Nisin (E234): The Bacterial Weapon in Your Food

Table of Contents

1. Key Effects at a Glance
2. Overview
3. Where It's Found (Exposure Routes)
4. How It Works
5. Health Effects
6. Antimicrobial Resistance
7. The Microbiome Paradox
8. Regulatory Status & Safety Thresholds
9. Emerging Research
10. Where Nisin Is and Is Not Used
11. Key Research Papers
12. Connections
13. Featured Videos

Key Effects at a Glance

• Antibiotic food additive – A lantibiotic that targets Lipid II in Gram-positive bacteria.
• Digestive inactivation – Rapidly hydrolyzed by chymotrypsin; negligible systemic absorption.
• Gut microbiome disruption – Inhibits Lactobacillus and Bifidobacterium in the upper gastrointestinal (GI) tract before full proteolytic inactivation.
• Antimicrobial resistance concerns – Nisin-resistant Listeria strains documented in food-processing environments; potential cross-resistance with vancomycin pathways.
• No known carcinogenicity – No cancer effect has been identified, but the European Food Safety Authority (EFSA) rates the older long-term animal studies as limited.
• ADI – The Joint FAO/WHO Expert Committee on Food Additives (JECFA) set 0–2.0 mg/kg body weight/day in 2013; EFSA set 1 mg nisin A/kg/day in 2017.

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1. Overview

Nisin (E234) is a lantibiotic — a class I bacteriocin — produced naturally by the lactic acid bacterium Lactococcus lactis subsp. lactis. It is the only bacteriocin currently approved as a food preservative worldwide, a distinction it has held since the 1950s. The commercial product is a standardized nisin preparation containing approximately 2.5% pure nisin in a sodium chloride and defatted milk solids matrix.

Nisin was first described in scientific literature in 1928 by Rogers and Whittier, who observed that certain strains of L. lactis — naturally present in dairy fermentation — produced a substance that inhibited the growth of competing bacteria during cheese making. The compound was named "nisin" from N-Inhibitory Substance. Systematic study of its structure and mechanism advanced considerably in the following decades, with its complete chemical characterization achieved in the 1970s and its three-dimensional structure resolved in the 1990s.

Nisin's approval as a food additive reflects its natural origin (produced by a bacterium used in fermentation for millennia), its peptide nature (making it susceptible to digestion), its narrow antibacterial spectrum, and its long history of incidental human consumption through fermented dairy products. However, like natamycin, its classification as both a food additive and an antibiotic creates inherent tensions with antimicrobial stewardship principles.

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2. Where It's Found

Nisin is used across a diverse range of processed food categories, reflecting its particular effectiveness against the Gram-positive bacterial spoilage organisms and pathogens most prevalent in dairy, heat-processed, and fermented foods:

• Processed cheese and cheese spreads: The primary commercial application. Nisin prevents the growth of Clostridium species responsible for "blowing" (gas production) and textural defects in processed cheese during extended ambient storage.
• Canned foods: Nisin is used in heat-processed canned vegetables, soups, and ready meals to provide additional protection against thermophilic spore-formers that survive retort processing, allowing reduction in thermal treatment intensity and improved product quality.
• Pasteurized liquid eggs: Prevents post-pasteurization contamination with Gram-positive pathogens during storage.
• Beer: Nisin controls bacterial spoilage — particularly Lactobacillus and Pediococcus species — in brewery production, extending shelf life without affecting yeast-mediated fermentation (since nisin is ineffective against yeasts).
• Crumpets and other baked goods: Nisin is incorporated into the dough to extend mold-free shelf life by suppressing bacterial rope disease (Bacillus subtilis) and certain mold-associated bacterial flora.
• Reconstituted and flavored milk products: Used in some markets to extend the shelf life of dairy-based beverages susceptible to Gram-positive spoilage organisms.
• Canned soups and sauces: Applied as a supplement to thermal processing in ambient-stable products.

