You don’t need to buy an entire batch of lipopolysaccharide or wait months for production and release – Saves you valuable time
Paying for as few as 50 vials of a proven product and purchasing as you need it, while supplies last, also saves you a tremendous amount of money
Proven quality, product in use worldwide in clinical trials
Get to Phase one quickly with available GMP products
Time is money. The more time spent waiting for your materials to be manufactured is time that you are not conducting your clinical trials. Contracting a manufacturer to produce GMP products can take a year or more for manufacture and release, but with a GMP compliant product in stock, you can purchase what you need when you are ready.
Help your budget with available GMP products
There are so many costs associated with research studies and clinical trials, who wouldn’t want to save a little money on their project? The expense of custom manufacturing can be steep – purchasing available GMP compliant products from List Labs can help alleviate some of those costs. Lipopolysaccharide is broadly used in many types of clinical trials such as in the study of tumor Ag-loaded IL-12 secreting semi-mature DC for the treatment of pediatric cancer.1
Lipopolysaccharide currently in use in clinical trials worldwide
List Labs’ GMP compliant version of HPT™ Lipopolysaccharide from Escherichia coli O113 has already been used by organizations around the world in clinical trials. The quality of this product is proven by the successful use in Phases one through three in past or ongoing clinical trials. This unique difference sets our GMP product apart from the competition and saves you the risk of an unknown product.
See how List Labs’ products have been used in research projects on our citations page.
Dohnal AM, Witt V, Hügel H, Holter W, Gadner H, Felzmann T. Phase I study of tumor Ag-loaded IL-12 secreting semi-mature DC for the treatment of pediatric cancer. Cytotherapy. 2007;9(8):755-70. Epub 2007 Oct 4. PMID: 17917887
By: Karen Crawford, PhD.
President, List Labs
Staphylococcal enterotoxin type B (SEB) is a powerful player in the family of toxins; in scientific terms, a superantigen. This enterotoxin binds to major histocompatibility complex (MHC) class II molecules on antigen-presenting cells and specific V-β chains of the T-cell receptors. This interaction between the three molecules leads to up-regulation of markers and proliferation of T-cells; additionally, it causes a massive release of proinflammatory cytokines including tumor necrosis factor (TNF), interleukins IL-1, IL-6 and interferon-gamma (INF-gamma) (1,2). SEB can form a complex with and activate T cell receptors even in the absence of MHC Class II antigens, making it a useful tool in stimulating T cells (3).
SEB Toxin’s Associations with Human Diseases
SEB is associated with staphylococcal food poisoning, along with TSST-1, is part of the toxic shock syndrome (4) and very likely has a role in human diseases such as atopic dermatitis (5) allergy and rhinitis (6) and the development of autoimmune diseases (7). A mouse model to simulate Toxic Shock Syndrome has been created by exposing mice to both SEB and lipopolysaccharide (8).
Staphylococcal enterotoxin B is on the Centers for Disease Control and Prevention Select Agents & Toxins list, because of high toxicity and the potential to be aerosolized for wide dissemination; however, the quantity which a principal investigator can possess without registration is sufficient for research. Despite the toxicity and potential danger, SEB is a useful tool in research.
Some papers utilizing SEB toxin are described below:
Busbee et al (9) cultured splenocytes in 96-well plates in the presence and absence of SEB. Supernatants were collected and analyzed for cytokine levels using ELISA kits purchased from Biolegend (San Diego, CA) for determining interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), interleukin-2 (IL-2), and IL-6.
Herter et al (10) investigated T cell movement between lymph nodes and sites of inflammation. In this study, SEB is used extensively as a positive control, stimulating an immune response in the mouse kidney and in various cultured cells.
Janik and Lee (11) has used SEB in mice to develop an understanding of the inhibitory effect SEB may have on pre-existing immunity to pathogens unrelated to the superantigen. These studies demonstrated that SEB in BALB/c mice selectively targets memory CD4 T cells.
Marrack P, Blackman M, Kushnir E, Kappler J (1990)The toxicity of staphylococcal enterotoxin B in mice is mediated by T cells.J. Exp. Med.171: 455–464.
