Biomaterial Surface Chemistry Dictates Adherent Monocyte/Macrophage Cytokine Expression in Vitro

Brodbeck, William G.; Nakayama, Yasuhide; Matsuda, Takehisa; Colton, Erica; Ziats, Nicholas P.; Anderson, James M.

doi:10.1006/cyto.2002.1048

Cited by 234 publications

(216 citation statements)

References 30 publications

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“…6,63,64 Consistent with this, Ch + Fg films triggered a distinct cell activation, as assessed by the amount of soluble factors, than Ch films without adsorbed protein, despite supporting equivalent numbers of adherent and fusing macrophages. Previous studies have demonstrated that preadsorption of Fg affected macrophage release of proinflammatory cytokines, in a surface-and time-dependent manner.…”

Section: Figsupporting

confidence: 64%

Adsorbed Fibrinogen Enhances Production of Bone- and Angiogenic-Related Factors by Monocytes/Macrophages

Maciel

Oliveira²,

Colton

et al. 2014

Tissue Engineering Part A

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Macrophages are phagocytic cells with great importance in guiding multiple stages of inflammation and tissue repair. By producing a large number of biologically active molecules, they can affect the behavior of other cells and events, such as the foreign body response and angiogenesis. Since protein adsorption to biomaterials is crucial for the inflammatory process, we addressed the ability of the pro-inflammatory molecule fibrinogen (Fg) to modulate macrophage behavior toward tissue repair/regeneration. For this purpose, we used chitosan (Ch) as a substrate for Fg adsorption. Freshly isolated human monocytes were seeded on Ch substrates alone or previously adsorbed with Fg, and allowed to differentiate into macrophages for 10 days. Cell adhesion and morphology, formation of foreign body giant cells (FBGC), and secretion of a total of 80 cytokines and growth factors were evaluated. Both substrates showed similar numbers of adherent macrophages along differentiation as compared with RGD-coated surfaces, which were used as positive controls. Fg did not potentiate FBGC formation. In addition, actin cytoskeleton staining revealed the presence of punctuate F-actin with more elongated and interconnecting cells on Ch substrates. Antibody array screening and quantification of inflammation-and wound-healing-related factors indicated an overall reduction in Ch-based substrates versus RGD-coated surfaces. At late times, most inflammatory agents were downregulated in the presence of Fg, in contrast to growth factor production, which was stimulated by Fg. Importantly, on Ch + Fg substrates, fully differentiated macrophages produced significant amounts of macrophage inflammatory protein-1delta (MIP-1d), platelet-derived growth factor-BB, bone morphogenetic protein (BMP)-5, and BMP-7 compared with Ch alone. In addition, other important factors involved in bone homeostasis and wound healing, such as growth hormone, transforming growth factor-b3, and insulin-like growth factor-binding proteins, as well as several angiogenic mediators, including endocrine gland-derived vascular endothelial factor, fibroblast growth factor-7, and placental growth factor, were significantly promoted by Fg. This work provides a new perspective on the inflammatory response in the context of bone repair/regeneration mediated by a pro-inflammatory protein (Fg) adsorbed onto a biomaterial (Ch) that does not otherwise exhibit osteogenic properties.

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Section: Figsupporting

confidence: 64%

Adsorbed Fibrinogen Enhances Production of Bone- and Angiogenic-Related Factors by Monocytes/Macrophages

Maciel

Oliveira²,

Colton

et al. 2014

Tissue Engineering Part A

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“…6,34 TNF-␣ also induces apoptosis in macrophages adherent to biomaterials, and IL-4 inhibits the apoptosisinducing abilities of TNF-␣. 21,35 More relevant to this study, Robinson et al 36 demonstrated that in the monocytic cell line THP-1 and in human peripheral blood monocytes, addition of rMCP-1 stimulated TNF-␣ expression, which in turn induced MMP-9 release. In addition, those authors demonstrated that by inhibiting the activity of TNF-␣, reduced expression of MMP-9 was observed.…”

Section: Discussionmentioning

confidence: 70%

“…One microgram of total RNA was translated into single-stranded cDNA using the Superscript II cDNA synthesis kit and Oligo-dT (both from Invitrogen Corp.) according to an established protocol. 21 Gene expression levels were determined using the IQ5 multicolor real-time PCR and SYBR Green supermix (Bio-Rad Laboratories, Inc., Hercules, CA). Amplification of each sample was performed in duplicate.…”

Section: Quantitative Pcr Analysismentioning

confidence: 99%

Lack of TNF-α–Induced MMP-9 Production and Abnormal E-Cadherin Redistribution Associated with Compromised Fusion in MCP-1–Null Macrophages

