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Leukemia inhibitory factor, interleukin-6, and their receptors are expressed transiently in the olfactory mucosa

B Nan1, M L Getchell, J V Partin

  • 1Sanders-Brown Center on Aging, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA.

The Journal of Comparative Neurology
|May 23, 2001
PubMed

Insights

Following olfactory bulb removal, infiltrating macrophages release leukemia inhibitory factor (LIF) and interleukin-6 (IL-6), promoting olfactory receptor neuron progenitor proliferation and nerve repair.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Olfactory receptor neuron (ORN) survival depends on synaptic targets in the olfactory bulb.
  • Olfactory bulb ablation (OBX) triggers ORN apoptosis and progenitor cell proliferation.
  • Intercellular signaling pathways regulate olfactory mucosa regeneration after injury.

Purpose of the Study:

  • To investigate the expression and role of leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) signaling in the olfactory mucosa post-OBX.
  • To identify the cellular sources and temporal dynamics of LIF and IL-6 expression.
  • To determine the function of these cytokines in olfactory progenitor cell proliferation and nerve repair.

Main Methods:

  • Immunohistochemistry to detect protein expression and cell infiltration in olfactory epithelium (OE) and olfactory nerve (ON) post-OBX.
  • Reverse transcriptase-polymerase chain reaction (RT-PCR) and Northern blot to analyze mRNA levels of LIF, LIFR, IL-6, IL-6R, and gp130.
  • Temporal analysis of cellular events at various time points after OBX.

Main Results:

  • Macrophage infiltration into the OE occurred by 16 hours post-OBX.
  • LIF expression increased by 2 days post-OBX, with LIF receptor (LIFR) upregulation on globose basal cells (GBCs), leading to peak GBC proliferation at 3-4 days.
  • LIF and IL-6 expression in macrophages and IL-6 in ensheathing cells were upregulated in the ON, coinciding with LIFR, IL-6R expression.

Conclusions:

  • Leukemia inhibitory factor (LIF) from infiltrating macrophages acts as a mitogen for olfactory progenitor cells (GBCs).
  • LIF and IL-6 from macrophages and ensheathing cells function as repair factors in the olfactory nerve.
  • These findings elucidate key molecular mechanisms driving olfactory nerve regeneration after injury.

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