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Dairy cows’ urinary nitrogen (N) excretion (UN; g/d) represents a significant environmental concern due to their contribution to nitrate leaching, nitrous oxide (a potent greenhouse gas), and ammonia emissions (contributor to N deposition). The first objective of the current study was to determine the adequacy of existing models to predict UN from total mixed ration (TMR)-fed and fresh forage (FF)-fed cows. Next, we aimed to develop equations to predict UN based on animal factors [milk urea nitrogen (MUN; mg/dL) and body weight (BW, kg)] and to explore how these equations are improved when dietary factors, such as diet type, dry matter intake (DMI), or dietary characteristics [neutral detergent fiber (NDF) and crude protein (CP) content], are considered. A dataset was obtained from 51 published experiments composed of 174 treatment means. The whole dataset was used to evaluate the mean and linear biases of three existing equations including diet type as an interaction term; all models had significant linear and mean biases and two of the three models had poor predictive capabilities as indicated by their large relative prediction error (RPE; root mean square error of prediction as a percent of the observed mean). Next, the complete data set was split into training and test sets, which were used to develop and to evaluate new models, respectively. The first model included MUN and BW, and there was a significant interaction between diet type and the coefficients. This model had the worst 1:1 agreement [Lin’s concordance correlation coefficient (CCC) = 0.50] and largest RPE (24.7%). Models that included both animal and dietary factors performed the best, and when included in the model, the effect of diet type was no longer significant (p > 0.10). These models all had very good agreement (CCC ≥ 0.86) and relatively low RPE (≤13.1%). This meta-analysis developed precise and accurate equations to predict UN from dairy cows in both confined and pasture-based systems.

The absence of tumor necrosis factor (TNF) causes lethal infection by Leishmania major in normally resistant C57BL/6J (B6.WT) mice. The underlying pathogenic mechanism of this fatal disease has so far remained elusive. We found that B6.WT mice deficient for the tnf gene (B6.TNF−/−) displayed not only a non-healing cutaneous lesion but also a serious infection of the liver upon L. major inoculation. Infected B6.TNF−/− mice developed an enlarged liver that showed increased inflammation. Furthermore, we detected an accumulating monocyte-derived macrophage population (CD45+F4/80+CD11bhiLy6Clow) that displayed a M2 macrophage phenotype with high expression of CD206, arginase-1, and IL-6, supporting the notion that IL-6 could be involved in M2 differentiation. In in vitro experiments, we demonstrated that IL-6 upregulated M-CSF receptor expression and skewed monocyte differentiation from dendritic cells to macrophages. This was countered by the addition of TNF. Furthermore, TNF interfered with the activation of IL-6-induced gp130-signal transducer and activator of transcription (STAT) 3 and IL-4-STAT6 signaling, thereby abrogating IL-6-facilitated M2 macrophage polarization. Therefore, our results support the notion of a general role of TNF in the inflammatory activation of macrophages and define a new role of IL-6 signaling in macrophage polarization downstream of TNF.