Krakauer T and Stiles BG (2013) The staphylococcal enterotoxin (SE) family: SEB and siblings Virulence 4: 759-773. PMID: 23959032
Hewitt CR, Lamb JR, Hayball J, Hill M, Owen MJ, O’Hehir RE (1992) Major histocompatibility complex independent clonal T cell anergy by direct interaction of Staphylococcus aureus enterotoxin B with the T cell antigen receptor. J Exp Med. 175:1493–1499. PMID: 1588277
Kashiwada T, Kikuchi K, Abe S, Kato H, Hayashi H, Morimoto T, Kamio K et al (2012) Staphylococcal enterotoxin B toxic shock syndrome induced by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). Intern. Med. 51: 3085–3088. PMID: 23124156
Breuer K, Wittmann M, Bosche B, Kapp A, Werfel T (2000)Severe atopic dermatitis is associated with sensitization to staphylococcal enterotoxin B (SEB). Allergy55: 551–555. PMID: 10858986
Pastacaldi C, Lewis P, Howarth P (2011)Staphylococci and staphylococcal superantigens in asthma and rhinitis: systematic review and meta-analysis. Allergy66: 549–555. PMID: 21087214
Principato M, Qian BF (2014)Staphylococcal enterotoxins in the etiopathogenesis of mucosal autoimmunity within the gastrointestinal tract.Toxins6: 1471–1489. PMID: 21535520
Huzella LM, Buckley MJ, Alves DA, Stiles BG, Krakauer T (2009) Central roles for IL-2 and MCP-1 following intranasal exposure to SEB: A new mouse model. Vet. Res. Sci. 86:241–247. PMID: 18793785
BusbeePB, Nagarkatti M, Nagarkatti PS (2014) Naturalindoles, indole-3-carbinol and 3,3′-diindolymethane, inhibit T cell activation by staphylococcal enterotoxin B through epigenetic regulation involving HDAC expression. Toxicol Appl Pharmacol.274: 7–16 PMID: 24200994
Herter JM, Grabie N, Cullere X, Azcutia V, RosettI F, Bennett P, Herter-Sprie GS, Eylaman W, Luscinakas FW, Lichtman AH and Mayadas TN (2015) AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation. Nature Communications6, Art. No.: 10182. PMID: 26680259
Janik DK, Lee WT (2015) Staphylococcal Enterotoxin B (SEB) Induces Memory CD4 T Cell Anergy in vivoand Impairs Recall Immunity to Unrelated Antigens. J Clin Cell Immunol. 6(4):1-8. PMID: 26807307
By: Rachel Berlin, Marketing Manager
Microbiome research is uncovering the enormous potential for developing drugs, such a live biotherapeutic products, from the microbiome. This burgeoning field is the future of medicine.
List Labs is excited and proud to support microbiome research by providing reagents to scientists studying the human microbiome. Below is a list of microbiome research studies that have used List Labs’ research reagents such as Athrax, Pertussis, Cholera and Difficile Toxins.
Following a botulism outbreak due to contaminated ham that severely sickened 10 and resulted in the death of three people in Ellezelles, Belgium, a review and case study on botulism was published by a researcher named Emile Van Ermengem (Van Ermengem 1897). While Van Ermengem was not the first to study this syndrome, his article supplied critical information defining botulism as a type of food poisoning having specific paralytic symptoms. He determined that the illness was an intoxication, not an infection, and that its cause was a bacterial toxin. He was also able to isolate and characterize the organism responsible for the toxin as an anaerobic spore-forming bacillus, which he named Bacillus botulinus (later renamed Clostridium botulinum). “Botulinus” is the latin word for sausages, and this nomenclature was used due to the historic link between botulism and improperly processed sausages, particularly blood sausages. His careful and painstaking research provided the foundation for future studies on botulism, its causes and treatments.
During this time, botulism was thought to be related specifically to improperly processed meat, such as sausages and ham, and caused by a single monospecific toxin. Within the next decade both of these theories were proven wrong. In 1904, Dr. G. Landmann isolated a botulinum toxin-producing bacterial strain from preserved bean salad which had caused 11 deaths in Darmstadt, Germany (Landmann 1904). This was the first reporting of botulism due to a source other than meat or fish. In 1910, Leuchs showed that the Ellezelles strain from Van Ermengem and the Darmstadt strain from Landmann were immunologically distinct toxins, providing the first evidence that all botulinum neurotoxins were not the same (Leuchs 1910). This marked the beginning of a century of study related to botulinum neurotoxin diversity which included clinical case reviews and morphological, immunological, and, most recently, genetic studies.
As the bacteria responsible for botulinum neurotoxins initially seemed to be nearly identical in morphology and cultural characteristics, early delineations were the result of serological studies, which were apparently the “hot new thing” of the day. Antisera produced using a particular bacterial strain was tested against other strains to determine relationships among both the toxins and the bacteria that produced them. The assays were both qualitative and quantitative and included agglutination, immuno-absorption, and neutralization techniques (Schoenholz and Meyer 1925). They were originally targeted to both the toxins and the bacteria that produced them, but the emphasis quickly shifted to neutralization of toxins using specific antisera. These antisera, which were predominantly of equine origin, were developed for treatment purposes as well, and they continue to be the only approved treatment for botulism to this day. In 1919, Georgina Burke produced antisera from three strains isolated in California, Oregon, and New York, and she was able to show that the toxins from the two West Coast strains were immunologically identical, while the New York toxin was distinct (Burke 1919). She identified these toxins as type A (West) and Type B (East). Later studies of U. S. strains by K. F. Meyer and B. Dubovsky substantiated her findings (Meyer and Dubovsky 1922).
