# Slippery dopamine–fluoropolymer hybrid surface for improving biliary stent longevity

**Authors:** Tae Young Kim, Won-Jong Lee, Yurim Lee, Seo Jung Kim, Sungjin Min, Seyong Chung, Soo A Kim, Keun-Young Yook, Chang-Hwan Moon, Yeontaek Lee, Kijun Park, Dae-Hyun Kim, Jungmok Seo

PMC · DOI: 10.1016/j.bioactmat.2026.02.003 · 2026-02-13

## TL;DR

A new coating called ELFS improves biliary stent longevity by reducing inflammation and biofilm formation.

## Contribution

The ELFS coating prevents stent occlusion through anti-fouling properties and inhibits early immune responses.

## Key findings

- ELFS reduced neutrophil recruitment by over 20-fold compared to non-coated stents.
- ELFS-coated stents remained free of biofilm for over six months in mice.
- Coated stents maintained patency in a rabbit model for two months without occlusion.

## Abstract

Biliary obstruction leads to bile retention and triggers a cascade of pathological events. Bile accumulation induces cholestasis and inflammation, progressing to hepatocellular injury, fibrosis, and ultimately liver failure. To restore bile flow, biliary stents are a necessary option due to their immediate patency. However, their high susceptibility to foreign body reaction (FBR) associated fibrosis, biofilm formation, and biliary sludge accumulation leads to frequent occlusion. To address this limitation, we developed the Enhanced Longevity by anti-fouling Functional coating for Stent (ELFS), a lubricant-infused coating that prevents stent occlusion. ELFS can be readily fabricated via a simple dip-coating solution process and employ a polydopamine (PDA) adhesion layer. Intravital imaging in mice confirmed that ELFS suppressed the FBR by blocking early neutrophil adhesion, which in turn prevented downstream immune-fibrotic cascades. At 3 h, neutrophil recruitment in the non-coated group was >20-fold higher than in ELFS-coated groups. Additionally, ELFS-coated stents remained free of biofilm for over six months in mice and maintained full open for two months in a rabbit common bile duct model. In contrast, non-coated stents resulted in complete occlusion, bile duct dilation (over 4 times), hepatomegaly (over 2 times), and fibrosis.

Image 1

•Clinical challenge: Biliary stents often fail due to bile viscosity, foreign body reaction, fibrosis, and biofilm-driven occlusion.•ELFS, a lubricant-infused antifouling coating, shows high mechanical stability without delamination under physiological flow.•ELFS is fabricated via a simple dip-coating process using a PDA adhesion layer.•ELFS reduced neutrophil recruitment by >20-fold, prevented biofilm for 6 months in mice, and maintained patency in rabbits.

Clinical challenge: Biliary stents often fail due to bile viscosity, foreign body reaction, fibrosis, and biofilm-driven occlusion.

ELFS, a lubricant-infused antifouling coating, shows high mechanical stability without delamination under physiological flow.

ELFS is fabricated via a simple dip-coating process using a PDA adhesion layer.

ELFS reduced neutrophil recruitment by >20-fold, prevented biofilm for 6 months in mice, and maintained patency in rabbits.

## Linked entities

- **Chemicals:** dopamine (PubChem CID 681)
- **Diseases:** cholestasis (MONDO:0001751), liver failure (MONDO:0100192)
- **Species:** Mus musculus (taxon 10090), Oryctolagus cuniculus (taxon 9986)

