Occasional plasma membrane rupture and cell collapse were seen. And a small amount of apoptotic cells could also be seen: cell volume reduced, matrix electron density increased, nuclear membrane invaginated, chromatin agglutinate until broken into many small pieces. Cell plasma membrane inward shrunk with the formation

of apoptotic bodies in which nuclear materials were visible. No significant changes in cell morphology occurred in the other three control groups (Fig. 4). Figure 4 The morphologic changes of each group cells observed by electromicroscope. Antisense group showed more cell degeneration and necrosis, with cell volume enlargement, chromatin margination and dissolving and lipid droplets within the cytoplasm increase, endoplasmic

reticulum dilation, and swelling of mitochondria Stem Cells inhibitor like vacuoles. Occasional plasma membrane rupture and cell collapse were also seen. (a: control group(original magnification × 10000 b: antisense group(original magnification × 4000). To further confirm the increasing apoptosis rate, we used flow cytometry to measure cell apoptosis. The results showed cell apoptosis rate of antisense group with Livin ASODN transfection (46.39 ± 9.23) % was significantly higher than PBS group (4.54 ± 1.84) %, liposome group (5.70 ± 1.61)%, and missense groups (5.10 ± 1.56)% with P < 0.01. The apoptosis rates of the latter three groups INK 128 purchase had no significant Obatoclax Mesylate (GX15-070) difference, P > 0.05. (Fig. 5). Figure 5 Cell apoptosis rate measurement. Antisense group showed increase of cell apoptosis rate (46.39 ± 9.23) %, while the other three groups did not have significant difference. *, p < 0.05. Cellular caspase3 activities were increased after transfection with Livin

ASODN As Caspase3 is an important apoptosis inducing kinase, we next detect the Caspase 3 activity in bladder cancer cells after transfect with Livin ASODN. Results of Caspase3 activity kinase method showed that after Livin ASODN transfection into 5637 cells, the Caspase3 activity was significantly increased with the relative activity of 0.062 ± 0.018 (fig 6). Compared with missense group (0.025 ± 0.011), liposome group (0.029 ± 0.016) and PBS group (0.032 ± 0.016), the difference was significant with P < 0.05. The latter three groups had no significant difference, P > 0.05. all this result indicated that Livin ASODN may through increasing Caspase 3 activity to induce bladder cancer cell apoptosis and thus inhibit its growth. Figure 6 Caspase3 activities in the cells of each group. The results of kinase method to detect Caspase3 activity showed that after Livin ASODN transfection with 5637 cells, the Caspase3 activity was significantly increased with the relative activity of 0.062 ± 0.018.

From Figure  7a, the resistances of Hy-rGO-based sensors could be calculated to be 12.3, 14.5, and 89.3 KΩ, respectively, when the assembly concentrations of GO were 1, 0.5, and 0.25 mg/mL. When the concentration was above 0.5 mg/mL, the resistances this website of the sensing devices had little changes. However, when the assembly concentration of GO solution decreased to 0.25 mg/mL, the resistance of the resultant device increased greatly. This might be due to the crack of the rGO sheets

during the reduction process, which inevitably destroyed the electrical circuit of the device. Similar situations occurred for Py-rGO devices, as shown in Figure  7b, the resistances of the devices were 13.5 and 28.2 KΩ respectively when the assembly concentrations of GO solution were 1 and 0.5 mg/mL. Further decrease of GO concentration to 0.25 mg/mL resulted in rapid increase of resistance of the resultant Py-rGO device (8.3 MΩ). This value was much higher than the resistances of Hy-rGO-based devices. This might be ascribed to the following two reasons: (1) hydrazine was a stronger reducing agent during the reduction process, and as a result, the resistances of the resultant Hy-rGO devices were generally lower than those of Py-rGO devices, and this was also in agreement with the results as shown in Figure  7a,b; (2) much more cracks existed during FK506 concentration the reduction

process when pyrrole was used as a reducing agent. This could be proved by the SEM images as shown in Figure  5e,f; comparing with Hy-rGO devices (as shown in Figure  4e, f), much more cracks appeared, which had great effects on the final resistances of the resultant rGO devices. Figure 7 The comparison of sensing properties of devices based on assembled rGO sheets. I-V curves of sensing devices based on Hy-rGO (a) and Py-rGO (b) fabricated with GO assembly concentration