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3. How It Works

Nisin operates through a dual mechanism that makes it one of the most potent and mechanistically sophisticated naturally occurring antibiotics known:

Mechanism 1: Lipid II Sequestration

Nisin binds with extremely high affinity (Kd in the nanomolar range) to Lipid II, the essential bactoprenol-anchored cell wall precursor that shuttles cell wall building blocks (N-acetylmuramic acid pentapeptide units) across the bacterial cell membrane. By capturing and sequestering Lipid II molecules, nisin physically blocks the transglycosylation and transpeptidation steps of cell wall synthesis — the same target exploited by vancomycin, a clinically critical antibiotic. This mechanism alone would be bacteriostatic, preventing new cell wall synthesis.

Mechanism 2: Pore Formation

Beyond sequestering Lipid II, nisin uses the captured Lipid II molecules as docking platforms to insert into the bacterial membrane and form transmembrane pores approximately 1–2 nm in diameter. These pores are large enough to allow passage of ions, amino acids, and small metabolites, rapidly dissipating the membrane potential and cellular energy charge. The pore-forming activity converts the bacteriostatic Lipid II inhibition into a bactericidal mechanism.

The synergy of these two mechanisms — using the same target molecule for both cell wall inhibition and membrane disruption — makes nisin exceptionally potent at very low concentrations (minimum inhibitory concentrations typically in the range of 0.01–10 μg/mL against susceptible organisms).

Spectrum of Activity

Nisin's spectrum is restricted to Gram-positive bacteria. This specificity arises because:

• Gram-positive bacteria have cell walls with externally accessible Lipid II molecules, allowing nisin to reach its target.
• Gram-negative bacteria possess an outer membrane that excludes nisin (a polycationic peptide) from reaching the inner membrane and its Lipid II target.

Key susceptible organisms include: Listeria monocytogenes, Clostridium botulinum, Clostridium tyrobutyricum, Staphylococcus aureus (including some methicillin-resistant Staphylococcus aureus (MRSA) strains), Bacillus cereus, and numerous Lactobacillus and Streptococcus species — including many probiotic and beneficial gut bacteria.

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4. Health Effects

Nisin's direct toxicological profile is among the most favorable of any food preservative:

• Rapid digestive inactivation: Nisin is a polypeptide of 34 amino acids (3,354 Da). In the gastrointestinal tract, it is rapidly hydrolyzed by pancreatic proteases — particularly chymotrypsin — into inactive amino acid fragments. Most ingested nisin is therefore handled by the body as a dietary protein, and systemic absorption of intact peptide is low. The word to resist is “complete”: a 2023 pig study recovered intact, still-active nisin from the gastrointestinal tract after oral dosing, so degradation is substantial but not total — see the microbiome section below.
• Cancer and long-term studies: No carcinogenic potential has been identified in animal studies, but EFSA's 2017 opinion rates the older chronic and cancer studies (from 1962 and 1970) as “limited and not adequate for hazard characterisation.” JECFA evaluated nisin in 1969 and again in 2013.
• Allergenicity: No credible reports of immunoglobulin E-mediated allergic reactions to nisin in food have been documented in the peer-reviewed literature. The peptide's rapid digestion substantially reduces its allergenicity compared to intact dietary proteins.
• High acute oral tolerance: A review gives a lethal dose (LD50) of approximately 6,950 mg/kg, without naming the species — extremely low toxicity. In a three-generation rat study, EFSA identified no adverse effect on mothers, reproduction or development at 5% nisin preparation in the diet, equivalent to 62.5 mg nisin/kg/day.

Gut Microbiome Concerns

This is the part of the nisin story where the honest answer is “it depends on the dose, and the evidence is genuinely mixed.” Nisin kills Gram-positive bacteria — and the two genera most people take deliberately as probiotics, Lactobacillus and Bifidobacterium, are Gram-positive. Whether that matters at the amounts found in food is a real question with real data on both sides, so here is what has actually been measured, in order of how directly it applies to a person eating cheese.