## Full-text entities

- **Genes:** Slc17a5 (solute carrier family 17 (anion/sugar transporter), member 5) [NCBI Gene 235504] {aka 4631416G20Rik, 4732491M05, AST, ISSD, NSD, SD}, Pecam1 (platelet/endothelial cell adhesion molecule 1) [NCBI Gene 18613] {aka Cd31, PECAM-1, Pecam}, Gpt (glutamic pyruvic transaminase, soluble) [NCBI Gene 76282] {aka 1300007J06Rik, 2310022B03Rik, ALT, ALT1, Gpt-1, Gpt1}, albumin [NCBI Gene 100034206], Alb (albumin) [NCBI Gene 11657] {aka Alb-1, Alb1, BCL001, BCL002, BPL001}, Adgre1 (adhesion G protein-coupled receptor E1) [NCBI Gene 13733] {aka DD7A5-7, EGF-TM7, Emr1, F4/80, Gpf480, Ly71}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Il1 (interleukin 1 complex) [NCBI Gene 111343] {aka Il-1}, alp (alopecia, recessive) [NCBI Gene 11691], Acta2 (actin alpha 2, smooth muscle, aorta) [NCBI Gene 11475] {aka 0610041G09Rik, Actvs, SMAalpha, SMalphaA, a-SMA, alphaSMA}, Ly6g (lymphocyte antigen 6 family member G) [NCBI Gene 546644] {aka Gr-1, Gr1, Ly-6G}, Ggt1 (gamma-glutamyltransferase 1) [NCBI Gene 14598] {aka CD224, GGT, GGT 1, GGT-1, Ggtp, dwg}
- **Diseases:** biliary cirrhosis (MESH:D008105), necrosis (MESH:D009336), hyperplasia (MESH:D006965), hepatic injury (MESH:D056486), hepatic failure (MESH:D017093), Biliary obstruction (MESH:D001658), bacterial biofilm (MESH:D001424), Cytotoxicity (MESH:D064420), impairment of hepatobiliary function (MESH:D004066), infection (MESH:D007239), bile duct obstruction (MESH:D002779), hypertrophy (MESH:D006984), bile retention (MESH:D016055), hepatomegaly (MESH:D006529), common bile duct obstruction (MESH:D003138), anemia (MESH:D000740), bile (MESH:D001649), bile stricture (MESH:D003251), acute cholangitis (MESH:D000208), jaundice (MESH:D007565), bile stasis (MESH:D014647), Hepatic fibrosis (MESH:D008103), swelling (MESH:D004487), malignancies (MESH:D009369), gallstone (MESH:D042882), bile duct, pancreatic, or gallbladder cancer (MESH:D001650), pain (MESH:D010146), bile leakage (MESH:D003763), acute and chronic inflammation (MESH:D007249), cholestatic liver disease (MESH:D008107), gallbladder (MESH:D005705), cirrhosis (MESH:D005355)
- **Chemicals:** DMSO (MESH:D004121), glucose (MESH:D005947), povidone-iodine (MESH:D011206), Cy5 (MESH:C085321), Dopamine hydrochloride (MESH:D004298), glutaraldehyde (MESH:D005976), acetate (MESH:D000085), potassium chloride (MESH:D011189), fluoropolymer (MESH:D005465), PFA (MESH:C003043), meloxicam (MESH:D000077239), Prolene (MESH:D011126), Zoletil (MESH:C006131), PDMS (MESH:C013830), Bupivacaine (MESH:D002045), polystyrene (MESH:D011137), Alexa Fluor 488 (MESH:C000711379), RFP (MESH:D012293), humic acid (MESH:D006812), Alexa 594 (MESH:C417664), CuSO4 (MESH:D019327), penicillin (MESH:D010406), Al (MESH:D000535), H2O2 (MESH:D006861), NaHCO3 (MESH:D017693), CAs (-), bile acids (MESH:D001647), H&amp;E (MESH:D006371), Lidocaine (MESH:D008012), TB (MESH:D014048), cholesterol (MESH:D002784), PE (MESH:D020959), ethanol (MESH:D000431), Perfluoropolyether (MESH:C078113), PDA (MESH:C568283), Ag (MESH:D012834), HCl (MESH:D006851), isoflurane (MESH:D007530), Alfaxan (MESH:C006477), PDS (MESH:D010165), Water (MESH:D014867), CCK-8 (MESH:D012844), amide (MESH:D000577), F (MESH:D005461), agar (MESH:D000362), FeCl3 (MESH:C024555), polymer (MESH:D011108), EO (MESH:D005027), streptomycin (MESH:D013307), Carbon (MESH:D002244), EG (MESH:D019855), bilirubin (MESH:D001663), TRITC phalloidin (MESH:C041085), xylene (MESH:D014992), N (MESH:D009584), Rompun (MESH:D014991), PEG (MESH:D011092), phalloidin (MESH:D010590), oxygen (MESH:D010100), paraffin (MESH:D010232)
- **Species:** Equus caballus (domestic horse, species) [taxon 9796], Oryctolagus cuniculus (domestic rabbit, species) [taxon 9986], Homo sapiens (human, species) [taxon 9606], Staphylococcus aureus (species) [taxon 1280], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395], Mus musculus (house mouse, species) [taxon 10090], Escherichia coli (E. coli, species) [taxon 562]
- **Cell lines:** NIH 3T3 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0594), NIT-3T3 — Mus musculus (Mouse), Transformed cell line (CVCL_U269), SNU-1079 — Homo sapiens (Human), Intrahepatic cholangiocarcinoma, Cancer cell line (CVCL_5008), ATCC CRL-1658 — Homo sapiens (Human), Nevoid basal cell carcinoma syndrome, Finite cell line (CVCL_2Z69), RAW 264.7 — Mus musculus (Mouse), Mouse leukemia, Cancer cell line (CVCL_0493), IH 3T3 — Homo sapiens (Human), Plasma cell myeloma, Cancer cell line (CVCL_WZ44), CCK-8 — Homo sapiens (Human), Colon adenocarcinoma, Cancer cell line (CVCL_2873), ATCC 6538 — Homo sapiens (Human), Lung adenocarcinoma, Cancer cell line (CVCL_0023)

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12924897/full.md

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Source: https://tomesphere.com/paper/PMC12924897