Microscopic Evidence of Selective Binding of Microplastics by Qi601™
Qi601™ is a novel, orally administered agent derived from Lactobacillus fermentum, a proprietary probiotic strain that has been heat-inactivated and processed under conditions that enhance its natural biofilm phenotype. This patented bacterial preparation and manufacturing process produce a self-aggregating particulate form, enabling Qi601 to function as a physical barrier and sequestration platform.
Upon ingestion, Qi601 acts as a Biofilm Shield™, selectively binding microplastic and nanoplastic contaminants present. These particles—commonly found in food, drinking water, and inhaled air—are a growing concern due to their potential to interaction with the human host. By potentially capturing these plastic particles before they can adhere to or penetrate the intestinal lining, Qi601 provides a non-absorptive, barrier-based strategy for reducing plastic exposure.
The probiotic source organism in Qi601 consists of aggregates of thousands of intact bacterial cells that naturally self-assemble into protective biofilm structures. The strain has been evaluated by the U.S. Food and Drug Administration (FDA) and holds Generally Recognized As Safe (GRAS) status under GRN No. 0988, supporting its safety for human consumption.
Description of Qi601 Aggregate Structure:
The Qi601 aggregate is composed of thousands of individual, heat-inactivated Lactobacillus fermentum bacteria that have retained their natural rod-shaped morphology. These cells, originally cultivated under biofilm-promoting conditions, self-assemble post-inactivation into dense, three-dimensional structures. This spontaneous aggregation mimics the extracellular organization typical of bacterial biofilms, resulting in a high-surface-area matrix capable of capturing environmental contaminants.
In this image of a representation of Qi601 seen below, each pale green rod represents a single bacterial unit within the larger Qi601 macrostructure. The irregular, non-spherical shape of the aggregate reflects the biological heterogeneity of spontaneous bacterial assembly. This natural clustering behavior is critical to Qi601’s function, enabling it to act as a “biofilm shield”—physically intercepting microplastics and nanoplastics and preventing them from contacting or adhering to epithelial surfaces. In laboratory studies Qi601 prevented the binding of nanoplastics to human colon epithelia cells by up to 83% when compared to untreated controls.
The overall structure is non-living, non-replicative, heat inactived bacteria sourced from a GRAS-approved probiotic (GRN 00988), making it a uniquely safe, scalable, and effective bio-inspired solution for gut-level environmental plastic sequestration.
Qi601
Selective Binding of 10 µm Microplastics to Qi601 Aggregates on a microscope slide.
Figure 1 below illustrates a fluorescence microscopy image capturing the interaction between Qi601 aggregates and 10 µm fluorescent microplastic spheres on a microscope slide. The light green shaded region is a Qi601 aggregate, while the bright fluorescent spheres are the microplastics particles. The image demonstrates a preferential and selective adherence of microplastic spheres to the surface of Qi601 on a microscope slide. Notably, regions lacking Qi601 show a corresponding absence of fluorescent signal, reinforcing both the specificity and spatial selectivity of this binding interaction. The microplastics appear to accumulate predominantly on and around the aggregate surface, indicating a non-random, affinity-based association.
Figure 1
The Qi601 aggregates seen in the top left panel above in figure 1, is magnified below in figure 2, is approximately 200 µm in diameter and present a high-surface-area scaffold capable of physically capturing microplastic particles in a test tube and potentially in the gastrointestinal lumen. This physical sequestration mechanism is consistent with Qi601’s proposed function as a non-absorptive, Biofilm Shield. The panel on the left below in figure 2 is a higher resolution, demonstrating the outline of the Qi601 aggregate on the microscope slide.
Figure 2
These images in figures 1 and 2 support the functional claim that Qi601 can act as a microplastic-binding agent in vitro on a microscope slide, and forms the basis for its inclusion as a gastrointestinal decontamination strategy targeting entrapping environmental plastic contaminants. The calculated volume of a single Qi601 particle with a diameter of approximately 200 microns is approximately 4,190,000 cubic micrometers (µm³)—a size that far exceeds the threshold for particles capable of passive absorption across the gastrointestinal (GI) barrier that is discussed later in the particle size absorption characteristics.
Selective Binding of Nanoscale particles (nanoplastic) to Qi601 Aggregates
Figure 3 below provides fluorescence microscopy evidence of selective nanoparticle binding to Qi601 aggregates in a laboratory test tube. The central pale green mass represents a Qi601 aggregate, while the surrounding bright fluorescence are the nanoscale particles dusting Qi601 larger aggregate.