• Nisin can survive the gut intact — the older “fully digested” story is too simple. A 2023 study in pigs (whose digestive tract is the standard stand-in for a human one) recovered orally dosed nisin from the gastrointestinal tract still intact and still biologically active, confirmed both by antimicrobial assay and by molecular weight. The pigs were given ultrapure (95%) nisin ZP, a natural variant, at 150 mg/kg body weight in feed, or an encapsulated form at 850 mg/kg (O’Reilly et al., 2023). So the reassurance that chymotrypsin destroys all of it before it can act is only partly true; some fraction gets through. A separate mouse study shows that how much gets through depends on what the nisin is eaten with (Gough et al., 2018; see below).
• At high doses it demonstrably reshapes the microbiome — and the change reverses. In the same pig study, nisin caused a decrease in Gram-positive bacteria and a corresponding relative rise in Gram-negative Proteobacteria, exactly the shift that had previously only been hypothesized. Functionally, the pathways for acetate and butyrate synthesis fell while propionate rose, and total short-chain fatty acids in stool dropped. Butyrate is the primary fuel of the colon lining, so that is a change worth taking seriously. The important qualifier is that these effects largely reversed after the four days of dosing stopped: ten days later the bacterial community was again comparable to untreated pigs and intact nisin was no longer detected, although the butyrate level was still significantly lower (p = 0.048).
• Pure nisin at one tested dose did not change fecal bacteria in rats. The counterweight comes from rats colonized with a human gut flora: dosing with pure nisin (EFSA describes this as feeding 60 mg of nisin A; the EU limit for cheese is 12.5 mg per kg of cheese) produced no significant change in the fecal microbiota, and DGGE profiles from nisin-dosed animals were indistinguishable from saline controls. Measured nisin concentrations were roughly ten-fold higher in the small intestine and two-hundred-fold higher in feces by immunoassay than by bioassay — meaning most of what was present had been degraded or inactivated. EFSA notes that some antimicrobial activity remained in the feces, and both L. lactis strains tested, with and without nisin production, raised Bifidobacterium in feces during the first 8 days (Bernbom et al., 2006).
• Protecting nisin from digestion is what makes the difference. Mice fed nisin inside resistant-starch matrices showed significantly altered gut microbiota, and the differences between the two nisin diets tracked how much nisin each matrix released rather than the nisin dose itself: mice ate three times as much nisin in starch dough, yet twice as much turned up in the feces of mice fed nisin in starch gel (Gough et al., 2018). This is the mechanistic bridge between the two results above: nisin that is shielded from proteases acts on the microbiome, and nisin that is not, mostly does not.
• What this adds up to for a person eating preserved cheese. The realistic dietary exposure is small, and the one rat experiment with pure nisin, at a dose well above food levels, found no change in fecal bacteria. The concern is not "cheese destroys your microbiome"; it is that nisin is not as inert as the older toxicology summaries imply, that the effect is dose- and matrix-dependent, and that nobody has run the long-term human study. No human study has tested whether spacing probiotics away from heavily nisin-preserved processed cheese makes any difference, including after antibiotics.

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5. Antimicrobial Resistance

Despite nisin's favorable direct toxicology, its role as an antibiotic food additive raises parallel AMR concerns to those documented for natamycin:

Documented Nisin Resistance in Listeria

Natural nisin resistance is common in Listeria monocytogenes, a priority foodborne pathogen. Of 356 field strains from foods, food production environments, animals and human infections, 66% were classed as resistant, 26% intermediate and 8% sensitive; higher resistance went with mutations in rsbU and pbpB3, and higher sensitivity with mutations in the sigB, vir and dlt genes (Wambui et al., 2020). In 282 German isolates from ready-to-eat foods, food-processing environments and patients, the concentration stopping 90% of them was under 1,500 IU/mL, and two resistant strains were sequenced (Szendy et al., 2019). A 2025 study linked a gtcA mutation in a food-plant strain to higher resistance (Mandinyenya et al., 2025). Resistance mechanisms include:

• Cell wall surface changes: Adding the amino acid D-alanine to the teichoic acids in the wall (D-alanylation) reduces the wall’s negative surface charge, so positively charged nisin binds less well. This is a change in charge, not in thickness; a thicker wall is a separate change, seen in the lab-made resistant Staphylococcus aureus described below.
• Membrane phospholipid modification: Incorporation of lysyl-phosphatidylglycerol into the membrane reduces nisin's ability to form stable pores.
• PrfA-regulated tolerance: Virulence regulator PrfA influences nisin tolerance through yet incompletely understood mechanisms.

