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. 2019 Mar 20;16(3):703–712. doi: 10.1111/iwj.13084

In vitro cellular viability studies on a concentrated surfactant‐based wound dressing

Rui Chen 1, Anne‐Marie Salisbury 1, Steven L Percival 1,✉
PMCID: PMC7948640  PMID: 30895731

Abstract

In this study, three cellular cytotoxic assays (direct contact assay, extraction assay, and cell insert assay) were applied to evaluate the effects of a concentrated surfactant gel preserved with antimicrobials and a concentrated surfactant gel with 1% silver sulfadiazine on both the mouse fibroblast cell line L929 and human dermal fibroblasts (HDFa). Also, the in vitro wound model was wounded by a 100 μL pipette tip and used to assess cell migration and wound closure after treatment with both gels. A needle‐scratched membrane disruption model was used to preliminarily evaluate membrane stabilisation and the membrane‐resealing effects of concentrated surfactant gels. It was demonstrated that the concentrated surfactant gel preserved with antimicrobials was not toxic to both L929 and HDFa. However, the concentrated surfactant gel with 1% silver sulfadiazine demonstrated a degree of cytotoxicity to both cell types. After treatment with a concentrated surfactant gel preserved with antimicrobials, cell movement to close the scratch gap was enhanced at 24 and 48 hours. The results also showed that cells treated with the concentrated surfactant gel preserved with antimicrobials decreased cell necrosis and improved cell resistance of the f‐actin rearrangement after a needle scratch. The results demonstrated that a concentrated surfactant gel preserved with antimicrobials is non‐cytotoxic and has ability to accelerate wound closure by enhancing cell mobility. Furthermore, the concentrated surfactant gel appeared to stabilise the plasma membrane and demonstrated a resealing ability and helped to retain the plasma membrane integrity and enhanced wound healing.

Keywords: cell membrane stabilisation and resealing, cytotoxicity, surfactant, wound closure, wound dressing

1. INTRODUCTION

Surfactant‐based wound dressings are available to the clinician, pharmacist, and patient to improve wound healing by aiding wound cleansing, suppressing protein aggregation and denaturation, sealing/repairing tissue or cell membranes, and stabilising antimicrobials and exerting antimicrobial activity themselves.1 To effectively manage wound infections, topical antimicrobial agents are used. The most common ones that are used and been shown to reduce microbial colonisation and infection include iodine, chlorhexidine, silver, and polyhexamethylene biguanide (PHMB).1, 2, 3 All antimicrobial dressings are now being evaluated for their antibiofilm ability because of the fact that biofilms are considered to be detrimental to wound healing.2, 4, 5, 6 However, antimicrobial‐based wound dressings inevitably change the physical and chemical microenvironment of the wound and the wound ecosystem where the healing process occurs. Wound healing is the interaction of a complex cascade of cellular events that include inflammation, proliferation, and remodelling. An ideal wound dressing provides wound cleaning and antimicrobial and antibiofilm ability without adversely impacting cellular activities vital to the wound‐healing process. Therefore, it is important to investigate cellular responses to the wound dressings as well as their antimicrobial and antibiofilm ability. Meanwhile, understanding the cellular events regulating wound healing will help to develop novel wound dressings aimed towards enhanced wound healing.

Wound dressings that are toxic to microbial cells may also be toxic to the skin cells. Cytotoxic wound dressings can affect cells in a variety of ways. The cells can stop growing and dividing and necrosis can be increased as a result of cell lysis. Such effects all decrease the cellular viability, proliferation, and mobility that will delay wound healing. There are many articles in the literature, which discuss the cytotoxicity of wound dressings, in particular those that are impregnated with antimicrobial agents.2, 4, 7, 8, 9, 10

Recently, multiple studies have shown the effectiveness of using surfactant‐based wound dressings with or without antimicrobial agents in wound healing and pain reduction.5, 11, 12, 13, 14 However, fewer studies have discussed the cells response to these surfactants.

The aim of this study was to develop different cellular test models to evaluate the effects of a concentrated surfactant gel preserved with antimicrobials and a concentrated surfactant gel impregnated with 1% silver sulphadiazine (SSD) on cellular behaviours. Within this study, we focused on fibroblast proliferation, viability, and mobility, as fibroblasts are the main residential cells that are responsible for restoring the main structural features of the skin. In addition, we studied whether a concentrated surfactant gel has the ability to improve cell survival by resuming the structural integrity of the cell plasma membrane to maintain homeostasis and protect intracellular organelles.

