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The PSMP-CCR2 interactions trigger monocyte/macrophage-dependent colitis.

Xiaolei Pei^1,2, Danfeng Zheng¹, Shaoping She¹

¹Department of Immunology, School of Basic Medical Sciences, and Key Laboratory of Medical Immunology of Ministry of Health, Peking University Health Science Center, Beijing, 100191, P.R. China.

Scientific Reports

|July 13, 2017

Summary

PC3-secreted microprotein (PSMP) is identified as a key chemokine in ulcerative colitis, driving monocyte migration to inflamed gut tissues. Targeting PSMP offers a novel therapeutic strategy for managing colitis and related inflammatory conditions.

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Area of Science:

Immunology
Gastroenterology
Molecular Biology

Background:

Monocytes and macrophages are crucial in colitis pathogenesis.
The specific chemokine initiating monocyte migration to colitis tissue is unknown.

Purpose of the Study:

To identify the key chemokine responsible for monocyte migration in colitis.
To investigate the role of PC3-secreted microprotein (PSMP) in colitis.

Main Methods:

Analysis of PSMP expression in human and mouse colitis and tumor tissues.
Investigating the effect of PSMP overexpression and anti-PSMP antibodies in DSS-induced colitis models.
Assessing PSMP's role in monocyte chemoattraction using chemotaxis and adoptive transfer assays.

Main Results:

PSMP is upregulated in colitis tissues and its overexpression exacerbates disease.
Anti-PSMP antibodies reduce inflammation by decreasing macrophage infiltration and key cytokine expression (IL-6, TNF-α, CCL2).
PSMP chemoattracts monocytes in a CCR2-dependent manner and promotes M1 macrophage CCL2 production.

Conclusions:

PSMP is a critical chemokine in ulcerative colitis, mediating monocyte/macrophage recruitment.
PSMP represents a novel mechanism influencing gut innate immunity.
PSMP is a potential therapeutic target for controlling colitis.