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Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment
09:00

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

Mycoplasma fermentans and TNF-beta interact to amplify immune-modulating cytokines in human lung fibroblasts

James P Fabisiak1, Fei Gao, Robyn G Thomson

  • 1Department of Environmental and Occupational Health, Center for Free Radical and Antioxidant Health, University of Pittsburgh Graduate School of Public Health, College of Medicine, Pittsburgh, PA 15219-3130, USA. fabs@pitt.edu

American Journal of Physiology. Lung Cellular and Molecular Physiology
|June 6, 2006
PubMed

Insights

Mycoplasma fermentans infection amplifies lung cell cytokine release, particularly IL-6, by interacting with TNF-beta. This interaction involves JNK/stress-activated protein kinase, offering insights into latent infections.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Mycoplasma infections can lead to chronic lung disease.
  • Understanding Mycoplasma's interaction with host cells is crucial for disease management.

Purpose of the Study:

  • To investigate how Mycoplasma fermentans affects immune-modulating cytokine release in lung cells.
  • To explore the synergistic effects of M. fermentans with other immune stimuli like TNF-beta.
  • To elucidate the signaling pathways involved in M. fermentans-induced cytokine production.

Main Methods:

  • Human lung fibroblasts (HLF) were exposed to live M. fermentans and its component MALP-2.
  • Cytokine release (IL-6, IL-8/CXCL8, MCP-1/CCL2, Gro-alpha/CXCL1) was measured.
  • Synergistic effects with TNF-beta were assessed.
  • NF-kappaB activation and MAPK pathways (p38, JNK) were analyzed using inhibitors.

Main Results:

  • M. fermentans significantly increased IL-6, IL-8/CXCL8, MCP-1/CCL2, and Gro-alpha/CXCL1 production.
  • M. fermentans and TNF-beta exhibited a synergistic effect on IL-6, CXCL8, and CXCL1 release.
  • The synergistic effect was dependent on prolonged incubation and TNF-beta pre-sensitization.
  • JNK/stress-activated protein kinase was identified as crucial for amplifying IL-6 release in the combined M. fermentans and TNF-beta response.

Conclusions:

  • M. fermentans amplifies lung cell cytokine production, especially IL-6, through synergistic interactions with stimuli like TNF-beta.
  • The JNK pathway plays a key role in amplifying this synergistic cytokine response.
  • This in vitro model provides a platform for dissecting the mechanisms of Mycoplasma-host interactions in lung cells.

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