In the following decades several additional serotypes were identified. In 1922, Dr. Ida Bengtson reported a toxin from a C. botulinum strain that was not neutralized by either type A or type B antisera, which she designated type C (Bengtson 1922). The bacterial strain was isolated from fly larvae that proved to be causative agents in the intoxication of chickens that had ingested these larvae. This illustrates that botulism is not restricted to humans but rather can be seen in a wide variety of animals as well. In fact, differential sensitivities of the toxins in animals has formed a background for discerning various toxin types. In addition, catastrophic losses due to botulism have been noted in domestic fowl, cattle, horses, and even minks and foxes, prompting the development and use of vaccines in these animals for protection. H. R. Seddon isolated a culture that apparently produced type C toxin from an outbreak in cattle in Australia (Seddon 1922). The toxin could be neutralized by Bengtson’s antisera, however, the reverse was not true. This “one-way” neutralization was the first of several anomalies that were discovered when serotyping botulinum neurotoxins.
In 1929, Meyer and Gunnison showed that the toxin from a culture isolated by Theiler and associates in South Africa was immunologically distinct from types A, B, or C. This toxin, which was also related to intoxication in cattle, was designated type D (Meyer and Gunnison 1929).
In the following decade, several botulism cases were noted that were related to ingestion of fish. While Russian scientists were the first to note these unusual cases of botulism, it was Dr. Janet Gunnison who determined the toxins were a new type, and Dr. Elizabeth Hazen who published initial reports on type E botulism cases (Gunnison, Cummings et al. 1936, Hazen 1937). Outbreaks due to dried, smoked, or fermented fish, fish eggs, whale blubber, and seal or walrus meat are common, but there have been rare type E cases related to other foods as well.
The first case due to type F was linked to an outbreak involving duck paste on Langeland Island, Denmark, in 1958 (Moller and Scheibel 1960). Reported cases due to type F are rare and have been restricted to humans so far. Type G was isolated from a cornfield in Argentina in 1969 as part of a soil sampling study conducted by Dr D. F. Gimenez and Dr. A. S. Ciccarelli (Gimenez and Ciccarelli 1970). This type is unusual in that there are no direct reports of intoxications due to type G in people or animals. However, a study of autopsy materials related to sudden deaths due to unknown causes in Switzerland identified type G producing organisms among the samples (Sonnabend, Sonnabend et al. 1981). Why type G is only found in Argentina or Switzerland is a mystery.
As of 1970, there were seven known immunologically distinct botulinum toxin types. However, as we will discover, this was just the beginning of our understanding of the diversity that is seen within botulinum neurotoxins.
Theresa Smith has studied botulinum neurotoxins for over 25 years, specializing in toxin countermeasure research, and is considered a leading expert regarding diversity in botulinum neurotoxins as well as the organisms that produce these toxins.
Bengtson, I. (1922). “Preliminary note on a toxin-producing anaerobe isolated from the larvae of Lucilia caesar.” Pub Health Repts37: 164-170.
Burke, G. S. (1919). “Notes on Bacillus botulinus.” J Bact4: 555-571.
Gimenez, D. F. and A. S. Ciccarelli (1970). “Another type of Clostridium botulinum.” Zentralbl Bakteriol Parasitenk Infektionskr Hyg Abt215: 221-224.
Gunnison, J. B., et al. (1936). “Clostridium botulinum type E.” Proc Soc Exp Biol Med35: 278-280.
Hazen, E. L. (1937). “A strain of B. botulinus not classified as type A, B, or C.” J Infect Dis60: 260-264.
Landmann, G. (1904). “Uber die ursache der Darmstadter bohnenvergiftung.” Hyg Rundschau10: 449-452.
Leuchs, J. (1910). “Beitraege zur kenntnis des toxins und antitoxins des Bacillus botulinus.” Z Hyg Infekt76: 55-84.
Meyer, K. F. and B. Dubovsky (1922). “The distribution of the spores of B. botulinus in the United States. IV.” J Infect Dis31: 559-594.
Meyer, K. F. and J. B. Gunnison (1929). “South African cultures of Clostridium botulinum and parabotulinum. XXXVII with a description of Cl. botulinum type D, N. SP.” J Infect Dis45: 106-118.