Skokos

Charokopos

Khan

et al. 2011

The American Journal of Pathology

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Homotypic cell fusion occurs in several cell types including macrophages in the formation of foreign body giant cells. Previously, monocyte chemoattractant protein-1 (MCP-1) was demonstrated to be required for foreign body giant cell formation in the foreign body response. The present study investigated the fusion defect in MCP-1-null macrophages by implanting biomaterials intraperitoneally in wildtype and MCP-1-null mice and monitoring the macrophage response at 12 hours to 4 weeks. MCP-1-null mice exhibited reduced accumulation and fusion of macrophages on implants, which was associated with attenuation of the foreign body response. Consistent with previous in vitro findings, the level of matrix metalloproteinase-9 (MMP-9) was reduced in MCP-1-null macrophages adherent to implants. In contrast, CCR2 expression was unaffected. In vitro studies revealed reduced tumor necrosis factor-␣ (TNF-␣) production and abnormal subcellular redistribution of E-cadherin and ␤-catenin during fusion in MCP-1-null macrophages. Exogenous TNF-␣ caused an increase in the production of MMP-9 and rescued the fusion defect. Addition of GM6001 (MMP inhibitor) or NSC23766 (Rac1 inhibitor) indicated two distinct induction pathways, one for E-cadherin/␤-catenin and one for MCP-1, TNF-␣, and MMP-9. Considered together, these observations demonstrate that induction of E-cadherin/␤-catenin is not sufficient for fusion in the absence of MCP-1 or the downstream mediators TNF-␣ and MMP-9. Moreover, attenuation of the foreign body response in intraperitoneal implants in MCP-1-null mice demonstrates that the process depends on tissue-specific factors.

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“…Polymers with increased hydrophobicity have been revealed to increase infl ammatory cells' (monocytes) attachment. [ 38 ] PLCL scaffold being relatively hydrophobic (around 80°, measured by water contact angle), [ 39 ] these scaffolds would also have greater affi nity for body fl uid proteins than the modifi ed scaffolds, which might lead to conformational changes in the proteins due to the hydrophobic interactions that are thought to be responsible for recruiting infl ammatory cells and causing a pronounced foreign body reaction. [ 31,40 ] After week 8, the majority of cells seen in all specimens were mononuclear and giant cells, representing the typical foreign body response to biomaterials.…”

Section: Discussionmentioning

confidence: 99%

In Vivo Host Response and Degradation of Copolymer Scaffolds Functionalized with Nanodiamonds and Bone Morphogenetic Protein 2

Suliman

Sun

Pedersen

et al. 2016

Adv Healthcare Materials

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The aim is to evaluate the effect of modifying poly[( L -lactide)-co-(ε-caprolactone)] scaffolds (PLCL) with nanodiamonds (nDP) or with nDP+physisorbed BMP-2 (nDP+BMP-2) on in vivo host tissue response and degradation. The scaffolds are implanted subcutaneously in Balb/c mice and retrieved after 1, 8, and 27 weeks. Molecular weight analysis shows that modifi ed scaffolds degrade faster than the unmodifi ed. Gene analysis at week 1 shows highest expression of proinfl ammatory markers around nDP scaffolds; although the presence of infl ammatory cells and foreign body giant cells is more prominent around the PLCL. Tissue regeneration markers are highly expressed in the nDP+BMP-2 scaffolds at week 8. A fi brous capsule is detectable by week 8, thinnest around nDP scaffolds and at week 27 thickest around PLCL scaffolds. mRNA levels of ALP, COL1α2, and ANGPT1 are signifi cantly upregulating in the nDP+BMP-2 scaffolds at week 1 with ectopic bone seen at week 8. Even when almost 90% of the scaffold is degraded at week 27, nDP are observable at implantation areas without adverse effects. In conclusion, modifying PLCL scaffolds with nDP does not aggravate the host response and physisorbed BMP-2 delivery attenuates infl ammation while lowering the dose of BMP-2 to a relatively safe and economical level.

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Biomaterial Surface Chemistry Dictates Adherent Monocyte/Macrophage Cytokine Expression in Vitro

Cited by 234 publications

References 30 publications

Adsorbed Fibrinogen Enhances Production of Bone- and Angiogenic-Related Factors by Monocytes/Macrophages

Adsorbed Fibrinogen Enhances Production of Bone- and Angiogenic-Related Factors by Monocytes/Macrophages

Lack of TNF-α–Induced MMP-9 Production and Abnormal E-Cadherin Redistribution Associated with Compromised Fusion in MCP-1–Null Macrophages

In Vivo Host Response and Degradation of Copolymer Scaffolds Functionalized with Nanodiamonds and Bone Morphogenetic Protein 2

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