This micrograph demonstrates that fluorescent nano-sized particles exhibit preferential adherence to the surface of Qi601 aggregates, forming a dense ring of fluorescence around the Qi601 aggregate boundary. Importantly, areas lacking Qi601 aggregates are devoid of fluorescent signal, supporting the hypothesis of selective and specific binding of these nanoplastic particles to Qi601 on a microscope slide.
The spatial exclusion of nanoplastic particles from Qi601-negative regions reinforces the conclusion that Qi601 not only physically interacts with microparticles (as shown previously) but also with nano-scale plastic contaminants, which are otherwise more likely to cross gastrointestinal barriers. This suggests a dual utility of Qi601 in microplastic sequestration across both micro- and nano-size ranges, providing a compelling potential mechanistic basis for its function as a gastrointestinal binding agent from these laboratory experiments.
Figure 3
The graph titled “Absorption of Nanoplastics (0.1 um Microplastics Measured by Spectrophotometry” demonstrates a dose-dependent relationship between the amount of Qi601 and its capacity to adsorb 100-nanometer (nm) fluorescent microplastic particles in a test tube. In this study, fixed quantities of 0.1 μm plastics (nanoplastics) were incubated in a test tube with increasing concentrations of Qi601 ranging from 0.5 mg to 10 mg. After incubation, samples, including the negative control, were lightly centrifuged, and the fluorescence of the supernatant was measured to determine the amount of plastic remaining unbound. The resulting percent change relative to the negative control reflects the amount of plastic adsorbed by Qi601.
At the lowest concentration (0.5 mg) in a test tube, Qi601 adsorbed 30.2% of the microplastics, with adsorption increasing significantly to 53.9% at 1 mg and 75.6% at 2 mg. A near-maximal binding effect was observed at 3 mg and 4 mg, with adsorption levels of 87.6% and 87.0%, respectively. Beyond this range, from 5 mg to 10 mg, adsorption remained relatively stable, ranging from 73.7% to 80.7%, suggesting that the system approached a saturation point where either all available microplastics were bound or the Qi601 binding sites had become saturated in the test tube.
These findings confirm that Qi601 in a test tube exhibits strong and selective binding capacity for nanoscale microplastics in a concentration-dependent manner, particularly up to 3–4 mg. Importantly, since particles in the 100 nm size range are more likely to cross epithelial barriers , Qi601’s ability to adsorb such particles may offer a significant protective mechanism as seen by these laboratory experiments. By forming these large physical aggregates, Qi601 could act as a physical barrier by binding nanoplastics, and may help reduce systemic exposure to these environmentally persistent contaminants.
Qi601 Reduces Microplastic Adherence to Human Colonic Epithelial Cells (CaCO₂) in a tissue culture model (figures 4 & 5)
Following the application of fluorescent microplastic spheres onto a monolayer of CaCO₂ human colonic epithelial cells in a typical tissue culture model, Qi601 was co-administered to assess its ability to mitigate particle adherence to the epithelial surface when compared to the negative controls. Both samples where treated equally with a gentle washing after application of microplastic particles with and without Qi601 to simulate gastric emptying.
Microplastic Particle Attachment to Human Colonic Cells in a test tube in the Absence of Qi601 (figure 4):
In the absence of Qi601, fluorescence microscopy reveals scattered adherence of fluorescent microplastic particles (10-6 nanometers) to the surface of human colonic epithelial cells (CaCO₂ human cell line) in a tissue culture model. These fluorescent, spherical microplastic particles appear irregularly distributed across the human cell monolayer, indicating surface interaction with the epithelial membrane. This pattern of diffuse microplastic binding to human cells highlights the potential for direct epithelial exposure and supports the rationale for using a sequestration agent, such as Qi601. In contrast, previous figures show that when Qi601 is present, microplastics preferentially bind to the Qi601 aggregates and are largely absent from epithelial surfaces, supporting Qi601 as a functional protective barrier.
Figure 4: Negative Control microplastics on human colon cells without Qi601.
In the presence of Qi601 on human colon cells in a tissue culture model (figure 5) the fluorescence microscopy image demonstrates a marked reduction of microplastic spheres associated with the epithelial surface, compared to untreated controls in figure 4. This finding provides compelling visual evidence that Qi601 effectively sequesters microplastic particles in a human tissue culture model, preventing their direct interaction with the human colonic epithelium.
