We used C and N stable isotope measurements to identify trophic position and feeding histories of fish from Lake Okeechobee, one of the largest lakes in North America. When δ15N values were used to estimate trophic levels, analyses of about 500 individual fish collected in two seasons at five sites showed that trophic level varied from 2 (herbivore) to 4.3 (second-level carnivore) among the 29 fish species examined. Lower trophic levels predominated among small fish caught at a littoral marsh site, and highest trophic levels were found among larger offshore fish. Marsh fish showed about three times the C isotope variation than did offshore fish, consistent with the wider array of foods in the marsh versus offshore food web. In addition to these community-level results, there were often unexpected large isotopic differences between individuals in almost all fish species examined, suggesting large differences in individual feeding behavior. Isotopic analyses indicate long-term differences in feeding among individuals, in addition to the short-term differences often observed in stomach content studies. Long-term individual variation in fish foraging may be important in understanding variation in other biochemical parameters measured in fish, such as Hg or PCB contents.
IL-6 affects tissue reparative and inflammatory properties of vascular endothelial cells (ECs). This cytokine can signal to cells through classic and trans-signaling mechanisms, which are differentiated based on the expression of IL-6 receptor (IL-6R) on the surface of target cells. The biological effects of these IL-6 signaling mechanisms are distinct and have implications for vascular pathologies. We have directly compared IL-6 classic and trans-signaling in ECs. Human ECs expressed IL-6R in culture and in situ in coronary arteries from heart transplants. Stimulation of human ECs with IL-6, to model classic signaling, triggered the activation of PI3K-Akt and ERK1/2 signaling pathways while stimulation with IL-6 + sIL-6R, to model trans-signaling, triggered activation of STAT3, PI3K-Akt and ERK1/2 pathways. IL-6 classic signaling reduced persistent injury of ECs in an allograft model of vascular rejection and inhibited cell death induced by growth factor withdrawal. When inflammatory effects were examined, IL-6 classic signaling did not induce ICAM or CCL2 expression but was sufficient to induce secretion of CXCL8 and support transmigration of neutrophil-like cells. IL-6 trans-signaling induced all inflammatory effects studied. Our findings show that IL-6 classic and trans-signaling have overlapping but distinct properties in controlling EC survival and inflammatory activation. This has implications for understanding effects of IL-6 receptor blocking therapies as well as for vascular responses in inflammatory and immune conditions.
Background.
The gut microbiota affects immune responses that cause organ transplant rejection, but the mechanisms by which this occurs remain poorly understood.
Methods.
We have examined, in a murine model, how disruption of the gut microbiota with antibiotics early in life alters this microbial community later in life to affect immune responses that injure vascular allografts.
Results.
Analysis of 16S rRNA and whole genome sequencing of the gut microbiota demonstrated that early life disruption of this microbial community with antibiotics caused a reduction in taxa and enzymatic genes involved in the synthesis of acetate, an immunoregulatory metabolite in mice and humans. When allograft vascular injury was examined, early life disruption of the gut microbiota increased neutrophil accumulation and related medial injury of transplanted arteries. Normalizing the gut microbiota by co-housing and oral administration of acetate prevented neutrophil-mediated vascular allograft injury.
Conclusions.
Dysbiosis of the gut microbiome that reduces its production of the immunoregulatory metabolite acetate exacerbates neutrophil-mediated allograft vascular injury.
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