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A transcriptomics study of hereditary angioedema attacks.

Giuseppe Castellano1, Chiara Divella1, Fabio Sallustio2

  • 1Nephrology Unit, Department of Emergency and Organ Transplantation, University "Aldo Moro," and the Center for Diagnosis and Treatment of Hereditary Angioedema, Bari, Italy.

The Journal of Allergy and Clinical Immunology
|May 7, 2018
PubMed
Summary
This summary is machine-generated.

Hereditary angioedema (HAE) attacks involve increased adrenomedullin and uPAR in PBMCs, potentially amplifying bradykinin and edema. This study identifies key genes in HAE pathogenesis, offering new insights into disease mechanisms.

Keywords:
C1 inhibitor deficiencyHereditary angioedemaacute attacksgenesperipheral blood mononuclear cellsplasminvascular permeability

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Area of Science:

  • Immunology
  • Genetics
  • Vascular Biology

Background:

  • Hereditary angioedema (HAE) is a lifelong disorder causing recurrent edema.
  • The kallikrein/bradykinin pathway is implicated in HAE attacks.
  • Variable clinical presentations suggest involvement of other genetic factors.

Purpose of the Study:

  • To investigate additional genes contributing to edema formation in HAE.
  • To explore the transcriptomic profile of patients during HAE attacks.

Main Methods:

  • PBMC microarray gene expression analysis comparing HAE patients during attacks and remission.
  • Validation of key gene expression using real-time PCR in additional HAE patients.
  • In vitro studies to assess the role of uPAR in bradykinin generation and endothelial leakage.

Main Results:

  • 23 genes were significantly modulated during HAE attacks, primarily in NK cell and leukocyte extravasation pathways.
  • Adrenomedullin and uPAR gene expression was upregulated in PBMCs during acute HAE attacks.
  • In vitro studies confirmed uPAR's involvement in bradykinin generation and endothelial leakage.

Conclusions:

  • Adrenomedullin and uPAR levels increase in PBMCs during acute HAE attacks.
  • Upregulation of these genes may amplify bradykinin production, contributing to edema.
  • These findings provide insights into the molecular mechanisms of HAE pathogenesis.