The protective effect in a tissue culture model is visually clear: regions containing residual Qi601 aggregates (white arrows in figure 5) show localized accumulation of microplastics on the aggregate surface of Qi601, rather than on the colon epithelial monolayer. Conversely, epithelial areas lacking Qi601 display minimal to no microplastic fluorescence, reinforcing the product’s binding sensitivity and specificity with functional barrier properties. Again, this observation supports the proposed mechanism by which Qi601 acts as a physical interception barrier protection agent, and can potentially reduce the burden of microplastic exposure at the gastrointestinal interface.
Figure 5: Treatment: Qi601 on human colon cells following exposure to microplastic spheres in a tissue culture model.
Nanoplastic Application on human colonic epithelium With and Without Qi601 in a tissue culture model.
The same experimental setup in a tissue culture model was repeated but this time using nanoscale fluorescent plastic particles. In the absence of Qi601, (Figure 6), diffuse nanoscale fluorescence was again observed directly on the human colon epithelial surface, indicating nonspecific particle-cell interactions. However, upon co-application of Qi601 (figure 7), the nanoparticles were sequestered onto Qi601 aggregates, and the epithelial cell layer appeared largely devoid of fluorescence, mirroring the protective effect seen with microplastics.
Figure 6: Nanoplastics without Qi601 in a tissue culture model.
Figure 7: Nanoplastics with Qi601 on human colon cells in a tissue culture model.
The composite fluorescence microscopy image in Figure 8 below provides visual and quantitative evidence of Qi601’s protective effect against microplastic adherence to human colonic epithelial cells (CaCO₂ cell line) in a tissue culture model. The experiment compares untreated control cells exposed to fluorescent microplastics (Panel A) versus cells treated with Qi601 alongside the same microplastic challenge (Panel B).
In Figure 8, Panel A below (Negative Control), a high density of green fluorescent microplastic particles is clearly visible, indicating widespread surface attachment to the CaCO₂ cells in a tissue culture model. This confirms that in the absence of Qi601, microplastics readily interact with and adhere to the human colon epithelial surface in this tissue model, posing a risk of cellular interaction and possible absorption.
In Figure 8 Panel B below (Qi601 + Microplastics), the fluorescent signal is dramatically reduced in this tissue culture model of human colon cells. Microplastic particles appear sparse and scattered, indicating that the presence of Qi601 effectively prevents microplastics from reaching or attaching to the epithelial surface in this tissue culture model of human colon cells. This visual observation is supported by quantitative analysis shown in Panel C, where the number of microplastics associated with CaCO₂ cells is reduced by 83% in the presence of Qi601, as measured by fluorescence signal quantification.
Together, these results demonstrate that Qi601 functions as a physical barrier, intercepting microplastics before they can reach the human colon intestinal epithelium in this tissue culture model. This effect further supports Qi601’s proposed mechanism of action as a “biofilm shield,” potentially reducing the likelihood of plastic particle absorption into systemic circulation.
Figure 8: Human colon cells in a tissue culture model (Panel A above no Qi601 with microplastics; panel B below Qi601 with microplastics)
Simulated Gastric Emptying Protocol in a Tissue Culture Model
In both microplastic and nanoparticle human tissue culture model experiments, a gentle wash protocol was performed post-application, designed to simulate gastric emptying and mucosal clearance conditions. Notably, the protective effect of Qi601 persisted under these conditions: micro- and nano-plastics remained adhered to Qi601 aggregates. They were then washed away, whereas in the absence of Qi601, residual particle fluorescence remained detectable on the epithelial surface even after washing.
Conclusion: Qi601 Sequesters Micro- and Nano-Plastic Particles, Protecting Human Colonic Epithelium in a Tissue Culture Model
A series of tissue culture models with in vitro fluorescence microscopy experiments were conducted using CaCO₂ human colonic epithelial cells to assess the interaction of plastic particles with the epithelial surface and to evaluate the protective sequestration capacity of Qi601, a GRAS-designated aggregate of heat-inactivated Lactobacillus fermentum (GRN 00988).
Upon application of fluorescent 10 µm microplastic spheres or 100 nanoplastic spheres another set of experiments to CaCO₂, a tissue culture model of human colon monolayer cells in the absence of Qi601, where scattered and irregular adherence of particles was observed across the apical surface. This distribution suggests non-specific binding of microplastics to the mucosal interface, which is a potential exposure risk through absorption across the gastrointestinal tract epithelium.