Cross-Resistance with Clinical Antibiotics

The Lipid II-binding mechanism shared between nisin and vancomycin raises concern about cross-resistance. While the binding sites on Lipid II differ between nisin (pyrophosphate) and vancomycin (D-Ala-D-Ala), the D-alanylation resistance mechanisms that reduce nisin efficacy may also reduce susceptibility to other cell wall-active antibiotics. Cross-tolerance between nisin and clinical glycopeptide antibiotics has been demonstrated in laboratory conditions, though its clinical prevalence in food-associated strains requires further investigation. In one such experiment, Staphylococcus aureus made resistant to the antibiotic ramoplanin in the lab also became cross-resistant to vancomycin and nisin, with a thickened cell wall, and lost the resistance after 18 days without the drug (Schmidt et al., 2010).

Horizontal Gene Transfer of Resistance Determinants

Nisin resistance genes (particularly nsr encoding the nisin resistance protein, and operon components from nisRK regulatory pathways) reside on mobile genetic elements capable of horizontal transfer between bacterial species in food environments. Transfer of nisin immunity genes from nisin-producing L. lactis to other Gram-positive organisms — including potential pathogens — has been demonstrated in laboratory and food matrix models.

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6. The Microbiome Paradox

Perhaps the most conceptually striking concern raised by dietary nisin is what might be called the microbiome paradox: nisin kills the very bacteria that the probiotic industry promotes as essential for health.

The probiotics market — now worth tens of billions of dollars annually — is anchored around oral supplementation with Lactobacillus and Bifidobacterium species. These genera are precisely the Gram-positive bacteria most susceptible to nisin at the concentrations achievable in the upper gastrointestinal tract before full proteolytic inactivation. Simultaneously, millions of people consuming probiotic supplements are regularly eating processed cheeses, canned soups, and other foods preserved with nisin.

The practical implications of this parallel are underexplored in published research:

• Probiotic viability reduction: Nisin present in the stomach and small intestine at the time of probiotic capsule transit could reduce the viable count of probiotic organisms reaching the large intestine, partially or fully negating the intended probiotic dose.
• Endogenous microbiome suppression: Beyond supplemented probiotics, nisin could suppress endogenous Lactobacillus populations in the small intestinal microbiome, where these organisms play roles in colonization resistance and mucosal immune modulation.
• Ecological shift toward Gram-negative dominance: Regular dietary nisin could exert selective pressure favoring Gram-negative bacteria in the gut, potentially contributing to dysbiosis characterized by increased lipopolysaccharide (LPS) burden from Gram-negative organisms — a state associated with systemic low-grade inflammation and metabolic disease risk.

Controlled human trials examining the gut microbiome composition of individuals with high versus low dietary nisin exposure — ideally using shotgun metagenomic sequencing to characterize community composition — are urgently needed to determine whether these theoretical concerns translate to measurable effects.

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7. Regulatory Status

Nisin holds regulatory approval across more than 50 countries, making it one of the most broadly accepted natural antimicrobial food preservatives globally:

• United States (U.S. Food and Drug Administration, FDA): Approved as generally recognized as safe (GRAS) for use in pasteurized cheese spreads and pasteurized process cheese spreads (with or without fruits, vegetables or meats), at a maximum of 250 parts per million of nisin in the finished product. Listed in 21 CFR 184.1538. Generally recognized as safe status has been extended by U.S. Food and Drug Administration notification for additional food categories.
• European Union: Approved as E234 under Regulation (EC) No 1333/2008 for use in clotted cream (maximum 10 mg/kg), mascarpone (maximum 10 mg/kg), ripened cheese, processed cheese and ripened and processed cheese products (maximum 12.5 mg/kg), pasteurized liquid egg (maximum 6.25 mg/kg), and semolina and tapioca puddings (maximum 3 mg/kg). In 2017 EFSA concluded that proposed use in unripened cheese (12 mg/kg) and heat-treated meat products (25 mg/kg) would not be of safety concern; whether those uses have since been authorized was not checked for this page. The EU imposes more restrictive permitted uses than the U.S. Food and Drug Administration.
• WHO/FAO (JECFA): At its 77th meeting in 2013, JECFA set an Acceptable Daily Intake (ADI) of 0–2.0 mg/kg body weight/day.
• EFSA (2017): Raised its own ADI from 0.13 to 1 mg nisin A/kg body weight/day, based on a 90-day rat study that found no adverse effects at 225 mg/kg/day, the highest dose tested. It estimated overall exposure to be below the new ADI for all population groups. EFSA also stated that possible antimicrobial resistance and effects on the gut microbiota had “deliberately not been considered,” as outside its remit, so this safety figure does not answer those two questions.
• Codex Alimentarius: Nisin is listed in the Codex General Standard for Food Additives for use in specific food categories including heat-treated cheese and cream.
• Organic foods: Like natamycin, nisin is not permitted in certified organic foods under USDA NOP or EU organic regulations, due to its antibiotic classification.

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8. Emerging Research

Beyond its established role as a food preservative, nisin has attracted substantial research interest in several emerging applications:

Anti-Cancer Activity

A series of studies beginning in the 2010s has investigated nisin's cytotoxic activity against cancer cells. Kamarajan et al. (2015) published significant findings demonstrating that nisin ZP (a variant form) exhibited potent cytotoxicity against head and neck squamous cell carcinoma (HNSCC) cells in vitro and in murine xenograft models. The mechanism the authors actually documented is apoptosis through a calpain-dependent pathway — and, importantly, that pathway was triggered in the carcinoma cells but not in normal human oral keratinocytes, which is the selectivity any candidate drug has to show. Nisin ZP also killed endothelial cells and reduced vascular sprouting in vitro, suggesting an anti-angiogenic contribution on top of the direct cytotoxicity. Keep the evidence tier in view: this is cell-culture and mouse work, there is no human trial of nisin as a cancer treatment, and the doses used are far above anything obtainable from food. Eating nisin-preserved cheese is not a cancer therapy, and nothing in this literature suggests otherwise. (DOI: 10.1371/journal.pone.0131008)

Nisin-Producing Probiotics

Research groups have explored the concept of engineering or selecting L. lactis nisin-producing strains as "therapeutic probiotics" — organisms that could colonize the gut and produce nisin in situ to suppress pathogenic Gram-positive bacteria including Clostridioides difficile and Listeria. This approach leverages nisin's natural origin but raises the same concern about suppression of beneficial Lactobacillus strains.

Bioengineered Nisin Variants

Through site-directed mutagenesis and combinatorial biosynthesis, researchers have generated hundreds of nisin analogs with modified activity spectra, enhanced stability, or improved activity against specific resistant pathogens. Nisin variants with activity against Gram-negative bacteria (achieved by combining nisin with membrane-permeabilizing agents such as EDTA) represent one avenue being explored for food safety applications against Salmonella and E. coli. Additionally, variants with increased activity against nisin-resistant Listeria isolates from food environments have been developed, addressing the practical resistance problem in food processing.

Synergistic Combinations

Nisin combined with other hurdle technologies — high pressure processing, essential oils (thymol, carvacrol), organic acids, or bacteriophages — shows synergistic activity that allows reduction of nisin concentrations needed for equivalent preservation, potentially reducing selection pressure for resistance.

New Variants and Gum Disease

A nisin variant, nisin G, has been found in Streptococcus salivarius from the human gut; the strain controlled Fusobacterium nucleatum, a bacterium associated with colorectal cancer, in a laboratory model of the colon with little effect on the surrounding bacteria (Lawrence et al., 2025). Nisin and a nisin-producing Lactococcus lactis reduced bone loss and inflammation in a mouse model of gum disease (Gao et al., 2022). Neither has been shown in people.