2. MATERIALS AND METHODS

2.1. Test wound dressing

Two non‐ionic surfactant‐based wound dressings were investigated in this study: a concentrated surfactant gel preserved with antimicrobials (CSG) and a concentrated surfactant gel with 1% silver sulphadiazine (CSG‐SSD). The CSG dressing is a water‐soluble primary wound dressing, intended for daily to three‐time weekly use.15

2.2. Cell culture

A mouse fibroblast cell line L929 and primary adult human dermal fibroblasts (HDFa) (ATCC, LGC Standards, UK) were maintained in Dulbecco's modified Eagle's medium (DMEM) GlutaMAX (Gibco, ThermoFisher Scientific, UK) supplemented with 10% foetal bovine serum (FBS) (HyClone, GE Healthcare Life Sciences, UK) and 100 units/mL penicillin‐streptomycin (Life Technologies, Paisley, UK). Cells were cultured until approximately 90% confluence was achieved before undertaking tests.

2.3. Cytotoxicity and cell proliferation assay

Three cytotoxic assay methods were applied to study the cell viability of L929 and HDFa after treatment with CSG and CSG‐SSD.

Direct contact: L929 and HDFa were seeded into 24 well plates at a concentration of 0.05 × 106/mL/well. After 1‐day culture, 100 μL CSG or CSG‐SSD were added into pre‐determined wells. Cell images were taken at days 1 and 7. At days 1 and 7, the cells were washed with phosphate‐buffered saline (PBS) and stored at −80°C.

Extraction assay: L929 and HDFa were seeded into 24 well plates at a concentration of 0.05 ×106/mL/well. At the same time, 100 μL CSG and CSG‐SSD were added into 20 mL of culture medium and then stored in an incubator. After 1‐day culture, all the media were changed with reagents dissolved the day before. Cell images were taken at days 1 and 7. At days 1 and 7, the cells were washed with PBS and stored in −80°C.

Cell insert model: L929 and HDFa were seeded into 24 well plates at a concentration of 0.05 × 106/mL/well. After 1‐day culture, 0.4 μm 24 well format cell culture inserts with 100 μL CSG or CSG‐SSD were placed into pre‐determined wells. Cell images were taken at days 1 and 7. At days 1 and 7, the cells were washed with PBS and stored at −80°C.

The qualitative evaluation of cytotoxicity was undertaken according to the international standard ISO 10993. All cells during the test periods were observed microscopically to evaluate general morphology, vacuolisation, detachment, cell lysis, and membrane integrity.

Quantitative evaluation of cytotoxicity was evaluated by cell viability with the CyQUANT cell proliferation assay kit (Molecular Probes, Invitrogen, UK). The basis for the CyQUANT assay is the use of a proprietary green fluorescent dye (CyQUANT GR dye) that exhibits a strong fluorescence enhancement when bound to cellular nucleic acids. Cells were lysed with a buffer containing the CyQUANT GR dye. Fluorescence was measured using an FLX800 fluorimeter with excitation at 485 nm and emission at 530 nm. Sample fluorescence values were converted into cell numbers from an HDFC reference standard curve. All the cell numbers were converted to percentage of cell numbers of the DMEM group at 1 day, which was 100%. The results are presented as the mean ± SEM of n = 3.

2.4. Cell migration study: Scratch wound assay

The in vitro scratch wound model was used to assess the wound closure of L929 and HDFa in response to the addition of CSG and CSG‐SSD. L929 and HDFa were seeded into 6‐well plates at a cell density of 1 × 105 cells/mL in DMEM. Viable cell numbers were determined using 0.4% Trypan Blue exclusion dye (Gibco, ThermoFisher Scientific, UK). Cells were cultured until approximately 95% confluence before the scratch study was undertaken. At the same time, 100 μL CSG and CSG‐SSD were added into 20 mL DMEM and mixed. DMEM were changed by the treatment solutions and cultured for another 24 hours before creating a scratch using a sterile 100 μL pipette tip. After scratching, cells were washed using PBS (Sigma‐Aldrich, UK) to remove cell debris caused from the scratch. Another 2 mL treatment solution was added on the cells. For each cell there was a control. One for L929 and one for HDFa.

