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Heightened endotoxin susceptibility of monocytes and neutrophils during familial Mediterranean fever

Tigran K Davtyan1, Vachagan A Harutyunyan, Gagik S Hakobyan

  • 1Armenicum Research Centre, CJSC Armenicum, Yerevan, Republic of Armenia. tigdav@excite.com

FEMS Immunology and Medical Microbiology
|February 26, 2008
PubMed

Insights

Familial Mediterranean fever (FMF) impairs monocyte endotoxin tolerance in patients during attack-free periods. This leads to heightened sensitivity to bacterial endotoxins and altered immune responses, impacting neutrophil function.

Area of Science:

  • Immunology
  • Genetics
  • Autoinflammatory Diseases

Background:

  • Familial Mediterranean fever (FMF) is a genetic autoinflammatory disorder caused by MEFV gene mutations.
  • Pyrin protein, encoded by MEFV, is crucial in neutrophil and monocyte function.
  • FMF patients exhibit altered monocyte endotoxin tolerance, particularly during attack-free periods.

Purpose of the Study:

  • To investigate the mechanisms behind impaired lipopolysaccharide (LPS) tolerance in FMF patients during attack-free periods.
  • To analyze the correlation between impaired LPS tolerance and proinflammatory cytokine synthesis.
  • To examine alterations in monocytic surface receptor expression (CD14, CD11b) and neutrophil apoptosis in FMF.

Main Methods:

  • Monocyte culture and stimulation with lipopolysaccharide (LPS).
  • Analysis of proinflammatory cytokine synthesis and monocytic surface marker expression (CD14, CD11b).
  • Assessment of neutrophil apoptosis in FMF patients.

Main Results:

  • Attack-free FMF patients showed impaired LPS tolerance induction in monocytes.
  • This impairment correlated with increased LPS-induced proinflammatory cytokine synthesis.
  • Alterations in CD14 turnover and CD11b retention on monocytes were observed, along with enhanced LPS-induced neutrophil apoptosis.

Conclusions:

  • Impaired monocyte LPS tolerance in FMF is linked to dysregulated cytokine production and altered immune cell surface receptor dynamics.
  • Neutrophils from FMF patients exhibit increased susceptibility to LPS-induced apoptosis.
  • These findings highlight immune dysregulation in FMF beyond acute attacks.

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