Taxonomic composition of the microbiome is altered upon burn injury.

Sunburst plots show the most abundant taxa at the phylum (A) and family (B) level in the cecum (data shown as means). Differentially abundant strains (C) were considered significant if their FDR-corrected p-value was less than or equal to 0.05 and the absolute value of the log-2 fold change was greater or equal to 1. Points at either end of the x-axis indicate infinite log-2 fold change (the other groups mean abundance is 0). 59 strains were tested and only the 9 significantly different strains are displayed.</p

Burn injury severely impacts overall health on post burn day 1.

Body weight (A) of mice was determined before and one day after burn or sham injury. Data are presented as weight change in g. Spleen-to-body weight ratios (B) were also determined. Serum G-CSF (C) and serum IL-6 (D) levels of the same mice were quantified by cytometric bead assay. For all experiments, each replicate is plotted (n = 7 mice/group), as well as mean ± SD. Asterisks indicate significant differences as assessed by unpaired, two-tailed Student’s t test: ** p < 0.01; ** p < 0.001.</p

Microbiome structure upon burn injury.

The richness (A) and Shannon index (B) of fecal samples collected from the cecum were used to estimate the level of diversity of the gut microbiome after burn injury (data shown as mean ± SD). Beta diversity was assessed by dimensional reduction of the Bray-Curtis distance between the microbiome samples, using the PCoA ordination method (C). For all experiments, each replicate is plotted (n = 7 mice/group), as well as mean ± SD. Asterisks indicate significant differences as assessed by Kruskal-Wallis rank sum test.</p

Pathway diversity is altered upon burn injury.

The degree of variation of signaling pathways within a sample was assessed after burn or sham injury (A). Each replicate is presented, as well as mean ± SD. Asterisks indicate significant differences as assessed by Kruskal-Wallis rank sum test. Differentially abundant pathways in the cecal microbiome (B) were considered significant if their FDR-corrected p-value was less than or equal to 0.05 and the absolute value of the log-2 fold change was greater than or equal to 1. Infinite log-2 fold changes indicate that the other groups mean abundance is 0. Out of the 331 pathways tested, only the 38 pathways, whose abundance was significantly altered, are reported.</p

Influence of ghrelin treatment (0.5 μg/g BW, twice a day, intraperitoneal (ip.)) on bacterial load after cecal ligation and puncture (CLP)-induced sepsis.

<p>Blood and peritoneal lavage fluid from control mice (ghrelin: n = 5/timepoint, untreated: n = 5/timepoint) and high fat diet (hfd) mice (ghrelin: n = 5/timepoint, untreated: n = 5/timepoint) were collected before, 24h and 48h following CLP. Blood of (A) control and (B) hfd mice and and peritoneal lavage fluid of (C) control and (D) hfd mice were plated on tryptic soy agar pour plates and incubated at 37°C for 48 hours. Bacterial colony forming units (CFU) were determined. All values are expressed as means ± SEM; * p < 0.05 of of two-way ANOVA for unmatched samples followed by a <i>post hoc</i> Bonferroni test for analyses between more than two groups or within groups over time. n.d. = not detected.</p

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Influence of ghrelin treatment (0.5 μg/g BW, twice a day, intraperitoneal (ip.)) on inflammatory mediators after cecal ligation and puncture (CLP)-induced sepsis.

<p>Serum was collected from control mice (ghrelin: n = 5–9/timepoint, untreated: n = 4–5/timepoint) and high fat diet (hfd) mice (ghrelin: n = 4–10/timepoint, untreated: n = 4–5/timepoint) before, 6h, 24h and 48h following CLP. Serum leptin levels of (A) control and (B) hfd mice, Interleukin (IL)-1ß levels of (C) control and (D) hfd mice and tumor necrosis factor (TNF)α levels of (E) control and (F) hfd mice were determined by ELISA (combined data from several independent experiments); * p < 0.05 of two-way ANOVA for unmatched samples followed by a <i>post hoc</i> Bonferroni test for analyses between more than two groups or within groups over time. All values are expressed as means ± SEM.</p

Influence of ghrelin treatment (0.5 μg/g BW, twice a day, intraperitoneal (ip.)) on peritoneal cellular immune response after cecal ligation and puncture (CLP)-induced sepsis.

<p>Peritoneal lavage fluid from control mice (ghrelin: n = 5/timepoint, untreated: n = 5–11/timepoint) and high fat diet (hfd) mice (ghrelin: n = 5/timepoint, untreated: n = 4–10/timepoint) were collected before, 24h and 48h following CLP. Numbers of neutrophils of control (A) and (B) hfd mice, natural killer (NK) cell numbers of (C) control and (D) hfd mice and γδ T cell numbers of (E) control and (F) hfd mice were were enumerated by flow cytometric analysis (combined data from two independent experiments). All values are expressed as means ± SEM; * p < 0.05 of unpaired t-test for comparison of baseline levels between two groups (hfd and control) and of two-way ANOVA for unmatched samples followed by a <i>post hoc</i> Bonferroni test for analyses between more than two groups or within groups over time.</p

Influence of ghrelin treatment (0.5 μg/g BW, twice a day, intraperitoneal (ip.)) on oxidative burst capacity of neutrophils after cecal ligation and puncture (CLP)-induced sepsis.

<p>Blood and peritoneal lavage were collected from controls (n = 5/timepoint), controls with ghrelin treatment (n = 5/timepoint), high fat diet (hfd) (n = 5/timepoint) and hfd with ghrelin treatment (n = 5/timepoint) before, 24h and 48h after CLP-induced sepsis. Ghrelin dependent changes of spontaneous oxidative burst capacity of neutrophils and capacity after stimulation with fMLP in serum of (A) control and (B) hfd mice and in peritoneal lavage fluid of (C) control and (D) hfd mice were measured in blood and peritoneal lavage by flow cytometric analysis (combined data from two independent experiments). All values are expressed as means ± SEM; * p < 0.05 of of two-way ANOVA for unmatched samples followed by a <i>post hoc</i> Bonferroni test for analyses between more than two groups or within groups over time.</p

Increased survival and decreased bacterial sepsis-associated tissue damage of mice with T-cell targeted deletion of HIF-1α.

<p><u>A: </u><i>Use of the hypoxic marker EF5 reveals that CD4+ and CD8+ T cells have been exposed to low oxygen tension (hypoxic) conditions in the peritoneum during sepsis in mice.</i> Single cell suspensions from peritoneal lavage fluid and spleens were analyzed by flow cytometry using anti-EF5 mAb (Elk3-52 Cy5). <u>B: </u><i>High Efficiency of Cre recombinase-mediated deletion of HIF-1</i> α <i>in T-Cells.</i> Efficiency of deletion was calculated by quantitative real-time PCR as described. Constitutively synthesized HIF-1 α mRNA was detected in control (lck-Cre negative) but not in (lck-Cre positive) HIF1 α gene targeted mice. N = 3 per group. <u>C: </u><i>T cell lineage specific HIF-1</i> α <i>deficient mice are more resistant to lethal sepsis after cecal ligation and puncture procedure.</i> Mice underwent CLP and were observed for mortality. N = 13 per group. p = 0.0326, Logrank (Mantel-Cox). <u>D: </u><i>T cell lineage specific HIF-1</i> α <i>deficient mice have less sepsis-associated liver damage as evaluated by levels of ALT transaminase activity in serum.</i> Serum samples obtained from mice 72 hrs after CLP. *:p<0.05 vs. WT, N = 5–6 per group.</p