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Repeat organic dust exposure-induced monocyte inflammation is associated with protein kinase C activity

Jill A Poole1, Todd A Wyatt, Susanna G Von Essen

  • 1Pulmonary, Critical Care, Sleep and Allergy Section, Department of Internal Medicine, University of Nebraska Medical Center, 985300 The Nebraska Medical Center, Omaha, NE 68198-5300, USA. japoole@unmc.edu

The Journal of Allergy and Clinical Immunology
|June 9, 2007
PubMed
Abstract

Insights

Repeat organic dust exposure alters monocyte inflammatory responses, potentially due to protein kinase C (PKC) pathway desensitization. This suggests new therapeutic targets for chronic respiratory diseases.

Area of Science:

  • Immunology
  • Occupational Health
  • Cell Biology

Background:

  • Organic dust exposure triggers inflammatory responses in the respiratory system.
  • Chronic or repeated exposure can lead to persistent respiratory diseases.
  • The precise mechanisms behind the modulated inflammatory response to repeated organic dust are not fully understood.

Purpose of the Study:

  • To investigate how repeated organic dust exposure affects inflammatory mediators and protein kinase C (PKC) activity in monocytes.
  • To compare the effects of single versus repeat organic dust exposure on these cellular responses.

Main Methods:

  • Organic dust from swine facilities was used to treat human monocytes and THP-1 cells.
  • Cells were exposed once or repeatedly to dust extract.
  • Levels of inflammatory mediators (TNF-alpha, IL-6, CXCL8, IL-10) and PKC isoform activation (alpha, delta, epsilon, zeta) were measured.
  • The role of endotoxin was assessed using depleted dust, LPS, and peptidoglycan.
  • PKC inhibitors were used to study their effect on TNF-alpha secretion.

Main Results:

  • Single organic dust exposure increased monocyte secretion of TNF-alpha, IL-6, CXCL8, and IL-10.
  • Repeated exposure diminished TNF-alpha and IL-6 responses but kept CXCL8 and IL-10 elevated.
  • Inflammatory responses were observed even with endotoxin-depleted dust, indicating an endotoxin-independent effect.
  • Organic dust induced significant activation of PKC isoforms (alpha, delta, epsilon, zeta).
  • PKC activation was reduced in cells exposed repeatedly to organic dust.
  • Inhibiting PKCalpha and PKCepsilon decreased TNF-alpha secretion.

Conclusions:

  • Repeated organic dust exposure modulates monocyte inflammatory mediator production independently of endotoxin.
  • The reduced ability of the protein kinase C (PKC) pathway to reactivate after repeat exposure may explain the altered inflammatory response.
  • Targeting PKC and specific mediators involved in repetitive organic dust exposure could lead to new therapeutic strategies for related respiratory conditions.

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