Moller, V. and I. Scheibel (1960). “Preliminary report of an apparently new type of Cl. botulinum ” Acta Path Microbiol Scand48: 80.
Schoenholz, P. and K. F. Meyer (1925). “The serologic classification of B. botulinus.” J Immunol10: 1-53.
Seddon, H. R. (1922). “Bulbar paralysis in cattle due to the action of a toxicogenic bacillus, with a discussion on the relationship of the condition to forage poisoning (botulism).” J Comp Path Ther35: 147-190.
Sonnabend, O., et al. (1981). “Isolation of Clostridium botulinum type G and identification of type G botulinal toxin in humans: report of five sudden unexpected deaths.” J Infect Dis143: 22-27.
Van Ermengem, E. (1897). “A new anaerobic bacillus and its relation to botulism (originally published as “Ueber einen neuen anaeroben Bacillus und seine beziehungen zum botulismus” in Zeitschrift fur Hygiene und Infektionskrankheiten, 26:1-56) ” Clin Infect Dis4: 701-719.
By: Rachel Berlin, Marketing Manager
Linda Shoer, Founder of List Labs, exhibiting at ASM in the 90’s
List Labs is proud to be exhibiting at the ASM Microbe Conference again this year. The meeting will be held June 7-11th in Atlanta, GA at the Georgia World Congress Center. List Labs has been exhibiting at this conference for over 20 years and is excited to be back in 2018. ASM Microbe showcases the best microbial sciences in the world and provides a forum to explore the complete spectrum of microbiology from basic science to translation and application.
Meet with usto discuss research projects, products you might need or services we can help you with!
By: Rachel Berlin, Marketing Manager
1978 was a great year for scientific advancement – NASA hired the first women astronauts, the first test tube baby was born and List Labs was founded. Linda Shoer, our founder, saw an opportunity when she realized there was a need for a commercial supplier of Cholera Toxin for studies in signal transduction and neuronal track tracing. On May 18, 1978, Linda started something more than a company, she started a family- the List Labs family.
List Labs carries on the values instilled by Linda Shoer and continues to grow our team, our capabilities and experience. We are excited to see what the next 40 years bring!
By: Rachel Berlin, Marketing Manager
List Labs manufactures biological toxins for use in research. While we sell products directly, we also have both domestic and international distributors. Worldwide we have over 30 distributors in nearly 20 countries. Distributors receive benefits like generous discounts on products, full access to List Labs’ marketing, promotion via website, email marketing and social media and leads directly from List Labs. A dedicated distributor coordinator will work directly with you to answer any of your questions, suggest ways to save money on orders and to help you be successful selling List Labs’ products!
So how does a company become a distributor for List Labs?
The answer is simple and can be done in three easy steps:
Qualifying Questions to see if your company would be a good fit as a distributor for List Labs’ products
Fill out our application and become approved as a buyer
Review and Sign the Contract
Answer the Qualifying Questions
First step in becoming a distributor for List Labs is answering a series of qualifying questions that will help us determine if your company will be a good fit for us as a distributor of our products. List Labs will assess the partnership potential based on the answers to the qualifying questions. If it seems like a good fit, List Labs will move forward with the distributor application.
Fill out the Distributor Application
Once both parties agree that this partnership would be mutually beneficial and wish to move forward, the potential distributor will fill out the official application. Because of the nature of List Labs’ product, we are required to obtain certain information per federal regulations. If the application is filled out correctly and with enough detailed information, the approval process generally takes one to three business days.
Review and Sign the Distributor Contract
If the application is approved we will draft a contract including terms for discount, outlining the benefits of becoming a distributor and the List Labs’ requirements. Sign the contract, then we will countersign it, send it back and that’s it!
List Labs is currently actively seeking distributors in Mexico, Indonesia and South America. If you are interested in becoming a domestic or international distributor for List Labs’ products, please contact us today!
By: Shawn Lyles, Marketing Manager
List Labs will be attending the 54th annual Interagency Botulism Research Coordinating Committee (IBRCC) this year from October 27-30th. The conference will be held in Ellicott City, MA at the Turf Valley Resort and Conference Center. This international forum presents state-of-the-art research on botulinum toxin and the deadly disease of botulism. This important conference provides the opportunity for federal and non-federal agencies to coordinate in the effort against botulism in all of it’s forms.
The following List Labs employees will be attending the conference:
List Labs currently has nearly 50 botulinumrelated products including recombinant light chain, heavy chain, antibodies and specific substrates in stock. See how scientists have used List Labs’ reagents in their research projects on our citations page.