Down-regulation of insulin receptors in Propionibacterium acnes-activated macrophages in the mouse
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Abstract:
Intraperitoneal administration of Propionibacterium acnes in CD-1 mice was associated with the reduction in number of insulin receptors in peritoneal macrophages (M phi), and with elevated levels of insulin in plasma and the peritoneal cavity. When insulin levels returned to normal, insulin receptors in P. acnes-M phi were still reduced. Insulin appears to contribute significantly to the down-regulation of the M phi-insulin receptors during the early stage of activation. Other biologically active substances released during M phi activation might assume greater influence on insulin resistance in activated M phi at a later stage. The induction of transient hyperinsulinemia in P. acnes-treated mice might be attributed to the effect of concurrently elevated interleukin-1 (IL-1) released in the early course of M phi activation.
Insights
Propionibacterium acnes infection reduces insulin receptors in mouse macrophages, leading to insulin resistance. This effect persists even after insulin levels normalize, suggesting a complex immune-mediated mechanism.
Area of Science:
- Immunology
- Endocrinology
- Metabolic Research
Background:
- Propionibacterium acnes (P. acnes) is a bacterium known to modulate immune responses.
- Macrophages (M phi) play a crucial role in both immunity and metabolic regulation.
- Insulin resistance is a hallmark of metabolic disorders like type 2 diabetes.
Purpose of the Study:
- To investigate the effect of P. acnes administration on insulin receptor expression in peritoneal macrophages.
- To explore the relationship between P. acnes-induced changes in macrophages and systemic insulin levels.
- To elucidate the role of insulin in the modulation of macrophage insulin receptors during bacterial activation.
Main Methods:
- Intraperitoneal injection of P. acnes into CD-1 mice.
- Quantification of insulin receptor numbers in peritoneal macrophages.
- Measurement of plasma and peritoneal insulin levels.
- Assessment of insulin receptor expression following normalization of insulin levels.
Main Results:
- P. acnes administration led to a significant reduction in insulin receptors on peritoneal macrophages.
- Elevated plasma and peritoneal insulin levels were observed post-P. acnes administration.
- Reduced insulin receptor expression persisted in macrophages even after insulin levels returned to baseline.
- Interleukin-1 (IL-1) elevation in early P. acnes infection may contribute to transient hyperinsulinemia.
Conclusions:
- Insulin plays a significant role in the early-stage down-regulation of macrophage insulin receptors during P. acnes-induced activation.
- Other inflammatory mediators released during macrophage activation may influence insulin resistance at later stages.
- P. acnes infection induces a complex interplay between immune activation and metabolic dysregulation, impacting insulin sensitivity.