0.05% per year for cattle fed in Cactus Feeders' operations. A change in the demographics of placements has also occurred, in that heavier weight cattle are being placed as compared to previous years. Morbidity rates are lower, but higher case fatality rates are observed when compared to years when lighter weight cattle were placed. More lung lesions of varying degree are documented at necropsy of new arrivals and there is greater perception of reduced response to therapy in animals identified with respiratory disease. As placement weights have increased, mortality in the early stages of the feeding period has decreased, resulting in a greater proportion of total death loss later in the period. This shift, in conjunction with an increasing long-term trend of total death loss, can lead to the interpretation of higher 'late day mortality'. Rather than relying solely on observation and distributions of the data, Cactus Feeders believes that the development of a predictive model is better suited to address the potential of 'late day mortality' in confined cattle feeding operations.

Interleukin-17 stimulates C-reactive protein expression in hepatocytes and smooth muscle cells via p38 MAPK and ERK1/2-dependent NF-kappaB and C/EBPbeta activation.

Elevated systemic levels of the acute phase C-reactive protein (CRP) are predictors of future cardiovascular events. There is evidence that CRP may also play a direct role in atherogenesis. Here we determined whether the proinflammatory interleukin (IL)-17 stimulates CRP expression in hepatocytes (Hep3B cell line and primary hepatocytes) and coronary artery smooth muscle cells (CASMC). Our results demonstrate that IL-17 potently induces CRP expression in Hep3B cells independent of IL-1beta and IL-6. IL-17 induced CRP promoter-driven reporter gene activity that could be attenuated by dominant negative IkappaBalpha or C/EBPbeta knockdown and stimulated both NF-kappaB and C/EBP DNA binding and reporter gene activities. Targeting NF-kappaB and C/EBPbeta activation by pharmacological inhibitors, small interfering RNA interference and adenoviral transduction of dominant negative expression vectors blocked IL-17-mediated CRP induction. Overexpression of wild type p50, p65, and C/EBPbeta stimulated CRP transcription. IL-17 stimulated p38 MAPK and ERK1/2 activation, and SB203580 and PD98059 blunted IL-17-mediated NF-kappaB and C/EBP activation and CRP transcription. These results, confirmed in primary human hepatocytes and CASMC, demonstrate for the first time that IL-17 is a potent inducer of CRP expression via p38 MAPK and ERK1/2-dependent NF-kappaB and C/EBPbeta activation and suggest that IL-17 may mediate chronic inflammation, atherosclerosis, and thrombosis.