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Decrease in alpha-1 antiproteinase antitrypsin is observed in primary Sjogren's syndrome condition.

Brij B Singh1,2, Joyce Ohm2, Fredice O Quenum Zanbede2

  • 1Department of Periodontics, School of Dentistry University of Texas Health Science Center, San Antonio, TX, USA.

Autoimmunity
|May 26, 2020
PubMed
Summary

Loss of alpha-1 antiproteinase antitrypsin contributes to primary Sjogren's syndrome (pSS). Epigenetic changes like DNA methylation and microRNA132 may inhibit its expression, leading to salivary gland dysfunction in pSS patients.

Keywords:
DNA methylationSjogren’s syndromealpha-1 antiproteinase antitrypsinmicroRNAssalivary glands

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Area of Science:

  • Immunology
  • Autoimmune Diseases
  • Molecular Biology

Background:

  • Primary Sjogren's syndrome (pSS) is a systemic autoimmune disease causing salivary gland dysfunction.
  • The exact factors driving salivary gland tissue changes in pSS remain unclear.

Purpose of the Study:

  • To investigate the role of alpha-1 antiproteinase antitrypsin (AAT) deficiency in pSS pathogenesis.
  • To explore the potential epigenetic mechanisms regulating AAT expression in pSS.

Main Methods:

  • Comparative analysis of AAT and elastase expression in pSS patient samples versus controls.
  • Examination of AAT deficiency and immune infiltration in IL14α transgenic mice.
  • Assessment of microRNA and DNA methylation patterns in salivary gland tissue from pSS patients.

Main Results:

  • AAT expression was significantly decreased, while elastase expression increased in pSS samples.
  • IL14α transgenic mice showed AAT loss, increased immune infiltration, and reduced saliva secretion.
  • pSS salivary glands exhibited increased microRNA132 and DNA methylation in the serpina gene promoter.

Conclusions:

  • Reduced AAT expression, potentially due to epigenetic modifications (DNA methylation, microRNA132), may contribute to pSS development.
  • These findings highlight a novel mechanism involving AAT and epigenetic regulation in salivary gland pathology of pSS.