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Histamine receptor 2 modifies iNKT cell activity within the inflamed lung
R Ferstl1, R Frei1,2, W Barcik1
1Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, Switzerland.
Allergy
|June 16, 2017
Summary
Activating histamine receptor 2 (H2R) can reduce lung inflammation. Blocking H2R worsened airway disease, while its activation improved it, suggesting H2R as a therapeutic target for chronic lung conditions.
Area of Science:
- Immunology
- Respiratory Medicine
- Pharmacology
Background:
- Histamine receptor 2 (H2R) is an immunoregulatory mediator that suppresses inflammation.
- Understanding H2R's role in lung inflammation is crucial for developing new therapies.
Purpose of the Study:
- To investigate the role of H2R in modulating lung inflammatory responses.
- To explore H2R's interaction with CD1d-mediated lipid antigen presentation to iNKT cells.
Main Methods:
- Utilized ovalbumin (OVA) and house dust mite (HDM) murine models of respiratory inflammation.
- Administered H2R blockers (famotidine) and activators (dimaprit).
- Employed H2R-deficient and CD1d/H2R-deficient mice to study lipid antigen presentation to iNKT cells.
Main Results:
- Famotidine exacerbated OVA-induced airway disease; dimaprit reduced it.
- H2R-deficient mice showed more severe OVA and HDM-induced lung inflammation.
- H2R deficiency increased CD1d+ dendritic cells and iNKT cells, leading to higher pro-inflammatory cytokine secretion.
- Targeting iNKT cells in H2R-deficient mice normalized lung inflammation.
Conclusions:
- H2R activation, or its downstream pathways, presents a potential therapeutic strategy for chronic lung inflammatory diseases.
- This approach is particularly relevant when CD1d-mediated lipid antigen presentation to iNKT cells drives pathology.
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