Cadherin-11 Regulates Macrophage Development and Function

Cadherin-11 (CDH11) is a cell-cell adhesion protein that has previously been reported to play an important role in the pathogenesis of pulmonary fibrosis. It is expressed on macrophages in the fibrotic lung. However, the role of CDH11 on macrophage biology has not yet been studied. We show using imm...

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Bibliographic Details
Published in:Frontiers in immunology 2022-02, Vol.13, p.795337-795337
Main Authors: To, Sarah, Chavula, Thandiwe, Pedroza, Mesias, Smith, Jennifer, Agarwal, Sandeep K
Format: Article
Language:English
Subjects:
Animals
Antigens, Ly - metabolism
Bleomycin - toxicity
Cadherin-11
Cadherins - deficiency
Cadherins - genetics
Cell Adhesion
Cell Differentiation
Disease Models, Animal
Immunology
macrophages
Macrophages - metabolism
Macrophages - physiology
Male
Mice
monocytes
Monocytes - metabolism
Myeloid Progenitor Cells - metabolism
phagocytosis
polarization
pulmonary fibrosis
Pulmonary Fibrosis - chemically induced
Pulmonary Fibrosis - metabolism
Pulmonary Fibrosis - pathology
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Summary:Cadherin-11 (CDH11) is a cell-cell adhesion protein that has previously been reported to play an important role in the pathogenesis of pulmonary fibrosis. It is expressed on macrophages in the fibrotic lung. However, the role of CDH11 on macrophage biology has not yet been studied. We show using immunophenotypic analyses that mice have fewer recruited monocyte-derived macrophages and Ly6C monocytes in the lungs compared to wild-type mice in the intraperitoneal bleomycin-induced pulmonary fibrosis model. Additionally, fewer Ly6C monocytes were detected in the bone marrow and peripheral blood of naive mice. Given that macrophages are derived from monocytes, we investigated the precursors of the monocyte/macrophage lineage in the bone marrow. We found increased numbers of CMPs and reduced numbers of GMPs and MPs/cMoPs in mice compared to wild-type mice, suggesting decreased differentiation towards the myeloid lineage in mice. Furthermore, we show using bone marrow cells that loss of CDH11 impaired monocyte to macrophage differentiation. We also demonstrate that CDH11 deficiency repressed the M2 program and impaired the phagocytic function of bone marrow-derived macrophages. Overall, our findings demonstrate a role for CDH11 in macrophage development, M2 polarization, and phagocytic function.
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.795337