Physical properties of Herschel selected galaxies in a semi-analytic galaxy formation model

[Abridged] We make use of a semi-analytic cosmological model that includes simple prescriptions for dust attenuation and emission to make predictions for the observable and physical properties of galaxies that may be detected by the recently launched Herschel Space Observatory in deep fields such as GOODS-Herschel. We compare our predictions for differential galaxy number counts in the PACS (100 & 160) and SPIRE (250, 350, and 500 micron) bands with available observations. We find very good agreement with the counts in the PACS bands, for the overall counts and for galaxies binned by redshift at z< 2. At z > 2 our model underpredicts the number of bright galaxies by a factor of ten. The agreement is much worse for all three SPIRE bands, and becomes progressively worse with increasing wavelength. We discuss a number of possible reasons for these discrepancies, and hypothesize that the effect of blending on the observational flux estimates is likely to be the dominant issue. We note that the PACS number counts are relatively robust to changes in the dust emission templates, while the predicted SPIRE number counts are more template dependent. We present quantitative predictions for the relationship between the observed PACS 160 and SPIRE 250 micron fluxes and physical quantities such as halo mass, stellar mass, cold gas mass, star formation rate, and total infrared (IR) luminosity, at different redshifts. We also present quantitative predictions for the correlation between PACS 160 micron flux and the probability that a galaxy has experienced a recent major or minor merger. Although our models predict a strong correlation between these quantities, such that more IR-luminous galaxies are more likely to be merger-driven, we find that more than half of all high redshift IR-luminous galaxies detected by Herschel are able to attain their high star formation rates without enhancement by a merger.Comment: Accepted for publication in MNRA

Effects of Lactobacilli on Cytokine Expression by Chicken Spleen and Cecal Tonsil Cells▿

Lactobacillus acidophilus, Lactobacillus reuteri, and Lactobacillus salivarius are all normal residents of the chicken gastrointestinal tract. Given the interest in using probiotic bacteria in chicken production and the important role of the microbiota in the development and regulation of the host immune system, the objective of the current study was to examine the differential effects of these bacteria on cytokine gene expression profiles of lymphoid tissue cells. Mononuclear cells isolated from cecal tonsils and spleens of chickens were cocultured with one of the three live bacteria, and gene expression was analyzed via real-time quantitative PCR. All three lactobacilli induced significantly more interleukin 1β (IL-1β) expression in spleen cells than in cecal tonsil cells, indicating a more inflammatory response in the spleen than in cecal tonsils. In cecal tonsil cells, substantial differences were found among strains in the capacity to induce IL-12p40, IL-10, IL-18, transforming growth factor β4 (TGF-β4), and gamma interferon (IFN-γ). In conclusion, we demonstrated that L. acidophilus is more effective at inducing T-helper-1 cytokines while L. salivarius induces a more anti-inflammatory response

TLR ligands induce antiviral responses in chicken macrophages.

Chicken macrophages express several receptors for recognition of pathogens, including Toll-like receptors (TLRs). TLRs bind to pathogen-associated molecular patterns (PAMPs) derived from bacterial or viral pathogens leading to the activation of macrophages. Macrophages play a critical role in immunity against viruses, including influenza viruses. The present study was designed to test the hypothesis that treatment of chicken macrophages with TLR ligands reduces avian influenza replication. Furthermore, we sought to study the expression of some of the key mediators involved in the TLR-mediated antiviral responses of macrophages. Chicken macrophages were treated with the TLR2, 3, 4, 7 and 21 ligands, Pam3CSK4, poly(I:C), LPS, R848 and CpG ODN, respectively, at different doses and time points pre- and post-H4N6 avian influenza virus (AIV) infection. The results revealed that pre-treatment of macrophages with Pam3CSK4, LPS and CpG ODN reduced the replication of AIV in chicken macrophages. In addition, the relative expression of genes involved in inflammatory and antiviral responses were quantified at 3, 8 and 18 hours post-treatment with the TLR2, 4 and 21 ligands. Pam3CSK4, LPS and CpG ODN increased the expression of interleukin (IL)-1β, interferon (IFN)-γ, IFN-β and interferon regulatory factor (IFR) 7. The expression of these genes correlated with the reduction of viral replication in macrophages. These results shed light on the process of immunity to AIV in chickens

Selected lactic acid-producing bacterial isolates with the capacity to reduce Salmonella translocation and virulence gene expression in chickens.