at 1, 0.5, and 0.25 mg/mL. Plot of normalized resistance change versus time for the sensing devices based on Hy-rGO (c) and Py-rGO (d) fabricated with GO assembly concentration at 1, 0.5, and 0.25 mg/mL (the concentration of NH3 gas is 50 ppm). NH3, a toxic gas, is very harmful to human health [47], and it is import to develop ammonia gas sensors and monitor for NH3 leaks. to Hence, we used NH3 here as analyte in order to probe the sensing properties of the resultant Hy-rGO- and Py-rGO-based sensors. All of the sensors based on Hy-rGO and Py-rGO, which were fabricated with different assembly concentrations of GO solution, were tested toward 50 ppm NH3 balanced in synthetic air. The sensor response (R) toward NH3 gas was calculated according to the following equation: (2) where R 0 is the resistance of rGO device before the exposure to NH3 gas, and R gas is the resistance of rGO device in the NH3/air mixed gas [29].

Science. 1998;279:509–14.PubMedCrossRef 20. Joberty G, Peterson C, Gao L, Macara IG. The cell polarity protein par6 links par3 and atypical protein kinase C to Cdc42. Nat Cell Biol. 2000;2:531–9.PubMedCrossRef 21. Saito S, Tatsumoto T, Lorenzi MV, Chedid M, Kapoor V, Sakata H, et al. Rho exchange factor ECT2 is induced by growth factors and regulates cytokinesis through the N-terminal cell cycle regulator-related domains. J Cell Biochem. 2003;90:819–36.PubMedCrossRef 22. Rojas R, Ruiz WG, Leung SM, Jou TS, Apodaca G. Cdc42-dependent

modulation of tight junctions and membrane protein traffic in polarized Madin–Darby canine kidney cells. click here Mol Biol Cell. 2001;12:2257–74.PubMed 23. Hughson MD, Johnson K, Young RJ, Hoy WE, Bertram JF. Glomerular size and glomerulosclerosis: relationships to disease categories, glomerular solidification, and ischemic obsolescence. Am J Kidney Dis. 2002;39:679–88.PubMedCrossRef”
“Introduction Recently, several large cohort studies investigating renal anemia therapy have highlighted the biologically

plausible, but erroneous assumption that the normalization of hemoglobin (Hb) iron should attenuate cardiovascular disease risks and lead to a decline in the mortality rate of patients with chronic kidney disease (CKD), both before and after the initiation of maintenance hemodialysis (MHD) treatment [1–4]. Erythropoiesis stimulating agent see more (ESA) treatment decisions and guidelines based on the questionable assumption that Hb should be normalized or nearly normalized in the majority of CKD patients need to be reconsidered [5]. The development of safe and effective strategies aimed at obtaining better patient survival remains a challenge. In recent years, high-dose intravenous (IV) iron supplementation Protirelin has become the standard of care; however, there are concerns as to whether this is the right approach. Recent studies on the mechanisms involved in iron metabolism have revealed that hepcidin is a master regulator of systemic iron availability [6, 7]. To maintain iron homeostasis, hepcidin tightly controls duodenal

iron absorption and iron recycling from senescent erythrocytes by tissue macrophages. Hepcidin is the principal hormone responsible for the physiological regulation of iron balance as well as its control in a variety of pathologic conditions, including the anemia of chronic disease (ACD). In this review, we address the mechanisms whereby pharmacological iron supplementation, especially via the IV route, may reduce the body’s capacity to absorb iron from the gut and to reutilize iron from endogenous sources [8], with particular focus on the importance of hepcidin in this process. ESA hyporesponsiveness Although normal or near-normal Hb levels in CKD patients were associated with reduced mortality in many observational studies [9–11], recent evidence from randomized clinical trials does not support a beneficial effect of Hb normalization on survival.