L929 and HDFa were incubated under humidified conditions at 37°C with 5% CO2 for 48 hours. To ensure images were taken in the same place each time, three lines were drawn evenly on the underside of the dish, perpendicular to the scratch. Three images of the scratch area were taken using ×10 magnification at the drawn lines for each sample at 0, 24, and 48 hours. The scratch areas were measured by ImageJ for all the groups. Wound closure was determined as percentage closure (%), which was subsequently calculated as follows:

wound closure=(scratch area at0hour−uncovered scratch areascratch area at0hour)×100 (1)

2.5. Cell membrane resealing study

Cell preparation: L929 and HDF were seeded onto sterile coverslips (=13 mm) in 24 well plates at a concentration of 0.05 × 106/mL/well and incubated at 5% CO2, 37°C, under humidified conditions overnight. At the same time, 100 μL CSG and CSG‐SSD were added into 20 mL culture medium and then stored in an incubator. After 1‐day culture, all the media were changed with reagents dissolved in medium and incubated overnight.

Plasma membrane disruption: L929 and HDFa monolayers were scratched with a sterile 22‐gauge needle (Sterican® B. Braun Melsungen AG, Germany) with # shapes on each coverslip.

Live‐dead assay: Fifteen seconds after the needle scratch, cells on the coverslips were quickly washed with PBS. A 100 μL of the live/dead solution (2 μM calcein AM and 4 μM EthD‐1, made from LIVE/DEAD Cell viability/cytotoxicity assay kit L3224, ThermoFisher Scientific, UK) was added onto the coverslips and incubated for 30 minutes at room temperature. The coverslips were washed with PBS gently, and the labelled cells were viewed immediately using a laser scanning confocal microscope (Carl Zeiss 510, Germany).

F‐actin staining: Fifteen seconds after the needle scratch, cells on the coverslips were rapidly fixed. Briefly, cells were immersed in PBS containing 5% glutaraldehyde and 3.7% formaldehyde for 10 seconds, washed in ice cold PBS, and fixed for a further 10 minutes with 4% paraformaldehyde. Fixed cells were washed three times in PBS and permeabilised in 0.1% Triton‐100 in PBS. The cells were then stained with ActinGreen ReadyProbes (ThermoFisher Scientific, UK). All samples were microscopically analysed using a laser scanning confocal microscope (Carl Zeiss 510, Germany).

Lactate dehydrogenase (LDH) assay: Fifteen seconds after the needle scratch, the supernatants in each well were collected and centrifuged, and stored in 1.5 mL Eppendorf microcentrifuge tubes. The attached cells were washed with PBS. All the supernatants and cells were stored at −80°C before undertaking the LDH assay by using the Pierce LDH cytotoxicity assay kit (ThermoFisher Scientific, UK).

2.6. Statistical analysis

All data were presented as mean ± SE. The differences were tested for statistical significance using a one‐way analysis of variance.

3. RESULTS

3.1. In vitro cytotoxicity of L929 and HDFa

The microscopy images of cell morphology with three different cellular assays at day 1 are shown in Figure 1. For both L929 and HDFa, in the direct contact assay, compared with the culture media control, some malformed or degenerated cells under and near the CSG were observed; floating of an increased number of cells and cell lysis were observed in the CSG‐SSD group. In the extraction cellular assay, there was no distinct morphology changes observed after CSG treatment for both L929 and HDFa; distinct cell lysis and shrinkage were observed after CSG‐SSD treatment, especially for HDFa. In the cell insert model, no distinct morphology changes and cell floating were observed in the CSG treatment; however, distinct cell lysis and shrinkage were observed after CSG‐SSD treatment, especially directly under the cell inserts.

Figure 1.

Figure 1

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Cell images after concentrated surfactant gel preserved with antimicrobials (CSG) and concentrated surfactant gel with 1% silver sulphadiazine (CSG‐SSD) treatment at day 1. Scale bar: 50 μm

Quantitative cell viability at day 1 for both the L929 and HDFa results is shown in Figure 2. Compared with the culture media, all the three tests results showed cell viabilities of CSG treatment were higher than 70% for both L929 and HDFa. Both direct contact and extraction assays showed cell viabilities of CSG‐SSD treatment were lower than 40%; but the cell insert model showed cell viabilities of CSG‐SSD treatment to be higher than 70% (73.69% for L929; 84.83% for HDFa).