BACKGROUND:Probiotics have been used to control Salmonella colonization/infection in chickens. Yet the mechanisms of probiotic effects are not fully understood. This study has characterized our previously-selected lactic acid-producing bacterial (LAB) isolates for controlling Salmonella infection in chickens, particularly the mechanism underlying the control. METHODOLOGY/PRINCIPAL FINDINGS:In vitro studies were conducted to characterize 14 LAB isolates for their tolerance to low pH (2.0) and high bile salt (0.3-1.5%) and susceptibility to antibiotics. Three chicken infection trials were subsequently carried out to evaluate four of the isolates for reducing the burden of Salmonella enterica serovar Typhimurium in the broiler cecum. Chicks were gavaged with LAB cultures (10(6-7) CFU/chick) or phosphate-buffered saline (PBS) at 1 day of age followed by Salmonella challenge (10(4) CFU/chick) next day. Samples of cecal digesta, spleen, and liver were examined for Salmonella counts on days 1, 3, or 4 post-challenge. Salmonella in the cecum from Trial 3 was also assessed for the expression of ten virulence genes located in its pathogenicity island-1 (SPI-1). These genes play a role in Salmonella intestinal invasion. Tested LAB isolates (individuals or mixed cultures) were unable to lower Salmonella burden in the chicken cecum, but able to attenuate Salmonella infection in the spleen and liver. The LAB treatments also reduced almost all SPI-1 virulence gene expression (9 out of 10) in the chicken cecum, particularly at the low dose. In vitro treatment with the extracellular culture fluid from a LAB culture also down-regulated most SPI-1 virulence gene expression. CONCLUSIONS/SIGNIFICANCE:The possible correlation between attenuation of Salmonella infection in the chicken spleen and liver and reduction of Salmonella SPI-1 virulence gene expression in the chicken cecum by LAB isolates is a new observation. Suppression of Salmonella virulence gene expression in vivo can be one of the strategies for controlling Salmonella infection in chickens

Expression of Antimicrobial Peptides in Cecal Tonsils of Chickens Treated with Probiotics and Infected with Salmonella enterica Serovar Typhimurium ▿

Several strategies currently exist for control of Salmonella enterica serovar Typhimurium colonization in the chicken intestine, among which the use of probiotics is of note. Little is known about the underlying mechanisms of probiotic-mediated reduction of Salmonella colonization. In this study, we asked whether the effect of probiotics is mediated by antimicrobial peptides, including avian beta-defensins (also called gallinacins) and cathelicidins. Four treatment groups were included in this study: a negative-control group, a probiotic-treated group, a Salmonella-infected group, and a probiotic-treated and Salmonella-infected group. On days 1, 3, and 5 postinfection (p.i.), the cecal tonsils were removed, and RNA was extracted and used for measurement of avian beta-defensin 1 (AvBD1), AvBD2, AvBD4, AvBD6, and cathelicidin gene expression by real-time PCR. The expressions of all avian beta-defensins and cathelicidin were detectable in all groups, irrespective of treatment and time point. Probiotic treatment and Salmonella infection did not affect the expression of any of the investigated genes on day 1 p.i. Furthermore, probiotic treatment had no significant effect on the expression of the genes at either 3 or 5 days p.i. However, the expression levels of all five genes were significantly increased (P < 0.05) in response to Salmonella infection at 3 and 5 days p.i. However, administration of probiotics eliminated the effect of Salmonella infection on the expression of antimicrobial genes. These findings indicate that the expression of antimicrobial peptides may be repressed by probiotics in combination with Salmonella infection or, alternatively, point to the possibility that, due to a reduction in Salmonella load in the intestine, these genes may not be induced

Real-time RT-PCR primer sequences for chicken target genes.

<p>Real-time RT-PCR primer sequences for chicken target genes.</p

The replication of low pathogenic H4N6 AIV in chicken macrophages (MQ-NCSU cell line).

<p>Chicken macrophages were infected with low pathogenic H4N6 AIV at a MOI of 1. Cell supernatants were collected at 0, 6, 16, 24, 31 and 42 hours post-infection. This figure is representative of three separate experiments with four biological replicates per time point. Virus titre is represented by the log₁₀ TCID₅₀. Significant differences (<i>P</i> ≤ 0.05) between the viral titer at a specific time point and the time of infection (time 0) are indicated by an *.</p

Expression levels of MHC class II, CD80 and CD86 on chicken macrophages stimulated with TLR ligands.

<p>MQ-NCSU cells were stimulated with LPS from <i>E. coli</i> 026∶B6 (1 µg/ml), Pam3CSK4 (10 µg/ml), class B CpG ODN 1826 (10 µg/ml), control ODN (10 mg/ml) or medium (no stimulation) for 24 hours. The cells were stained with FITC conjugated anti-chicken MHC class II molecules (Clone 2G11-IgG1), Alexa Fluor 647-conjugated mouse anti-chicken CD80 (clone AV82- IgG2a), Alexa Fluor 647-conjugated mouse anti-chicken CD86 (clone AV88- IgG1) or isotype controls.</p