These transmission routes are in agreement with both the incongruent evolutionary history of Asaia and its host species, and with the high frequency of infections with multiple Asaia strains in mosquitoes [21]. However, very little is

known about the rate and mechanisms of horizontal transfer of Asaia in hemipterans like S. titanus. Horizontal transfer in this species has been only indirectly demonstrated by the capability of Asaia to be established in leafhopper individuals fed with bacterial cells and by the ability to colonize insect salivary glands [2]. The exploitation of symbiotic microorganisms of insect vectors is recently emerging as a strategy to limit the diffusion of arthropod-borne diseases through the development of “symbiotic Selleck beta-catenin inhibitor control” strategies [22]. This approach could represent a promising alternative to current FD control methods, which are limited to the use of chemical insecticides and to the removal of infected plants. To set up a symbiotic control strategy, a microbial symbiont that meets the requirements needed for a control agent must be firstly identified. Such requirements include stable association with the vector,

selleckchem dominance within its microbial community, co-localization with the pathogen, predisposition to in vitro manipulation, and, last but not least, an efficient spread system within insect populations [23]. Asaia and other acetic acid bacteria have such features in relation to dipteran mosquitoes, so they have been indicated as potential agents for natural or paratransgenic symbiotic control [4, 6, 24]. However, the capacity of Asaia to be transmitted horizontally among S. titanus has not been yet investigated. The objective of this work was to evaluate

whether Asaia is horizontally transmitted among S. titanus individuals by the oral and the venereal transmission routes. This could contribute to the evaluation of the ecology of this acetic acid bacterium in leafhopper populations. Results and discussion Donor insects Insects destined to test transmission of infection (‘donors’) were of infected with a marked strain of Asaia. To this end, donors were fed with diets added of Gfp-tagged Asaia for 48 hours and then allowed to release the symbiont for 48 hours in diets supplemented with kanamycin. Afterwards the diets, in which Gfp-tagged Asaia was released, were exposed to recipient individuals for 24, 48, 72 and 96 hours, respectively. At the same time, the 98 individuals used as donor specimens were collected to be tested in q-PCR. All of them were positive for the gfp gene, with an average titre of 1.1 × 106 gfp gene copies / pg of insect 18S rRNA gene (Figure 1, Table 1). Furthermore, Gfp Asaia represented 12.

The genomic DNA of these collected isolates was then extracted for polymerase chain reaction to verify the cagA-genotype by primers used in our published article [19]. To analyze the p-CagA intensity of each strain, H. pylori strains (2 × 108 cells) were suspended in 0.5 mL of phosphate-buffered saline (PBS) and were co-cultured with 2 × 106 AGS cells at a multiplicity of infection (MOI) of 100 for 5 hours. Afterward, the culture medium was removed and the AGS cells were lysed after five times washing with PBS. The AGS lysates were applied to SDS-PAGE gel electorphoresis

and transferred to membranes for western blots analysis. A phosphorylated tyrosine antibody and anti-actin antibody (Santa Cruz Biotechnology, selleck inhibitor Inc, Santa Cruz, CA) were used to detect the p-CagA and β-actin proteins. A clinical H. pylori strain (Hp830) which had a strong p-CagA band in the western blots was used as reference. In each western blots procedure, 7-9 clinical strains and the selleck chemicals reference strain were analyzed in the same run. The relative immunoblot density of the p-CagA and β-actin proteins were quantitated by scanning the images on a gel analysis system (BioSpectrum AC Imaging System, Vision Work LS software, Upland, CA) for each strain and defined as [p-CagA] and [Bactin]. The amount of p-CagA and β-actin proteins of the reference strain in the same run were also semi-quantified as reference and defined as [p-CagA-ref]

and [Bactin-ref]. The p-CagA intensity HSP90 of each strain was calculated by the formula: p-CagA value = ([p-CagA]/[Bactin])/([p-CagA-ref]/[Bactin-ref]). Strains with a p-CagA value <0.2, 0.2-0.8, and >0.8 were defined as sparse, weak, and strong p-CagA intensity. The immunoblot gel imaging of the representative

strain in each subgroup and the reference strain (Hp830) were showed in Figure 1. Figure 1 The p-CagA and β-actin immunoblot gel imaging of the reference strains (Hp830) and the representative strain in each subgroup. Statistical analysis SPSS software version 12.0 for Windows (SPSS Inc., Chicago, IL) was used for the statistical analysis. The differences in the p-CagA intensity among the subgroups of patients were analyzed by Pearson chi-square test. The odds ratio on the risk of IM and corpus-predominant gastritis between the different subgroups were analyzed by the logistical regression. All tests were two-tailed, and a p value less than 0.05 were considered significant. Results H. pylori isolates with diverse p-CagA intensity From the 469 patients, we sampled 146 strains for the analysis of the p-CagA intensity. The clinical characteristics of these patients were shown in Table 1. In each sampled group, age and gender were matched between the sampled patients and the entire group of patients (p = NS). All of the 146 enrolled H. pylori isolates were cagA-genopositive and the p-CagA intensity was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates.