In contrast in the same tissue culture models, microplastic and nanoplastic application to human colon cells (CaCO2) when Qi60 was co-administered with microplastic spheres in one set of experiments, or in the second set of experiments using nanoplastic spheres, the fluorescence microscopy images revealed a marked reduction of microplastic particles on the epithelial surface. Furthermore, the microplastics were preferentially bound to any residual Qi601 aggregates that were not washed away, demonstrating spatial selectivity and high binding specificity. Quantitative analysis further reinforced these findings. When Qi601 was applied with microplastic particles, an 83% reduction in particle attachment to CaCO₂ cells was observed compared to untreated controls. This was determined by measuring fluorescence intensity, indicating that Qi601 not only prevented plastics from reaching the cell surface but also retained those particles within the aggregate matrix, even following simulated gastric emptying through a gentle wash protocol. Together, these results provide clear visual, functional, and quantitative evidence that Qi601 selectively and specifically binds both microplastic and nanoplastic particles i. The ability of Qi601 to significantly reduce epithelial contact in this tissue culture model of human colon cells and to maintain this protective effect post-washing supports its intended role as a physical barrier for environmental plastic contaminants.
These experiments evaluating Qi601 with the application of micro and nano plastics consistently exhibited a corresponding absence of fluorescence on human colonic epithelial cells in these tissue culture model experiments, suggesting that Qi601 effectively intercepted the microplastics interaction on the epithelial surface. These findings provide visual and functional evidence that Qi601 selectively and specifically binds both microplastic and nanoplastic particles, significantly reducing their contact with intestinal epithelial surfaces. The persistence of this effect following simulated gastric emptying supports Qi601’s intended role as a Biofilm Shield as a physical barrier agent to environmental plastic contaminants.
Absorption of particles and nutrients across the GI barrier:
The gastrointestinal (GI) tract has selective permeability, and particle absorption across the intestinal epithelium depends on multiple factors, including size, solubility, and transport mechanisms.
Average Particle Size for Absorption:
- Small molecules (e.g., glucose, amino acids, vitamins):
Typically < 1 nanometer (nm). These are absorbed via specific transporters or diffusion. - Peptides and small proteins:
Can be absorbed intact if they’re < ~1–2 kilodaltons, roughly 1–3 nm in size, via transcytosis or endocytosis, though this is rare. - Nanoparticles (e.g., drug delivery systems):
Research suggests particles up to 50–200 nanometers can occasionally be absorbed through M cells in Peyer’s patches by endocytosis or phagocytosis. - Microparticles:
Particles >500 nm are very poorly absorbed. A few immune cells in specialized regions (e.g., M cells) might take up particles up to 5 microns, but systemic absorption is minimal. - The information provided on particle absorption across the gastrointestinal (GI) tract is grounded in well-established biomedical and pharmacological research. A list of key peer-reviewed sources and reference texts commonly used in the field, along with the relevant topics they support.
These references provide detailed insights into the mechanisms and factors influencing the absorption of particles across the GI tract. Full citations for the key references used in the discussion on particle absorption across the gastrointestinal (GI) tract are listed below:
| Particle Size | Typical Absorption Mechanism | Absorbed? |
| <1 nm | Passive diffusion, active transport | Yes |
| 1–10 nm | Transporters, endocytosis | Limited |
| 10–100 nm | Endocytosis (esp. via M cells) | Possible (low efficiency) |
| 100–500 nm | Phagocytosis, limited uptake | Rare |
| >1 micron (1000 nm) | Not absorbed, possible immune sampling | Extremely rare |
These references cited below support the conclusion that:
- Particles <50–100 nm may cross the GI epithelium via endocytosis.
- Particles 100–500 nm are sometimes taken up by M cells, but inefficiently.
- Particles >1 μm are mostly excluded from absorption, except for immune sampling.
- Qi601 Aggregates are greater than >100 microns, mostly 200 microns in diameter and by size alone, unlikely to be absorbed by the GI.
How nanoplastics are absorbed across the GI.