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9. Where Nisin Is and Is Not Used

• Cheese labels list it as “nisin” or “E234.”
• U.S. Department of Agriculture (USDA) Organic and EU Organic cheeses: both standards prohibit nisin as an antibiotic-category additive.
• Shelf-stable processed cheese spreads and canned cheese products are the largest volume use of nisin.
• Artisanal and farmstead cheese producers typically rely on controlled aging rather than added bacteriocins.
• Probiotics and meals: taking probiotics separately from meals containing nisin-preserved foods is described as reducing overlap of transit in the upper gastrointestinal tract; no human study has tested it.

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Connections

• All Toxins
• Preservatives
• Natamycin
• Sodium Nitrite
• Potassium Sorbate
• BHA and BHT
• US vs EU Food Safety
• Banned Additives
• Food Additives
• Cancer
• Gut-Brain Axis
• Probiotics
• Gut Microbiome
• Fermented Foods
• Food Dyes Banned Worldwide
• Milk
• Staphylococcus Aureus
• Bacillus Subtilis

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Key Research Papers

1. Breukink E, de Kruijff B. Lipid II as a target for antibiotics. Nature Reviews Drug Discovery. 2006;5(4):321–332. — doi:10.1038/nrd2004
2. Campion A, Casey PG, Field D, Cotter PD, Hill C, Ross RP. In vivo activity of nisin A and nisin V against Listeria monocytogenes in mice. BMC Microbiology. 2013;13:23. — doi:10.1186/1471-2180-13-23
3. Wambui J, Eshwar AK, Aalto-Araneda M, Pöntinen A, Stevens MJA, Njage PMK, Tasara T. The Analysis of Field Strains Isolated From Food, Animal and Clinical Sources Uncovers Natural Mutations in Listeria monocytogenes Nisin Resistance Genes. Frontiers in Microbiology. 2020;11:549531. — doi:10.3389/fmicb.2020.549531
4. Kamarajan P, Hayami T, Matte B, Liu Y, Danciu T, Ramamoorthy A, Worden F, Kapila S, Kapila Y. Nisin ZP, a bacteriocin and food preservative, inhibits head and neck cancer tumorigenesis and prolongs survival. PLOS ONE. 2015;10(7):e0131008. — doi:10.1371/journal.pone.0131008
5. Delves-Broughton J. Nisin and its uses as a food preservative. Food Technology. 1990;44(11):100–112.
6. European Food Safety Authority. Opinion of the Scientific Panel on food additives, flavourings, processing aids and materials in contact with food (AFC) related to The use of nisin (E 234) as a food additive. EFSA Journal. 2006;4(3):314. — doi:10.2903/j.efsa.2006.314
7. EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS). Safety of nisin (E 234) as a food additive in the light of new toxicological data and the proposed extension of use. EFSA Journal. 2017;15(12):5063. — doi:10.2903/j.efsa.2017.5063
8. JECFA (Joint FAO/WHO Expert Committee on Food Additives). Specifications for the identity and purity of food additives and their toxicological evaluation: some antibiotics. Twelfth Report of the Joint FAO/WHO Expert Committee on Food Additives. No 430. World Health Organization, Geneva; 1969.
9. JECFA (Joint FAO/WHO Expert Committee on Food Additives). Evaluation of certain food additives and contaminants. Seventy-seventh report of the Joint FAO/WHO Expert Committee on Food Additives. No 983. World Health Organization, Geneva; 2013.
10. Cotter PD, Ross RP, Hill C. Bacteriocins — a viable alternative to antibiotics? Nature Reviews Microbiology. 2013;11(2):95–105. — doi:10.1038/nrmicro2937