We observed two main differences in relation to earlier experiments:

(i) previously [19], waves have been observed to either reflect, refract or collapse (depending on the agar concentration, pH and strains used) but not to split into simultaneous combinations of these options. We observe that all three outcomes are simultaneously possible at a single collision, although there is a large variation buy Galunisertib between experiments in the distribution of the incoming wave over these components (Figure 3); (ii) previously [38], it has been observed that a localized population (formed after a collision) can emit a reflected wave after about one hour (a timescale which has been argued to be required by the cells to switch to a different nutrient). In contrast, the reflected waves observed in our devices reverse direction within 10 minutes, without first forming an observable stationary population. Driven by the results described above we designed a third type of device

(type-3; Figure 5A) with which we demonstrated that traveling populations confined to separate, but chemically coupled, habitats still influence each others Protease Inhibitor Library cell assay colonization dynamics and exhibit “collisions”, despite having exclusive access to vacant patches (Figure 5). This shows that chemical interactions are the main mechanisms underlying the collision patterns of colonization waves as well as of expansion fronts. These interactions could possibly be mediated by small diffusible molecules. Using a typical diffusion constant of D = 5·10−6 cm2/s for such molecules, we find that diffusion between the two coupled habitats takes place on the order of 0.1 s, while the diffusional Ibrutinib range at the time-scales probed in this study (i.e. 10 min) is on the order of 1 mm (i.e. 7 patches). Therefore diffusible molecules could indeed be involved in the observed interactions of population waves and in the short-range interactions between population fronts. The long distance interactions (over

~1 cm, Figure 4E,F) however, happen at time scales much faster (~1 h) than those of diffusion (~15 h). These interactions might therefore be mediated by different mechanisms. Nevertheless, it is likely that at least the short range (d ~ 1 mm) interactions are caused by some form of habitat conditioning (e.g. consumption of nutrients, excretion of metabolites, chemoattractants and/or repellents) and/or by cell-signaling. It is interesting to note that when two strains are co-cultured together before inoculation, they colonize a habitat together and form a mixed metapopulation (Figure 4G and Additional file 7). In contrast, if the strains are cultured independently and invade the habitat from opposite ends, they form two distinct and competing metapopulations that do not mix when they meet in the habitats (Figure 4).

Understanding systems biology as adjustable size may

break through the barrier of complex tumor-stroma-interactions in a therapeutically relevant way: Comparatively high efficacy at moderate toxicity. Structured systems-directed Selleckchem Z-VAD-FMK therapies in metastatic cancer may get a source for detecting tumor-associated complex aggregated action effects as adjustable sizes available for targeted biomodulatory therapies. Poster No. 201 The Distribution of Markers of Drug Effect Following Chemotherapy and Hypoxia-Activated Pro-Drug Treatment Jasdeep K. Saggar 1 , Ian F Tannock1 1 Division of Applied Molecular Oncology and Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada Previous work from our laboratory has used quantitative immunohistochemistry (IHC) to show limited distribution from tumour blood vessels of the auto-fluorescent drugs doxorubicin and mitoxantrone. Analysis of the distribution of other anticancer drugs is more difficult because most are not fluorescent, and they are not recognized directly by available antibodies. Here we investigate the use of IHC to determine the

distribution of markers of drug effect, and compare that to the distribution of the fluorescent drugs mitoxantrone and AQ4N/AQ4. AQ4N is an inactive pro-drug that is selectively bioreduced www.selleckchem.com/products/Maraviroc.html in hypoxic environments to the cytotoxic metabolite, AQ4; it is structurally related to mitoxantrone, and like mitoxantrone binds with high affinity to DNA, and inhibits topoisomerase II. We have shown that AQ4N/AQ4 accumulates selectively in hypoxic regions of tumours (Tredan et al, Cancer Res 2009;69:940–7) Here, we use quantitative IHC to analyse the spatial distribution of the following molecular markers of drug effect in relation to blood vessels (recognized

by an antibody to CD31) and regions of hypoxia (recognized by an antibody to EF5) of tumours treated with mitoxantrone alone, AQ4N alone, or these drugs in combination: cleaved caspase 3 (a marker of apoptosis), gammaH2AX (a marker of DNA damage) and Ki67 (a marker of cell proliferation). Preliminary data show that compared to controls, mitoxantrone Clomifene treatment causes perivascular apoptosis, while AQ4N-treated tumours have greater levels of apoptosis farther away from blood vessels. Similarly, gammaH2AX staining is increased in drug-treated tumours compared to untreated tumours, and AQ4N-treated tumours show greater gammaH2AX activation farther away from blood vessels. Quantitative statistical analysis of the distributions of markers of drug effect in relation to tumour blood vessels and to regions of tumour hypoxia is in progress, and will be compared to the fluorescence distributions of mitoxantrone and AQ4N/AQ4. Poster No.

