Induction of monocyte chemoattractant protein-1 by Mycoplasma hominis in respiratory epithelial cells

J Baier1, T E Kruger

  • 1Department of Pediatrics, Louisiana State University Medical Center, Shreveport 71130-3932, USA. jbaier@lsumc.edu

Abstract

Insights

Mycoplasma hominis (Mh) can trigger inflammation in preterm infants by increasing monocyte chemoattractant protein-1 (MCP-1) in lung cells. This suggests Mh contributes to bronchopulmonary dysplasia (BPD) development.

Area of Science:

  • Neonatal respiratory diseases
  • Pulmonary inflammation
  • Microbial pathogenesis

Background:

  • Bronchopulmonary dysplasia (BPD) risk increases in preterm infants with genital mycoplasmas in the trachea.
  • Early BPD stages involve inflammation, potentially driven by mononuclear cell recruitment and activation.
  • Monocyte chemoattractant protein-1 (MCP-1) produced by lung epithelial cells is critical for mononuclear cell lung migration.

Purpose of the Study:

  • To investigate the capacity of Mycoplasma hominis (Mh) to induce MCP-1 gene expression and protein production.
  • To examine the role of pulmonary epithelial cells in the inflammatory response to Mh.

Main Methods:

  • A549 cells, a type II pulmonary epithelial cell line, were used to study Mh effects.
  • MCP-1 mRNA and protein levels were measured after stimulation with live or inactivated Mh.
  • The impact of polymyxin B, IL-1ra, and antibodies to IL-1α, IL-1β, and TNF-α on Mh-induced MCP-1 production was assessed.

Main Results:

  • Mh significantly induced MCP-1 mRNA and protein in a dose- and time-dependent manner.
  • MCP-1 induction by Mh was not inhibited by polymyxin B, IL-1ra, or antibodies against IL-1α, IL-1β, or TNF-α.
  • IL-1α, IL-1β, and TNF-α were not detected in the cell culture media after Mh stimulation.

Conclusions:

  • Mh directly stimulates pulmonary epithelial cells to produce MCP-1.
  • This induction of MCP-1 by Mh contributes to the inflammatory processes in BPD.
  • Mh may play a role in recruiting and activating mononuclear cells in the lungs of affected infants.