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A novel monocyte differentiation pattern in pristane-induced lupus with diffuse alveolar hemorrhage
Shuhong Han1, Haoyang Zhuang1, Rawad Daniel Arja1
1Division of Rheumatology, Allergy, & Clinical Immunology, University of Florida, Gainesville, United States.
Elife
|October 20, 2022
Summary
Pristane exposure activates monocytes, leading to lung injury and diffuse alveolar hemorrhage (DAH) in mice. This study identifies specific monocyte markers associated with DAH, revealing a novel inflammatory pathway.
Area of Science:
- Immunology
- Pathology
- Toxicology
Background:
- Pristane induces lupus and lung microvascular injury with diffuse alveolar hemorrhage (DAH) in C57BL/6 mice.
- Mineral oil (MO) causes inflammation but not lupus or DAH.
- Monocyte depletion prevents DAH, highlighting their critical role.
Purpose of the Study:
- To investigate the specific role of monocytes in pristane-induced DAH.
- To identify molecular changes in monocytes contributing to DAH pathogenesis.
Main Methods:
- Used Ccr2-/- mice to assess monocyte recruitment.
- Analyzed monocyte surface markers (annexin-V, CD138) and gene expression (TremL4, TNFα).
- Examined monocyte egress from bone marrow and plasma membrane asymmetry.
Main Results:
- Impaired monocyte egress in Ccr2-/- mice prevented DAH.
- Pristane-treated monocytes showed increased annexin-V staining without apoptosis.
- Nr4a1-regulated Ly6C(lo/-) monocytes from pristane-treated mice expressed CD138 and TremL4, producing excess TNFα.
Conclusions:
- Pristane alters monocyte development, generating inflammatory Ly6C(hi) and Ly6C(lo/-) subtypes.
- CD138+, high TremL4-expressing patrolling monocytes are associated with DAH susceptibility.
- These findings reveal a novel mechanism of pristane-induced lung injury involving monocyte activation.