Overall, these studies revealed presence of two clonal

groups among biovar 1A strains. These studies also showed that clinical and non-clinical serotype O:6,30-6,31 (biovar 1A) strains clustered into two separate groups but failed to reveal any unequivocal associations between genotypes and the source of isolation. Multilocus enzyme electrophoresis (MLEE) is an important tool used to study genetic relationships where allelic variations in housekeeping genes are indexed using electrophoretic mobilities of corresponding enzymes [20, 21]. The technique has been used to study epidemiology of several pathogenic bacteria [22–26]. Multilocus restriction typing (MLRT), a recently developed tool, analyses restriction fragment length polymorphism of several housekeeping https://www.selleckchem.com/products/bmn-673.html genes [27–29]. The objective of this study was to use MLEE and MLRT to gain further insight

into the genetic heterogeneity and relationships among clinical and non-clinical strains of Y. enterocolitica biovar 1A. Methods Bacterial strains Eighty one strains of Y. enterocolitica biovar 1A were examined in this study. Of these, sixty-five were isolated from clinical and non-clinical sources in India viz. diarrheic human patients (35), wastewater (18), swine (7) and pork (5) [30–32]. All isolates have been authenticated, and deposited with Yersinia National Reference Laboratory this website and WHO Collaborating Centre, Institut Pasteur, Paris (France). Of the remaining 16 isolates, ten were obtained from Elisabeth Carniel (Yersinia National Reference Laboratory and WHO Collaborating Centre, Institut Pasteur, Paris, France) and six from Jürgen Heesemann (Max von Pattenkofer Institute, Munich, Germany). Y. enterocolitica 8081 (biovar 1B, serotype O:8), kindly provided by Mikael Skurnik (Haartman Institute, Finland) was used

as the reference strain for both MLEE and MLRT. The serotypes, sources of isolation, country of origin and reference laboratory accession numbers of these strains have been reported previously [17]. All strains were maintained as glycerol stocks at -40°C. Multilocus enzyme electrophoresis (MLEE) The enzyme Axenfeld syndrome extracts were prepared as per the method described by Selander et al [20]. Briefly, cultures grown overnight in tryptone soy broth (TSB) were harvested by centrifugation at 10,000 g for 10 min at 4°C. The cells were washed twice in potassium phosphate buffer (0.15 M, pH 7.0) and the pellet was resuspended in 2 ml of buffer (10 mM Tris-HCl, 1 mM EDTA and 0.5 mM NADP, pH 6.8). The bacteria were lysed by sonication (Sonics) on ice and centrifuged at 13,000 g for 30 min at 4°C to obtain the supernatant (enzyme extract), which was stored in aliquots of 200 μl each at -40°C until use. The enzyme extracts were subjected to horizontal gel electrophoresis in 0.

The adapted SHIME consisted of a succession of three reactors: the first two reactors are of the fill-and-draw principle to simulate different steps in food uptake and digestion by simulating, respectively, stomach and small intestine; the last compartment, simulating the ascending colon (AC), was a continuously stirred reactor with constant volume, pH control and inoculation with fecal IWR-1 purchase microbiota. As described in more detail in the ‘Methods’ section, two HMI modules were connected to the AC vessel of the SHIME during the last three days of the control and of the treatment week