Figure 2.

Figure 2

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Cell viability of L929 (left) and human dermal fibroblasts (HDFa) (right) in different cytotoxic tests after concentrated surfactant gel preserved with antimicrobials (CSG) and concentrated surfactant gel with 1% silver sulphadiazine (CSG‐SSD) treatment at day 1

The microscopy images of cell morphology with the three different cellular assays at day 7 are shown in Figure 3. For both the L929 and HDFa, in the direct contact assay, cell shape recovery under and near CSG was observed; there were no distinct differences observed in the extraction assay and cell insert model to the control group at day 7. Cell lysis and degeneration were observed in the CSG‐SSD group in all the three test methods; however, L929 and HDFa away from the bottom of the cell inserts in the cell insert model showed a similar morphology to the control group.

Figure 3.

Figure 3

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Cell images after concentrated surfactant gel preserved with antimicrobials (CSG) and concentrated surfactant gel with 1% silver sulphadiazine (CSG‐SSD) treatment at day 7. Scale bar: 50 μm

The quantitative cell viability results (Figure 4) showed that compared with the culture media control (100%), CSG treatment did not decrease proliferation of both L929 and HDFa in all the three test models. CSG‐SSD treatment distinctly decreased proliferation of L929 in the direct contact assay and extraction assay. CSG‐SSD treatment distinctly decreased proliferation of HDFa in all the three test models. The results also showed that CSG may enhance proliferation of HDFa in the direct contact assay.

Figure 4.

Figure 4

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Cell viability of L929 (left) and human dermal fibroblasts (HDFa) (right) in different cytotoxic tests after concentrated surfactant gel preserved with antimicrobials and concentrated surfactant gel with 1% silver sulphadiazine treatment at day 7. **P < 0.01 vs. Control by one‐way analysis of variance

3.2. In vitro cell migration

The in vitro scratch wound model is a commonly used model to assess cell migration and wound closure because of its simplicity, reproducibility, and cost effectiveness. Figures 5 and 6 showed the typical images regarding cell migration of L929 and HDFa after being scratched at 0, 24, and 48 hours. Table 1 showed the calculated wound closure percentage for both L929 and HDFa with and without CSG treatment. The results showed that CSG enhanced both L929 and HDFa migration from the edge of scratch in comparison with the medium control group. Compared with the medium control group, wound closure percentage increased from 39.43 ± 5.99 to 54.26 ± 8.44 after 24 hours and from 58.71 ± 10.17 to 90.55 ± 4.60 after 48 hours for L929; and increased from 41.21 ± 7.66 to 49.68 ± 5.81 after 24 hours and from 60.27 ± 8.35 to 83.55 ± 10.29 after 48 hours for the HDFa. The results implied that the concentrated surfactant in the wound gel improved the cell mobility. There were no cell migration images of the CSG‐SSD treatment. It was impossible to distinguish the edge of the scratch after CSG‐SSD treatment because of a large number of cells detaching after the tip‐scratch. This may be because of the fact that the SSD in the CSG decreases extracellular protein secretion by both cells, which resulted in the cells detaching more readily following the scratch.

Figure 5.

Figure 5

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Representative L929 cell images after tip scratch with/without pre‐treatment with concentrated surfactant gel preserved with antimicrobials at 0, 24 and 48 hours. Scale bar: 50 μm

Figure 6.

Figure 6

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Representative human dermal fibroblast (HDF) images after tip scratch with/without pre‐treatment with concentrated surfactant gel preserved with antimicrobials at 0, 24, and 48 hours. Scale bar: 50 μm

Table 1.

Percentage of wound closure with CSG treatment and without treatment (control)

0 hours 24 hours 48 hours
L929 Control 0 39.43 ± 5.99 58.71 ± 10.17
CSG 0 54.26 ± 8.44 90.55 ± 4.60
HDFa Control 0 41.21 ± 7.66 60.27 ± 8.35
CSG 0 49.68 ± 5.81 83.55 ± 10.29
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3.3. Cell membrane resealing

To investigate the effects of CSG and CSG‐SSD on cell membrane resealing, we studied the cell live/dead ratio and actin rearrangement after cell membrane rupture by 22G needles with and without treatment.