11. Rogers LA, Whittier EO. Limiting factors in the lactic fermentation. Journal of Bacteriology. 1928;16(4):211–229. — doi:10.1128/jb.16.4.211-229.1928
12. Wiedemann I, Breukink E, van Kraaij C, Kuipers OP, Bierbaum G, de Kruijff B, Sahl HG. Specific binding of nisin to the peptidoglycan precursor lipid II combines pore formation and inhibition of cell wall biosynthesis for potent antibiotic activity. Journal of Biological Chemistry. 2001;276(3):1772–1779. — doi:10.1074/jbc.M006770200
13. Field D, Cotter PD, Ross RP, Hill C. Bioengineering of the model lantibiotic nisin. Bioengineered. 2015;6(4):187–192. — doi:10.1080/21655979.2015.1049781
14. O’Reilly C, Grimaud GM, Coakley M, O’Connor PM, Mathur H, Peterson VL, O’Donovan CM, Lawlor PG, Cotter PD, Stanton C, Rea MC, Hill C, Ross RP. Modulation of the gut microbiome with nisin. Scientific Reports. 2023;13:7899. — doi:10.1038/s41598-023-34586-x
15. Gough R, Cabrera Rubio R, O’Connor PM, Crispie F, Brodkorb A, Miao S, Hill C, Ross RP, Cotter PD, Nilaweera KN, Rea MC. Oral delivery of nisin in resistant starch based matrices alters the gut microbiota in mice. Frontiers in Microbiology. 2018;9:1186. — doi:10.3389/fmicb.2018.01186
16. Bernbom N, Licht TR, Brogren C, Jelle B, Johansen AH, Badiola I, Vogensen FK, Nørrung B. Effects of Lactococcus lactis on composition of intestinal microbiota: role of nisin. Applied and Environmental Microbiology. 2006;72(1):239–244. — PubMed PMID: 16391049
17. Szendy M, Kalkhof S, Bittrich S, Kaiser F, Leberecht C, Labudde D, Noll M. Structural change in GadD2 of Listeria monocytogenes field isolates supports nisin resistance. International Journal of Food Microbiology. 2019;305:108240. — PubMed PMID: 31202151
18. Mandinyenya T, Wambui J, Muchaamba F, Stevens MJA, Tasara T. Nisin resistance is increased through GtcA mutation induced loss of cell wall teichoic acid N-acetylglucosamine modifications in Listeria monocytogenes. International Journal of Food Microbiology. 2025;428:110954. — PubMed PMID: 39566380
19. Schmidt JW, Greenough A, Burns M, Luteran AE, McCafferty DG. Generation of ramoplanin-resistant Staphylococcus aureus. FEMS Microbiology Letters. 2010;310(2):104-11. — PubMed PMID: 20659164
20. Lawrence GW, Garcia-Gutierrez E, O’Mahony AK, Walsh CJ, O’Connor PM, Begley M, Guinane CM, Cotter PD. A gut-derived Streptococcus salivarius produces the novel nisin variant designated nisin G and inhibits Fusobacterium nucleatum in a model of the human distal colon microbiome. mBio. 2025;16(2):e0157324. — PubMed PMID: 39692472
21. Gao L, Kuraji R, Zhang MJ, Martinez A, Radaic A, Kamarajan P, Le C, Zhan L, Ye C, Rangé H, Sailani MR, Kapila YL. Nisin probiotic prevents inflammatory bone loss while promoting reparative proliferation and a healthy microbiome. NPJ Biofilms and Microbiomes. 2022;8(1):45. — PubMed PMID: 35672331
22. Agriopoulou S, Stamatelopoulou E, Sachadyn-Król M, Varzakas T. Lactic Acid Bacteria as Antibacterial Agents to Extend the Shelf Life of Fresh and Minimally Processed Fruits and Vegetables: Quality and Safety Aspects. Microorganisms. 2020;8(6). — PubMed PMID: 32599824
23. European Commission. Regulation (EC) No 1333/2008 of the European Parliament and of the Council on food additives. Official Journal of the European Union. 2008;L354:16–33.
24. FDA. Code of Federal Regulations, Title 21, Section 184.1538: Nisin preparation. U.S. Food and Drug Administration. 2023.

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