(Figures 3 and 4). Figure 3 Scheme of the adapted SHIME system (consisting of stomach, small intestine and ascending colon – AC – compartments) used for the long-term study. Two HMI modules have Selleckchem Cabozantinib been connected in parallel to the vessel simulating the AC compartment in order to obtain information on bacterial adhesion and host response after 24 and 48 h. The SHIME system was fed three times per day with SHIME feed; the medium in the lower compartment of the HMI modules (containing Caco-2 cells) was fully replaced every 6 hours by means of an automatic pump. The exhausted medium

was collected in order to analyze the concentration of IL-8. Figure 4 Scheme of the long-term experiment and of the relative sampling points for the different analyses. The experiment consisted of a 2-week startup period, 1-week control and 1-week treatment. The HMI modules were connected to the ascending colon compartment of a SHIME system during the last 3 days of the control and treatment periods. Samples from the lumen of the SHIME were collected for SCFA and DNA analyses. Samples from the surface of the double functional layer of the HMI modules were collected for DNA analyses. Samples from the lower compartment of the HMI module were collected for IL-8 measurements. DNA = qPCR and DGGE. DNA* = qPCR, DGGE and FISH (the latter only at 48 h). Considering the average of three sampling points

in the SHIME experiment (Figure 4), the treatment with the dried-fermented yeast product induced enough a 35% increase in total short chain fatty acids (SCFA) production in the lumen of the simulated AC (from 73.6 ± 1.4 to 99.7 ± 3.5 mmol/L) with a 41% increase of acetate (from 37.8 ± 2.4 to 53.2 ± 2.4 mmol/L), a 6% increase of propionate (from 17.0 ± 1.0 to 18.1 ± 1.1 mmol/L) and a 31% increase of butyrate (from 13.6 ± 0.5 to 17.8 ± 0.6 mmol/L) (p < 0.05). Quantitative PCR data at luminal level in the AC showed that at the moment of connecting the HMI module to the SHIME during the treatment period, the concentration of all the analysed microbial groups was lower as compared to the respective time point during the control period. Despite this, at the end of the 48 h-treatment period, the bacteria concentration of all groups were equal or higher than the respective sampling points during the control period (Table 2).

A) Representative micrographs of Hematoxylin- and Eosin-stained lung sections from mice 42 h after infection. Note that the high statin fed mice exhibit reduced cellularity and vascular hemorrhage. Original magnification, 10X. B) Vascular integrity was determined by assessing the amount of albumin present in the BAL fluid by ELISA prior to and following infection (n = 3/group for uninfected and n = 6/group for infected mice). Data are presented as the mean ± SEM. Statistics were determined by a two-tailed student’s t-test. P < 0.05 was considered significant in comparison to Control fed mice. We subsequently

examined the impact of oral simvastatin therapy R428 order on development of bacteremia. Following intratracheal challenge at 24 hpi, bacterial titers in the blood were not significantly different among all three groups tested; although mice receiving HSD had lower median titers compared to mice on the control diet (P = 0.12) (Figure 3). Between 24 and 36 h, pneumococcal titers in the blood increased at a similar rate for all see more mice, nonetheless mice on HSD had significantly fewer pneumococci in their blood compared to control mice (P = 0.007). After

36 h, mice receiving the control diet continued to experience bacterial replication whereas those on a simvastatin diet maintained or began to clear bacteria from the blood. At 42 hpi, mice on the HSD continued to have significantly less bacterial titers in the blood compared to control fed mice (P = 0.03). Figure 3 Mice on simvastatin prophylaxis show enhanced protection from bacteremia. Bacterial titers in the blood of challenged mice 24, 36 and 42 h after infection. Mice on Control (n = 11), Low (n = 11) or High (n = 12) diet were challenged intratracheally with 1 X 105 cfu. Mice receiving statins

had significantly fewer bacteria in the blood. Data are presented as the mean ± SEM. Statistics were determined by a two-tailed student’s t-test. P < 0.05 was considered significant. High-dose simvastatin reduces chemokine production in the lungs Statins have been reported to reduce cytokine Myosin production following LPS stimulation of monocytes and decrease lung inflammation following instillation of LPS in healthy human volunteers [18, 19]. Thus we investigated the effect of simvastatin therapy on the local and systemic production of cytokines and chemokines during pneumococcal pneumonia. At 24 hpi, before bacterial titers in the lungs were significantly different, no differences were observed for TNFα, IL-6, IL-10, IL-12, MCP-1, KC and IFNγ in the BAL fluid or serum of mice on LSD versus controls (Figure 4A, B). In contrast, mice on HSD had significant reductions in MCP-1 (P = 0.03) and KC (P = 0.02) in the BAL fluid but not serum. No differences were observed for all other cytokines or chemokines in the BALF or in the serum of HSD mice.