The development of an immune response of immunocompetent BALB/c and C57BL/6 mice with different levels of resistance to microsporidial infection and immunodeficient SCID mice was analysed in relation to the route of infection with Encephalitozoon intestinalis. Cell-mediated immune responses were characterised by measurement of IFN-γ and quantification of CD4+, CD8+ and NK cells. Intraperitoneal (i.p.) infection induced higher levels of IFN-γ in ex vivo cultures of peritoneal exudate cells or splenocytes than peroral (p.o.) infection. Numbers of CD4+ and CD8+ T lymphocytes in the spleen increased markedly at later time points (14 and 21 DPI) after i.p. infection of BALB/c mice, whereas in C57BL/6 mice the highest increase was after p.o. infection. Considerable IFN-γ production in ex vivo cultures of Peyer's patch lymphocytes of both mouse strains was observed after p.o. infection. Intraperitoneal infection of SCID mice induced marked influx of inflammatory cells into the peritoneum with NK cells. The results contribute to the development of an animal model of microsporidiosis caused by E. intestinalis.
In humans, antidiabetics thiazolidinediones (TZDs) upregulate stearoyl-CoA desaturase 1 (SCD1) gene in adipose tissue and increase plasma levels of Scd1 product palmitoleate, known to enhance muscle insulin sensitivity. Involvement of other tissues in the beneficial effects of TZDs on plasma lipid profile is unclear. In our previous study in mice, in which lipogenesis was suppressed by corn oil-based high-fat (cHF) diet, TZD rosiglitazone induced hepatic Scd1 expression, while liver triacylglycerol content increased, VLDL-triacylglycerol production decreased and plasma lipid profile and whole-body glycemic control improved. Aim of this study was to characterise contribution of liver to changes of plasma lipid profile in response to a 8-week-treatment by rosiglitazone in the cHF diet-fed mice. Rosiglitazone (10 mg/kg diet) upregulated expression of Scd1 in various tissues, with a stronger effect in liver as compared with adipose tissue or skeletal muscle. Rosiglitazone increased content of monounsaturated fatty acids in liver, adipose tissue and plasma, with palmitoleate being the most up-regulated fatty acid. In the liver, enhancement of Scd1 activity and specific enrichment of cholesteryl esters and phosphatidyl cholines with palmitoleate and vaccenate was found, while strong correlations between changes of various liver lipid fractions and total plasma lipids were observed (r=0.74-0.88). Insulin-stimulated glycogen synthesis was increased by rosiglitazone, with a stronger effect in muscle than in liver. Conclusions: changes in plasma lipid profile favouring monounsaturated fatty acids, mainly palmitoleate, due to the upregulation of Scd1 and enhancement of Scd1 activity in the liver, could be involved in the insulin-sensitizing effects of TZDs.
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