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Infiltration of M2-polarized macrophages in infected lymphatic malformations: possible role in disease progression
W Zhang1,2, K-F He1,2, J-G Yang1
1The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, 430079, China.
Background:
Lymphatic malformations (LMs), slow-flow vascular anomalies resulting from abnormal development of lymphatic channels, often progress rapidly after trauma or infection.
Objectives:
To explore the possible mechanism by which local infection promotes the progression of LMs.
Methods:
Immunohistochemistry in serial sections and immunofluorescence were performed to label polarized macrophages. Tertiary lymphoid organs (TLOs) in LMs were identified using antibodies against CD3 (a T-cell marker), CD20 (a B-cell marker) and PNAd (a high endothelial venule marker). Pearson's correlation and cluster analysis were carried out to delineate the relationship between macrophage infiltration and TLO formation. Rat models of LM were established to examine the role of lipopolysaccharide in LM development.
Results:
Compared with normal skin tissues, both M1- and M2-polarized macrophages were prevalent in LMs. Moreover, M2-polarized macrophages were significantly increased in infected LMs with an elevated density of TLOs. M2-polarized macrophages were observed in the centre of TLOs accompanied by intensive staining of macrophage colony-stimulating factor, a strong chemotactic factor for monocytes/macrophages, suggesting that macrophages might be recruited through TLOs. Cluster analysis and Pearson's correlation suggested a close relationship between macrophage infiltration and TLO formation. Furthermore, the expression of CD68 was also correlated with that of vascular endothelial growth factor (VEGF)-C and Ki67. Importantly, in an established LM rat model, lipopolysaccharide promoted the progression of the malformations with increased macrophage infiltration and TLO formation.
Conclusions:
M2-polarized macrophages that may be recruited through TLOs in infected LMs may contribute to the progression of the disease by secreting VEGF-C, and therefore accelerating the proliferation of lymphatic endothelial cells.
Insights
Infection promotes lymphatic malformations (LMs) progression via M2-polarized macrophages and tertiary lymphoid organs (TLOs). These macrophages, recruited through TLOs, secrete VEGF-C, accelerating LM development.
Area of Science:
- Vascular biology
- Immunology
- Pathology
Background:
- Lymphatic malformations (LMs) are slow-flow vascular anomalies of lymphatic channels.
- LMs can progress rapidly following trauma or infection.
Purpose of the Study:
- To investigate the mechanism by which local infection exacerbates LM progression.
- To explore the role of macrophages and tertiary lymphoid organs (TLOs) in LM pathogenesis.
Main Methods:
- Immunohistochemistry and immunofluorescence to identify polarized macrophages (M1/M2) and TLO markers (CD3, CD20, PNAd).
- Correlation and cluster analysis to assess macrophage-TLO relationships.
- Lipopolysaccharide-induced LM rat models to study disease progression.
Main Results:
- Both M1 and M2 macrophages were increased in LMs; M2 macrophages and TLOs were significantly higher in infected LMs.
- M2 macrophages were found within TLOs, associated with macrophage colony-stimulating factor, suggesting recruitment via TLOs.
- Macrophage infiltration correlated with TLO formation, VEGF-C, and Ki67 expression. Lipopolysaccharide enhanced LM progression, macrophage infiltration, and TLOs in a rat model.
Conclusions:
- M2-polarized macrophages, potentially recruited via TLOs in infected LMs, contribute to disease progression.
- These macrophages may secrete VEGF-C, promoting lymphatic endothelial cell proliferation and LM growth.
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