IL-1beta and IL-10 have dual effects on enteric glial cell proliferation

Neurogastroenterol Motil. 2001 Feb;13(1):89-94. doi: 10.1046/j.1365-2982.2001.00245.x.


Inflammatory bowel disease is typically accompanied by functional and structural changes of the enteric nervous system. In pathological studies, cellular loss and axonal degeneration have been described in the myenteric plexus. However, more recent studies suggest that the proliferation rate of myenteric glial cells is enhanced in animal models of intestinal inflammation. Therefore, we have investigated the effect of different cytokines on the proliferative response of enteric glial cells (EGCs), comparing transformed enteric glial cell lines, primary astrocyte cultures and transformed oligodendrocytes. Cells were incubated in serum-free chemically defined medium in the presence or absence of either interleukin (IL)-1beta or IL-10 at concentrations ranging between 0.1 and 100 ng mL(-1) for 48 h. Subsequently, [3H]thymidine was added to each culture dish for an additional 6 h, and the amount of incorporated [3H] was assessed. IL-1beta significantly and dose-dependently suppressed [3H]-uptake by EGCs. In contrast, IL-10 induced a biphasic response; IL-10 at low concentrations (0.1 ng mL(-1)) caused a significant suppression of [3H]-uptake, whereas high concentrations (5-100 ng mL(-1)) significantly enhanced [3H] uptake. These results indicate that EGC proliferation can be modulated by cytokines. The differential effects of IL-1beta and IL-10 suggest that during intestinal inflammation there may be a regulatory interplay between different classes of cytokines modulating EGC proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / drug effects
  • Cell Division / drug effects
  • DNA / biosynthesis
  • Enteric Nervous System / cytology*
  • Enteric Nervous System / drug effects*
  • Enteric Nervous System / metabolism
  • Interleukin-1 / pharmacology*
  • Interleukin-10 / pharmacology*
  • Nerve Tissue Proteins / biosynthesis
  • Neuroglia / drug effects*
  • Neuroglia / metabolism
  • Oligodendroglia / drug effects
  • Rats


  • Interleukin-1
  • Nerve Tissue Proteins
  • Interleukin-10
  • DNA