Even mild hyponatremia in the elderly should be considered a risk factor for falls. Correction of hyponatremia in the elderly may reduce morbidity and mortality, and at the same time, it has a huge impact on socioeconomic status.
ObjectiveTo determine if oral infection will result in an increase in markers of inflammation that are known to augment atherogenesis.IntroductionIt is known that patients with inflammation or infection of the oral cavity have a higher risk of acquiring susceptibility and being in a state of systemic inflammation increasing their risk of having vascular abnormalities. In the present study we sought to examine if infection of the oral cavity would result in an increase in the levels of markers of atherogenesis.MethodsFour month old female Apo E mice were treated with P. Gingivitis or with vehicle for 10 days. Plasma was prepared using heparinized capillary tubes and plasma separators and was cryopreserved. Circulating levels of interleukin 6 and 13‐HODE were determined using a commercially available ELISA kit and LC‐ESIMS/MS employing a Q4000 Quadrupole system. The data were analyzed using one way ANOVA taking advantage of GraphPad Prism application.ResultsIn mice receiving the P. Gingivitis treatment the levels of circulating IL‐6 and 13‐HODE were significantly higher (p=0.011 and p=0.031, respectively). There was no difference in the levels of 20‐ HETE which is known not to increase in inflammation.ConclusionThe present study indicates that oral infection with P. Gingivitis results in increases in the levels of circulating inflammatory molecules that are known to contribute to vascular dysfunction and increased vulnerability to atherogenic reactions.
ObjectiveTo determine the role of intestine in systemic inflammation.IntroductionThe small intestine receives various ingredients from food and water and the interplay between them, luminal microbiota and the enterocytes appears to play role in many digestive interactions.Objectivewe sought to determine if in a mouse model of inflammatory stress a high fat diet would affect the circulating levels of 12‐ hydroxyeicosatetraenoic acid (12‐HETE) an inflammatory metabolite of arachidonic acid and of serum amyloid A (SAA) a major marker of inflammation.MethodsMale ApoE deficient mice (n=10 per treatment group) were maintained on the laboratory chow or on a Western Type Diet containing 1.25% cholesterol for two weeks. Blood was removed from fasting mice according to UCLA IRB guidelines, plasma was separated and analyzed using a commercial ELISA system.Results12‐HETE an SAA levels were significantly higher in the circulation of the mice on the high fat diet (p=0.012 and p=0.023 respectively. These molecules have systemic effect and their high levels would result in a cascade of interactions producing high levels of other inflammatory molecules.Conclusiondietary factors such as lipids can affect intestine and result in elevated levels of inflammatory components. Systemic inflammation brought about by dietary ingredients can in turn produce pathological conditions in various organs and throughout the organism. This emphasizes the importance of the small intestine and the dietary habits in general health and well being.
We sought to test whether antibody repertoire development is abnormally regulated in mice that are genetically susceptible to the development of autoimmune disease. We have previously generated a transgenic strain of BALB/c mice whose DH locus has been altered to force use of amino acids from the inverted reading frame of the DSP2.2 gene segment. This sequence contains Arg, His, and Asn. The transgenic IgHa DH allele is termed Δ-iD, for deleted DH locus with a single, inverted D gene segment. On a BALB/c background, these mice evidence two partial blocks in B cell development. The first occurs in the bone marrow in the transition from the early to the late pre-B cell stage (Hardy Fraction C to D). Transition through this checkpoint requires the H chain to successfully create a pre-B cell receptor. The second occurs in the periphery, in the transition from the immature, transitional B cell to the follicular cell stage. These blocks are associated with progressive selection for a less highly charged CDR-H3 repertoire. We backcrossed the Δ-iD allele for ten generations to MRL and for seven generations to C57BL/6. The latter were then crossed with C57BL/6 mice congenic for three intervals derived from the autoimmune NZM2410 strain. Evaluation of B cell development in C57BL/6 by FACS revealed a similar block in development in the bone marrow in the transition from Fraction C to D, but no further loss in absolute B cell numbers was observed in the periphery. A similar pattern was observed in the sle1 congenic strain. The early block in development was also observed in the sle2 and sle3 congenic strains, but unlike controls the absolute number of follicular cells normalized in these latter strains. On an MRL background, no blocks in B cell development were observed. These results suggest that the sle2 and sle3 susceptibility loci have altered late-stage repertoire development, whereas repertoire development may be abnormal both centrally and peripherally in MRL.
TCDD was well tolerated without apparent side effects. Weight gain in exposed B/W mice and control mice was identical through 32 weeks of age. In DDT-exposed female B/W mice, the development of albuminuria was accelerated compared to control mice, but there was no significant effect on total IgG, anti-DNA antibodies, thymic/splenic cellularity, or mortality. In contrast, TCDD-exposed B/W mice had lower total IgG concentrations, significantly lower levels of anti-DNA (p < .05), lower incidence of albuminuria, significantly lower thymic and splenic weight and cellularity (p < .05), decreased CD4/CD8 ratio, and markedly reduced mortality compared to control and DDT exposed B/W mice (p < .05).
Conclusion:The environmental xenoestrogen DDT increased the incidence of albuminuria in lupusprone mice but did not significantly alter other disease parameters or mortality. In contrast, TCDD, a different environmental estrogen, suppressed markers of autoimmunity and the development of autoimmune glomerulonephritis compared to control mice. These results suggest that environmental estrogens, at molar concentrations similar to endogenous 17estradiol, do not markedly accelerate autoimmunity, and, in the case of TCDD, are immunosuppressive, either through a direct immunotoxic effect on thymus and spleen or indirectly through hormonal mechanisms. Further studies of dose-response relationships, specific mechanisms, and synergistic effects may elucidate environmental influences on human SLE and immune response.
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