Nanoplastics—plastic particles typically <1000 nanometers (nm) in size—can be absorbed across the gastrointestinal (GI) tract, but the extent and mechanisms depend heavily on their size, surface chemistry, and charge. Here’s how they can cross the intestinal barrier:
Main Absorption Mechanisms:
- Endocytosis by Enterocytes (intestinal lining cells)
- Nanoplastics <100 nm may be internalized by clathrin- or caveolin-mediated endocytosis.
- Most efficient for particles <50 nm.
- Typically ends up in endolysosomal compartments, which may lead to partial degradation or cellular stress.
- Transcytosis via M Cells in Peyer’s Patches
- Specialized immune cells in the ileum sample the luminal contents.
- Can transport particles up to ~200–500 nm across the epithelium to the underlying immune tissue.
- Provides a route for immune system exposure rather than systemic absorption.
- Paracellular Transport (Very limited)
- Nanoplastics <5–10 nm might transiently slip between cells if tight junctions are disrupted.
- Normally minimal, unless inflammation or barrier dysfunction is present.
- Dendritic Cell Sampling
- Dendritic cells can extend processes between enterocytes to capture particles.
- Mainly leads to immune activation rather than bloodstream absorption.
Efficiency of Absorption:
- Extremely low (<1% of ingested dose) in most models.
- Uptake depends on:
- Size: Smaller = more likely to cross.
- Surface properties: Hydrophobic, charged, or protein-coated particles behave differently.
- GI conditions: pH, enzymes, bile salts, and microbiome all affect plastic fate.
The information cited is not from Quorum Innovations’ primary research and is synthesized from peer-reviewed studies, authoritative reviews, and toxicological reports on nanoplastic absorption. Journal articles cited a list of key sources and types of literature typically used to support this content.
Relevance:
In a series of tissue culture fluorescence microscopy experiments, Qi601 demonstrated protective effects against both microplastic and nanoplastic particle adherence to human colonic epithelial cells (CaCO₂) in laboratory experiments. When fluorescently labeled 10 μm microplastic or 100 nm nanoplastic spheres were applied to CaCO₂ monolayers without Qi601, significant surface attachment of the particles to the epithelial cells was observed, indicating unimpeded interaction. In contrast, co-administration of Qi601 resulted in a marked reduction of plastic particle adherence, with the majority of particles selectively bound to Qi601 aggregates instead of the epithelial surface. These aggregates acted as localized sequestration platforms, displaying spatial selectivity and strong binding affinity for both micro- and nanoplastics. Quantitative image analysis showed that Qi601 reduced microplastic attachment to epithelial cells by 83% relative to untreated controls.
To simulate physiological clearance conditions in these tissue culture model experiments, all samples underwent a gentle wash protocol designed to mimic gastric emptying. This washing step was sufficient to remove Qi601, along with the microplastics and nanoplastics bound to it, while leaving the epithelial monolayer intact for evaluation. Notably, fluorescence remained minimal after washing in Qi601-treated samples, indicating that the bound plastic particles were effectively trapped by Qi601 and eliminated through this simulated gut clearance process. In contrast, in the absence of Qi601, plastic particles persisted on the epithelial surface using the same post-wash protocols to simulate gastric emptying.
Qi601’s performance is directly attributed to its biofilm-like, particulate aggregate structure, composed of heat-inactivated Lactobacillus fermentum cultivated under biofilm-inducing conditions. The resulting aggregates—approximately 200 µm in diameter—are by them selves generally too large to be absorbed across the intestinal barrier and could be naturally eliminated in the stool. This structural profile potentially enables Qi601 to serve as a non-systemic, “biofilm shield” that can potentially intercepts environmental plastic particles in the gastrointestinal tract.
Qi601 is supported by a favorable safety profile. Its source component has been reviewed by the U.S. Food and Drug Administration ( FDA) and granted GRAS status under GRN No. 00988 after FDA review and approval, confirming its suitability for human consumption. It is a non-living, large aggregate, and paired with its demonstrated efficacy in binding and removing plastic contaminants in human tissue culture models, positions Qi601 as a novel, potential solution for addressing environmental microplastics and nanoplastics.