Images of live/dead staining (Figure 7) showed that dead cells decreased distinctly by CSG treatment for both L929 and HDFa compared with the DMEM control. For the CSG‐SSD treatment, the dead cells also decreased despite both cells showing increased detachment. We also measured percentage of LDH release into the supernatant to show if CSG prevented membrane stress‐induced leakage of LDH from the needle‐ruptured cells in vitro. The percentage of LDH in the supernatant of both L929 and HDFa (Figure 8) showed that LDH released into the supernatants of CSG‐SSD treatment was higher than that of the control (DMEM) (P < 0.01) and CSG treatment (P < 0.01). This was because of detachment of the cells following addition of CSG‐SSD. The percentages of LDH in the supernatant of the CSG treatment were lower than the control group, which implied CSG treatment may have the ability to stabilise the membrane by resealing it.

Figure 7.

Figure 7

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Live and needle‐scratch killed L929 cells and human dermal fibroblasts (HDFa) stained with the LIVE/DEAD cell viability/cytotoxicity assay kit L3224. Live cells fluorescence bright green, whereas dead cells with disrupted membranes fluoresce red‐orange. Scale bar: 50 μm

Figure 8.

Figure 8

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LDH in supernatants versus the total LDH released by HDFa. LDH Wound dressing gels, Plurogel PSSD increase LDH release of HDFa cells. The figure showed LDH released in supernatants vs. the total LDH released by the cells on the coverslips and in supernatants. P < 0.05 vs. CSG; **P < 0.01 versus control by one way analysis of variance

F‐actin staining of L929 and HDFa following the needle scratch is shown in Figure 9. Compared with the no disruption control, L929 cells in the control (DMEM medium) were elongated and showed actin rearrangement after the needle scratch; L929 cells in the CSG treatment showed less morphological changes after the needle scratch (Figure 9, up‐row). For HDFa, compared with the no disruption control, f‐actin of the cells in control (DMEM medium) rearranged at the edge of the needle scratch; but f‐actin arrangement in CSG treatment looked similar to the cells without the needle scratch (Figure 9, bottom‐row). The results of both cells implied that the CSG treatment improved cell resistance to shape changes after the needle scratch.

Figure 9.

Figure 9

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Confocal imaging of needle‐scratched L929 cells and HDFa after rapid fixed, actin was stained using the ActinGreenTM 488 ReadyProbes reagent. Scale bar: 50 μm

4. DISCUSSION

Surfactants have been widely added into wound cleansers to improve their effectiveness in wound cleaning and irrigation in chronic and complicated wounds.1 Furthermore, researchers have demonstrated that surfactant‐based wound dressings reduce bacterial biofilms in a porcine skin explant model.16 Percival et al5 have also shown that the application of surfactant‐based wound dressings to a biofilm can cause a dispersive effect coupled with encapsulation of the microorganisms. Besides the efficacy of surfactants in controlling biofilms and enhancing wound cleansing, there are few in vivo studies that have demonstrated the safety of surfactant‐based wound dressing when topically applied in human and animal trials.17, 18 Furthermore, there is limited evidence regarding the effects of surfactant‐based wound dressing on skin cells. Consequently, the objective of this study was to assess the efficacy of concentrated surfactant gels on cell viability and to investigate the cellular mechanism involved in the regulation of wound healing.

Cytotoxicity is a very important aspect in wound healing, as destruction of healthy living cells around and in the wound will have a negative impact on the healing process.19 Kant et al18 have demonstrated that topically applied surfactants similar to the surfactant present in the CSG materials studied does not interfere with the healing of full‐thickness skin wounds in animal models. Further to this, in our study, three types of cellular test assays were used to evaluate a concentrated surfactant gel preserved with antimicrobials (CSG) and a concentrated surfactant gel with 1% silver sulfadiazine (CSG‐SSD) and its cytotoxicity profile. The result showed that the CSG was non‐toxic in all three tests, which demonstrated CSG was safe for daily use. Addition of SSD into the CSG resulted in the wound dressing exhibiting cytotoxic effects. In our test models, it was demonstrated that the CSG‐SSD was toxic to L929 and HDFa cells in both the direct contact and extraction assay. This is principally because of the fact that silver ions (Ag+) can bind to proteins and cell membranes, which leads to skin cell denaturation and mitochondrial dysfunction.6, 9 Interestingly, the cell viabilities were higher than 70% for both L929 and HDFa in the cell insert model, which means that CSG‐SSD was non‐cytotoxic−/low‐cytotoxic. This may be because of lower silver release from the cell insert to the wells where cells were growing in the culture plate.

