Experimental infection of Salmonella Enteritidis in quails submitted to forced molting by feed fasting

This study aimed at evaluating bacterial shedding, as detected in swabs, feces, and eggs of quails submitted to forced molting by feed fasting and experimentally infected with a Salmonella Enteritidis (SE) strain. In the experiment, 84 40-week-old Italian female quails were distributed in the following groups: FI (quails induced to molt by fasting and inoculated with Salmonella Enteritidis - SE); CI (quails fed with a laying diet and inoculated with SE); FNI (quails induced to molt by fasting and not inoculated with SE); and CNI (quails fed with a laying feed and not inoculated with SE). Feces, cloacal swabs, and eggs were collected on day 1, 3, 7 and 14 post-inoculation (dpi) and submitted to bacteriological analyses. All samples obtained from cloacal swabs were negative for SE. None of the quails of the non-inoculated groups (FNI and CNI) were positive for SE in the fecal samples. Among the inoculated quails, the FI group presented significantly higher (p< 0.05) SE shedding in the feces on 1 dpi than the CI group. On 4 dpi, no significant difference was observed (p< 0.05) in SE shedding between the inoculated quail groups. On 7 dpi, only the FI group shed SE in the feces, whereas on 14 dpi, none of the groups shed SE. According to the results, we concluded that quails submitted to molting by fasting have higher possibility of shedding SE in the feces

Cot/tpl2-MKK1/2-Erk1/2 controls mTORC1-mediated mRNA translation in Toll-like receptor-activated macrophages

Creative Commons Attribution Non-Commerical Share Alike 3.0 License.-- et al.Cot/tpl2 is the only MAP3K that activates MKK1/2-Erk1/2 in Toll-like receptor-activated macrophages. Here we show that Cot/tpl2 regulates RSK, S6 ribosomal protein, and 4E-BP phosphorylation after stimulation of bone marrow-derived macrophages with lipopolysaccharide (LPS), poly I:C, or zymosan. The dissociation of the 4E-BP-eIF4E complex, a key event in the cap-dependent mRNA translation initiation, is dramatically reduced in LPS-stimulated Cot/tpl2-knockout (KO) macrophages versus LPS-stimulated wild-type (Wt) macrophages. Accordingly, after LPS activation, increased cap-dependent translation is observed in Wt macrophages but not in Cot/tpl2 KO macrophages. In agreement with these data, Cot/tpl2 increases the polysomal recruitment of the 5´ TOP eEF1α and eEF2 mRNAs, as well as of inflammatory mediator gene-encoding mRNAs, such as tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and KC in LPS-stimulated macrophages. In addition, Cot/tpl2 deficiency also reduces total TNFα, IL-6, and KC mRNA expression in LPS-stimulated macrophages, which is concomitant with a decrease in their mRNA half-lives. Macrophages require rapid fine control of translation to provide an accurate and not self-damaging response to host infection, and our data show that Cot/tpl2 controls inflammatory mediator gene-encoding mRNA translation in Toll-like receptor-activated macrophages.This work was supported by SAF 2011-24481 and Mutua Madrileña grants to S.A. and by FIS 2009-80145 and Universidad Autónoma de Madrid CM-CCG10-4911 grants to G.S. PD 0325901 was a gift from Philip Cohen, rapamycin was from Victor Calvo, and the biscitronic pcDNA3rLuc-polIRESfLuc plasmid was generously provided by Alexey Benyumov. M.L.P. is a recipient of an FPU Fellowship from the Universidad Autónoma de Madrid. S.G. holds a research contract from the Ramón y Cajal Program of Spain.Peer reviewe