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Single-cell Transcriptomics Inference Of Neutrophil-mast Cell Communication Programs In Periodontitis.

Home
Single-cell Transcriptomics Inference Of Neutrophil-mast Cell Communication Programs In Periodontitis.

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Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Single-cell Transcriptomics Inference of Neutrophil-mast Cell Communication Programs in Periodontitis.

Lina Liu¹, Miaomiao Xue¹

¹Department of General Dentistry, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.

Current Gene Therapy

|June 19, 2026

View abstract on PubMed

Summary

This summary is machine-generated.

Neutrophil dysregulation in periodontitis (PD) involves distinct neutrophil states interacting with mast cells. This communication axis contributes to the inflammatory microenvironment in PD, offering new therapeutic targets.

Keywords:

Periodontitis cell communication immune microenvironment molecular network.neutrophils single-cell sequencing

Related Experiment Videos

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

Area of Science:

Immunology
Genomics
Computational Biology

Background:

Neutrophil dysregulation is a hallmark of periodontitis (PD).
Understanding cellular heterogeneity and interactions is crucial for PD pathogenesis.
Single-cell transcriptomics offers a powerful tool to dissect complex cellular microenvironments.

Purpose of the Study:

To delineate neutrophil heterogeneity in periodontitis.
To predict mast cell communication networks within the PD microenvironment.
To identify novel therapeutic targets for periodontitis.

Main Methods:

Analysis of a public single-cell RNA sequencing dataset (GSE171213) from gingival tissues.
Utilized Seurat and Harmony for data processing and clustering.
Employed CellChat, NicheNet, and SCENIC for cell-cell communication and regulatory program prediction.
Performed in vitro experiments on HMC-1.2 mast cells treated with TGFB1.

Main Results:

Identified ten distinct cell types in periodontitis, including two neutrophil transcriptional states.
Predicted significant interactions between inflammatory neutrophils (Subtype 2) and mast cells via IL6 and SEMA4D signaling.
Inferred neutrophil-derived TGFB1, OSM, and IL1B influence mast cell responses in proliferation, migration, and inflammation.
In vitro TGFB1 treatment modulated mast cell proliferation, migration, and cytokine production in a TGFBR1-dependent manner.

Conclusions:

Neutrophil heterogeneity and mast cell interactions represent a key communication axis in the periodontitis inflammatory microenvironment.
Computational single-cell transcriptomics revealed testable hypotheses for periodontitis mechanisms.
Identified potential therapeutic targets for periodontitis based on neutrophil-mast cell crosstalk.