Conclusion and Summary:
Qi601 is a novel, non-living, orally administered therapeutic derived from heat-inactivated probiotic, a probiotic strain cultured under biofilm-inducing conditions to promote natural self-aggregation into high-surface-area macrostructures. This process yields a particulate “biofilm shield” approximately 200 micrometers in diameter—a size that significantly exceeds the normal threshold for gastrointestinal absorption, with the potential for Qi601 to remain confined to the gut lumen and be eliminated naturally. Functionally, Qi601 is able to bind and sequester both microplastic and nanoplastic particles, as observed in human tissue culture models and potentially within the gastrointestinal tract. Fluorescence microscopy studies demonstrate its selective binding capacity, with plastic particles adhering preferentially to Qi601 aggregates while avoiding human colonic epithelial cells (CaCO₂ line) in these human tissue culture models. In contrast, when Qi601 is absent, microplastics and nanoplastics are found attached directly to the epithelial surface in these same human tissue culture models. After simulated gastric emptying via post-treatment washes in the same tissue culture models, Qi601 retains sequestered plastic particles, reinforcing the concept of a mechanical barrier function. By intercepting plastic contaminants before they can contact the human colon cells, Qi601 offers a potential strategy to reduce systemic absorption of micro- and nanoplastics. The bacterial strain from which Qi601 is derived has been evaluated by the U.S. Food and Drug Administration and designated Generally Recognized As Safe (GRAS) under GRN No. 00988, ensuring a high safety profile for human use. In sum, Qi601 represents a bio-inspired, potential solution to a growing environmental and physiological threat of micro- and nanoplastics in humans.
References Used in Scientific Understanding of GI Absorption of Nanoplastics:
- Cox, K. D., et al. (2019) – Human Consumption of Microplastics.
Environmental Science & Technology.- Discusses ingestion and estimated exposure routes.
- Stock, V., et al. (2019) – Uptake and Effects of Orally Ingested Polystyrene Micro- and Nanoplastics in Mice.
Environmental Science: Nano.
- Animal study showing systemic distribution and organ accumulation.
- Bouwmeester, H., et al. (2015) – Potential health impact of environmentally released micro- and nanoplastics in the human food production chain: experiences from nanotoxicology.
Environmental Science & Technology.
- Reviews uptake mechanisms and parallels with engineered nanoparticles.
- EFSA Panel on Contaminants (2016) – Presence of microplastics and nanoplastics in food, particularly seafood.
European Food Safety Authority (EFSA) Journal.
- Evaluates absorption, biodistribution, and risk.
- Wright, S. L., et al. (2017) – Plastic and Human Health: A Micro Issue?
Environmental Science & Technology.
- Comprehensive review of potential health impacts and absorption pathways.
- Walczak, A. P., et al. (2015) – Bioavailability and biodistribution of differently charged polystyrene nanoparticles upon oral exposure in rats.
Journal of Nanoparticle Research.
- Shows how size and charge affect GI uptake.
- Fackelmann, G., & Sommer, S. (2019) – Microplastics and nanoplastics in food and beverages: current evidence and future perspectives.
Current Opinion in Food Science.
References on Particle Absorption Across the GI Tract:
- Artursson, P., & Karlsson, J. (1991).
Correlation between oral drug absorption in humans and apparent drug permeability coefficients in human intestinal epithelial (Caco-2) cells.
Biochemical and Biophysical Research Communications, 175(3), 880–885.- Fundamental reference for molecular permeability based on size and physicochemical properties.
- Desai, M. P., et al. (1996).
Gastrointestinal uptake of biodegradable microparticles: effect of particle size.
Pharmaceutical Research, 13(12), 1838–1845.
- Classic study showing that uptake efficiency drops significantly for particles >1 micron.
- Florence, A. T. (2005).
Nanoparticle uptake by the oral route: Fulfilling its potential?
Drug Discovery Today, 10(4), 237–243.
- Reviews the cellular and physiological barriers to nanoparticle absorption in the GI tract.
- Jani, P., et al. (1990).
Nanoparticle uptake by the rat gastrointestinal mucosa: quantitation and particle size dependency.
Journal of Pharmacy and Pharmacology, 42(12), 821–826.
- Early and influential work showing that particles <100 nm can be taken up by intestinal M cells.
- Yeh, T. H., et al. (2011).
Oral delivery of nanoparticles: strategies to overcome gastrointestinal barriers.
Therapeutic Delivery, 2(5), 603–614.
- Outlines endocytosis mechanisms and limits to nanoparticle uptake in various GI regions.
- Powell, J. J., et al. (2007).
An in vitro model of particle uptake across the human gut epithelium: Characterizing particle size and surface dependency.
Environmental Health Perspectives, 115(3), 417–423.
- Discusses uptake efficiency in relation to particle size, surface charge, and shape.