Lmo-InlA-mur-lux infected A/J mice displayed high IFN-γ levels (F

Lmo-InlA-mur-lux infected A/J mice displayed high IFN-γ levels (Figure 5F) whereas C57BL/6J mice showed low serum concentrations for all of these cytokines and the CCL2 chemokine (Figure 5E-H). Thus, the elevated susceptibility of C3HeB/FeJ mice and their inability to control Listeria replication correlated with an exaggerated production of pro-inflammatory mediators. Serum levels of IL-10 were also high in

Lmo-InlA-mur-lux infected C3HeB/FeJ mice (data not shown). However, this apparently did not result in downregulation of pro-inflammatory responses. Figure 5 Chemokine and cytokine Geneticin production of different mouse inbred strains after oral CP673451 in vitro infection with Lmo-EGD-lux and Lmo-InlA-mur-lux. Female C3HeB/FeJ (A), A/J OlaHsd (B), BALB/cJ (C) and C57BL/6J mice (D) were orally infected with 5 × 109 CFU Lmo-EGD-lux or Lmo-InlA-mur-lux. Blood samples were collected at 3 and 5 d.p.i. and cytokine and chemokine levels were determined using Luminex bead assays. 3d and https://www.selleckchem.com/products/yap-tead-inhibitor-1-peptide-17.html 5d indicate Lmo-EGD-lux infected animals at 3 and 5 d.p.i., respectively; 3d mur and 5d mur indicate Lmo-InlA-mur-lux infected animals at these timepoints (n = 8). For each timepoint, chemokine and cytokine concentrations were determined in triplicate for each inbred mouse and L. monocytogenes strain. Data represent means

± SEM. (E-H) Comparison of chemokine and cytokine production across Lmo-InlA-mur-lux infected mice from the different inbred mouse strains at 5 d.p.i.. Shown are statistical significant differences of indicated cytokine and chemokine levels in the peripheral blood between groups of mice of the analysed inbred mouse strains. Data represent means ± SEM; *p < 0.05, non-parametric Mann–Whitney-U-test. One out of two representative experiments Temsirolimus price is shown (A-H). Oral infection with murinised Lmo-InlA-mur-lux is associated with increased induction of interferon-β An important factor which determines the virulence of Listeria monocytogenes is

the amount of type I interferons produced in the host during infection. High levels of interferon-β (IFN-β) have been demonstrated to be associated with host susceptibility to Listeria infection and mice deficient for IFN-β signalling components such as the type I interferon receptor (Ifnar) gene or the interferon regulatory factor 3 (Irf3) gene are more resistant to lethal L. monocytogenes infection [20–25]. Furthermore, variations in the induction of IFN-β responses in the host by different Listeria strains have been linked with differences in strain virulence [26–29]. To analyse and compare kinetics of Ifnb1 induction after intragastric infection challenge with Lmo-InlA-mur-lux and Lmo-EGD-lux we developed a dual luciferase detection model.

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