Serum amyloid P: a systemic regulator of the innate immune response

Cox, Nehemiah; Pilling, Darrell; Gomer, Richard H.

doi:10.1189/jlb.1mr0114-068r

Cited by 79 publications

(69 citation statements)

References 70 publications

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“…Fibrocytes also promote angiogenesis by secreting VEGF, bFGF, IL-8, and PDGF and promote fibroblast proliferation, migration, and collagen production by secreting TGF-β and CTGF (13,14). Fibrocyte recruitment and differentiation is regulated by a variety of factors (3,15). In vitro, monocytes can differentiate into fibrocytes without the addition of any exogenous factors (5,11,12,(16)(17)(18)(19)(20)(21)(22).…”

mentioning

confidence: 99%

Fibroblasts secrete Slit2 to inhibit fibrocyte differentiation and fibrosis

Pilling

Zheng

Vakil

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Significance A key question in fibrosing diseases is why monocytes do not become fibrocytes in healthy tissues but can become fibrocytes in fibrotic lesions. We show that fibroblasts secrete a signal that inhibits the differentiation of monocytes into fibrocytes. We identify the signal as Slit2 and show that Slit2 levels are low in fibrotic lesions. We also show that injection of Slit2 prevents fibrosis in a mouse model of lung fibrosis. The identification of Slit2 as a key signal in normal tissues that prevents entering monocytes from becoming fibrocytes represents a major advance in our understanding of the regulation of the innate immune system and how fibrosis propagates, as well as a potential novel therapeutic for fibrosis.

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confidence: 99%

Fibroblasts secrete Slit2 to inhibit fibrocyte differentiation and fibrosis

Pilling

Zheng

Vakil

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…fibrocyte | lumican | fibrosis | inflammation | decorin D uring wound healing, monocytes leave the circulation, enter the tissue, and differentiate into fibroblast-like cells called fibrocytes (1)(2)(3)(4)(5)(6). Fibrocytes are also found in the scar tissue-like lesions associated with fibrotic diseases such as pulmonary fibrosis, congestive heart failure, cirrhosis of the liver, and nephrogenic systemic fibrosis (3,(7)(8)(9)(10)(11).…”

mentioning

confidence: 99%

TNF-α–stimulated fibroblasts secrete lumican to promote fibrocyte differentiation

Pilling

Vakil

Cox

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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In healing wounds and fibrotic lesions, fibroblasts and monocyte-derived fibroblast-like cells called fibrocytes help to form scar tissue. Although fibrocytes promote collagen production by fibroblasts, little is known about signaling from fibroblasts to fibrocytes. In this report, we show that fibroblasts stimulated with the fibrocyte-secreted inflammatory signal tumor necrosis factor-α secrete the small leucine-rich proteoglycan lumican, and that lumican, but not the related proteoglycan decorin, promotes human fibrocyte differentiation. Lumican competes with the serum fibrocyte differentiation inhibitor serum amyloid P, but dominates over the fibroblast-secreted fibrocyte inhibitor Slit2. Lumican acts directly on monocytes, and unlike other factors that affect fibrocyte differentiation, lumican has no detectable effect on macrophage differentiation or polarization. α2β1, αMβ2, and αXβ2 integrins are needed for lumican-induced fibrocyte differentiation. In lung tissue from pulmonary fibrosis patients with relatively normal lung function, lumican is present at low levels throughout the tissue, whereas patients with advanced disease have pronounced lumican expression in the fibrotic lesions. These data may explain why fibrocytes are increased in fibrotic tissues, suggest that the levels of lumican in tissues may have a significant effect on the decision of monocytes to differentiate into fibrocytes, and indicate that modulating lumican signaling may be useful as a therapeutic for fibrosis.

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“…Preclinical cell and animal experiments suggested that SAP could reduce bleomycin-induced lung fibrosis 38,[83][84][85] . Intravenous administration of recombinant form of human SAP (PRM-151) resulted in a 30-50% decrease in fibrocyte numbers 24 h post-dose in pulmonary fibrosis patients 86 .…”

Section: Potential Therapy Targeted On Circulating Fibrocyte and Cxcr4mentioning

confidence: 99%

Role of CXCL12/CXCR4-Mediated Circulating Fibrocytes in Pulmonary Fibrosis

Xie¹,

Zhao²

2017

J. Biomed

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Pulmonary fibrosis is characterized by excessive deposition of extracellular matrix (ECM) and remodeling of the lung architecture, with clinically irreversible loss of lung function. The exact molecular and cellular mechanisms of pulmonary fibrosis are complicated. Many types of cells are involved in the pathogenic processes. The chemokine (C-X-C motif) ligand 12 (CXCL12) can attract circulating fibrocytes trafficking into lungs via chemokine (C-X-C motif) receptor 4 (CXCR4) to promote tissue repair or impertinently worsen fibrotic lesions. In this review, we briefly summarize the existing experimental and clinical findings about fibrocytes in pulmonary fibrosis and discuss the potential therapeutic target CXCL12/CXCR4 biological axis.

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Serum amyloid P: a systemic regulator of the innate immune response

Cited by 79 publications

References 70 publications

Fibroblasts secrete Slit2 to inhibit fibrocyte differentiation and fibrosis

Fibroblasts secrete Slit2 to inhibit fibrocyte differentiation and fibrosis

TNF-α–stimulated fibroblasts secrete lumican to promote fibrocyte differentiation

Role of CXCL12/CXCR4-Mediated Circulating Fibrocytes in Pulmonary Fibrosis

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