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Related Concept Videos

Histone Modification02:32

Histone Modification

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Intra-tracheal Administration of Haemophilus influenzae in Mouse Models to Study Airway Inflammation
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Extracellular Acetylated Histone 3.3 Induces Inflammation and Lung Tissue Damage.

Mario C Rico1, Oscar Perez-Leal1, Mary F Barbe2

  • 1Pharmaceutical Sciences Department, Temple University School of Pharmacy, Philadelphia, PA 19140, USA.

Biomolecules
|September 28, 2023
PubMed
Summary

Extracellular acetylated histone H3.3 (AcH3.3) significantly worsens lung tissue damage and inflammation in mice, suggesting a role in chronic obstructive pulmonary disease (COPD) progression.

Keywords:
COPDH3.3HDACalveolar damagecytokinescytotoxicityhistoneshyperacetylationsinflammation

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Area of Science:

  • Pulmonary Medicine
  • Cellular Biology
  • Immunology

Background:

  • Extracellular histones, damage-associated molecular patterns (DAMPs), are released from dying cells and cause toxicity.
  • Chronic obstructive pulmonary disease (COPD) lungs show abundant extracellular histone H3.3, often hyperacetylated (AcH3.3).
  • The specific role of AcH3.3 in COPD-induced lung damage is not fully understood.

Purpose of the Study:

  • To investigate the impact of extracellular acetylated histone H3.3 (AcH3.3) on lung tissue damage and inflammation.
  • To determine if AcH3.3 exacerbates lung injury compared to non-acetylated histone H3.3.

Main Methods:

  • Administration of recombinant histones (rH2A, rH3.3, rAcH3.3) or vehicle to mice via intratracheal instillation.
  • Evaluation of lung tissue damage, histological changes, apoptosis (caspase 3 and 9), and systemic inflammatory markers (TNF-α, IL-6, MCP-3, CXCL-1) 48 hours post-instillation.
  • Micro-CT analysis and confocal imaging for structural changes and immune cell infiltration (lymphocytes, monocytes/macrophages).

Main Results:

  • Intratracheal instillation of rAcH3.3 caused more severe lung tissue damage than rH3.3 or vehicle.
  • Histological analysis revealed alveolar wall rupture, epithelial damage, and immune cell infiltration in rAcH3.3 treated mice.
  • rAcH3.3 increased apoptosis, triggered systemic inflammation markers, and led to leukocytosis and lymphocytosis, with confirmed lymphocytic and monocytic/macrophage infiltration.

Conclusions:

  • Extracellular AcH3.3 induces significant cytotoxicity and acute inflammatory responses in the lungs.
  • AcH3.3 plays a critical role in promoting lung tissue damage and inflammation.
  • These findings suggest AcH3.3 is a potential driver of lung damage progression in COPD.