Consistent with our findings, a previous study showed that the parasite numbers in the livers of CCR5−/− mice were higher than those of the C57BL/6 wild-type animals, while the parasite numbers were similar in other organs of the WT and CCR5−/− mice [27]. Therefore, TgCyp18-mediated CCL5 production might contribute to macrophage migration to the site of infection and the

Selleckchem GDC-0994 transport of T. gondii-infected cells to the liver. Besides CCR5, CCL5 has been shown to interact with other receptors, including CCR3 and CCR1. Therefore, activation of CCR1- and CCR3-signaling may contribute to CCL5-mediated pathology during T. gondii infection. Hence, the chemokines up-regulated in CCR5−/− mice infected with RH-OE may play a crucial role in CCR5-independent macrophage migration. To test this idea in our study, the expression levels of chemokines related to macrophage migration were investigated. In vitro analysis showed that TgCyp18 increased the expression of CCL6 in a CCR5 independent manner. However, the in vivo data showed that a higher level of CCL6 was observed in the livers of the CCR5−/− mice infected RH-GFP at 3 dpi compared with those infected with RH-OE. Although we do not know the reason for the difference between the in vitro and in vivo data, it is possible that CCL6 expression might have been induced before 3 dpi in the livers of the CCR5−/−

mice infected with RH-OE. It is interesting to note that CCL2 expression was slightly increased in macrophages treated with recombinant TgCyp18. Moreover, the expression levels of CCL2 selleck and selleck screening library CXCL10 were significantly higher at 3 dpi in the livers of CCR5−/− mice infected with RH-OE compared with the uninfected mice. Thus, TgCyp18-mediated production of CCL2 and CXCL10 in the liver may trigger transport

of T. gondii-infected macrophages via a CCR2 and CXCR3-dependent mechanism, respectively. CCR2−/− mice have profound defects in monocyte recruitment although constitutive trafficking remains unaffected [28]. CCR2−/− mice or CCL2−/− mice failed to Metalloexopeptidase recruit Gr1+ inflammatory monocytes, which are required for mucosal resistance to T. gondii[29], or to control systemic toxoplasmosis by intraperitoneal infection [30]. Furthermore, another group reported that the CXCR3 ligands, CXCL9, CXCL10 and CXCL11, were induced markedly at the levels in the spleen, lung, and liver following infection with T. gondii[27]. Induction of these chemokines was similar in WT and CCR5−/− mice up to day 5 [27]. CXCL10 is required to maintain T-cell populations and to control parasite replication during chronic ocular toxoplasmosis [31]. These results suggest that CCR2 and CCL2, or CXCR3 and its ligands, play a crucial role in cell migration and control of T. gondii infection. Diana et al. [32] showed that a T. gondii excreted-secreted antigen induced recruitment and migration of human DCs in a CCR5-dependent fashion. Other studies in mice have reported that T.

03 Al2O3 27.76 Fe2O3 0.62 FeO 4.99 MnO 0.08 CaO 5.00 MgO 1.43 Na2O 0.14 K2O 0.90 Particle size distributions were obtained from the TEM micrographs. The particle size distributions of as-received and acetylene-treated coal fly ash (at different temperatures) were also determined using a Malvern particle size analyser (Master Sizer 2000, Malvern Instruments Ltd., Worcestershire, click here UK). Both these materials were analysed by dispersing them in two different solutions: (1) water and (2) a Dolapix solution (100 ml water:2 ml Dolapix (Zschimmer & Schwarz, Lahnstein, Germany)). Laser Raman spectroscopy was used to ascertain the

type of carbonaceous materials that were formed. The thermal stability of the acetylene-treated fly ash products was determined by using a PerkinElmer Pyris 1 thermogravimetric analyser (TGA; PerkinElmer, Waltham, MA, USA). In these measurements, a 10 mg sample was heated to 900°C at a rate of 10°C/min under air (20 ml/min). The specific surface areas

of approximately 200 mg of as-received and acetylene-treated fly ash materials (between 400°C and 700°C) were determined using the Brunauer-Emmett-Teller mTOR phosphorylation (BET) surface area method by N2 adsorption using an ASAP 2000 Micrometrics Tristar surface area and porosity analyser (Micromeritics Instrument Co., Norcross, GA, USA). Both materials were degassed at 150°C for 4 h under nitrogen before testing to remove the moisture. Mössbauer spectroscopy measurements were carried out in transmission mode with a 10 miC 57Co(Rh) source. Measurements were performed at room

temperature on the as-received and acetylene-treated fly ash samples at 700°C. Results and discussion Morphological studies The sizes, shapes and morphologies of the as-received and acetylene-treated fly ash were investigated using TEM. The results can be observed in Figure 1a,b,c,d,e,f. The as-received fly ash materials (Figure 1a) appeared to be spherically shaped. Fly ADP ribosylation factor ash agglomerates shaped like these have often been observed with inorganic salts and may be caused by inter-particulate fusion during the cooling of the fly ash [40]. In Figure 1b,c,d,e, it was observed that the glassy, smooth-shaped fly ash particles began to be coated with regularly and irregularly shaped CNFs when subjected to acetylene. In Figure 1c,d, it was noted that the types of CNMs that were formed varied from large CNFs to smaller CNTs. While the exact growth mechanism of CNTs/CNFs formed from fly ash as a catalyst has not been fully ascertained, it appeared that tip growth could not be discounted (as seen by the red-coloured circles in Figure 1e,f). This type of growth has typically been observed when either iron (Fe) or cobalt (Co) was used as a catalyst for CNM formation. While it is known from previous studies that at least 2.5% of iron is required as a catalyst for CNF STI571 mw formation when using fly ash [36], the XRF data (Table 1) obtained for the South African coal fly revealed that at least 5.

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