Wound closure is one of the vital steps of wound healing. The in vitro scratch wound model is a commonly used model to assess cell migration and wound closure because of its simplicity, reproducibility, and cost effectiveness.20, 21 Using this model, we found that CSG enhanced the mobility of both L929 and HDFa and increased the speed of closure by more than 20%. Cell proliferation and migration play significant roles in creating contractile force for wound closure.22 This result implied that CSG may have pro‐healing ability to enhance wound healing in vivo.18

The results of the cytotoxicity tests and scratch wound models implied that the concentrated surfactant gel preserved with antimicrobials (CSG) has potential to protect cells and accelerate healing processes in vitro. Maintenance of the integrity of the plasma membrane is essential for maintenance of cellular function and prevention of cell death. Palumbo and colleagues14 demononstrated that copolymer surfactants, such as Poloxamer 188 (P188) and Poloxamine 1107 (P1107), have the ability to restore cellular integrity. P188 has been shown to seal membrane pores in skeletal muscle cells23 and fibroblasts24 after heat shock. One of the main components of the concentrated surfactant gel preserved with antimicrobials is specific tri‐block copolymers (P188). To further understand the CSG's efficacy on cell viability and its pro‐healing effects,18 we set up a plasma membrane disruption model to investigate the ability of CSG to restore cellular integrity. Using a syringe needle to scratch cell monolayers has been proved successful to investigate plasma membrane disruption as demonstrated by Swanson and McNeil25 and Miyake et al26

In our study, the plasma membrane disruption model was successfully established by scratching confluent cell monolayers with a sterile 22‐gauge syringe needle to study whether there was a protective effect provided by the CSG on plasma membrane integrity. The surfactant P188 in CSG has shown the ability to seal, or repair tissue/cell membranes, to avoid further accumulation of cellular damage potentially by P188 insertion into damaged portions of the plasma membranes.

5. CONCLUSION

In this study, a series of test methods were used to investigate the cell viability following treatment with wound‐dressing materials and the cell protection mechanism of a concentrated surfactant gel. The research demonstrated that a concentrated surfactant gel preserved with antimicrobials is a non‐cytotoxic wound dressing when evaluated in the test models used in this study. The results of the scratch wound model demonstrated that the concentrated surfactant gel, preserved with antimicrobials, has the ability to accelerate wound closure by enhancing cell mobility. Furthermore, the concentrated surfactant gel preserved with antimicrobials reduced cell necrosis and improved cell resistance to the f‐actin rearrangement after the use of the needle scratch, which may be because of its ability to stabilise the plasma membrane and enhance membrane resealing.

Our results also indicated that a concentrated surfactant gel with 1% silver sulphadiazine (CSG‐SSD) is moderately cytotoxic in the direct contact and extraction assay; but CSG‐SSD was non‐cytotoxic in the cell insert assay model. We should be aware that the use of in vitro cell cytotoxic models does have some inherent limitations and may not be representative of cell‐tissue repair and wound healing in wound tissue in vivo. Recently, a multi‐center study including 1036 patients reported that more than 70% patients achieved wound closure, 56% of these non‐healing wounds achieved wound closure within 11 weeks after treated with CSG‐SSD.14 Consequently, a combination of both in vitro and in vivo studies is needed to determine the effect of surfactant‐based wound dressings such as CSG‐SSD on cell‐tissue repair and wound healing, not only on their cytotoxicity, but also their effects on wound closure, inflammation, and pain.

ACKNOWLEDGEMENTS

Funding for these research studies was provided by Medline Industries, Inc.

Chen R, Salisbury A‐M, Percival SL. In vitro cellular viability studies on a concentrated surfactant‐based wound dressing. Int Wound J. 2019;16:703–712. 10.1111/iwj.13084

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