Tag Archives: gut-health

NeoGenesis’ New Topical Probiotic Products, MB-2 and MB-3, Feature 5 Strains of Live, Colonizing Symbiotic Bacteria

Based on many recent scientific studies of using live, symbiotic bacteria in a topical application, NeoGenesis has launched a new probiotic, topical skin care product (MB-2) and will be launching MB-3 soon. I briefly explain some of the science for using topical probiotic products in this post.

I’ve been publishing about (Maguire and Maguire, 2017) and developing topical probiotic products (MB-1 was launched in 2015) for well over a decade. The data for topical symbiotic bacteria colonizing and benefiting the skin are rapidly accumulating. For example, topically applied Lactobacilli have been found to temporarily colonize the skin and to directly compete with skin pathogens through adhesion inhibition, production of antimicrobial metabolites, and by influencing pathogen metabolism. The competitive anti-pathogenic action of Lactobacilli has been described mechanistically for common skin pathogens, such as Staphylococcus aureus, Cutibacterium acnes, and Candida albicans (DeLanghe et al, 2021). Recently, studies of live Lactobacillus crispatus (LBC) demonstrated benefit to the skin when compared to inactivated LBC biomass, stimulating collagen in vitro. Moreover, the live LBC was stable in formulations not containing antimicrobial preservatives and was found to improve dermis density and wrinkle appearance in vivo.

Microbes and human cells have co-evolved for billions of years, through which they have been exposed to many types of molecules produced by each other and acting in bidirectional signaling pathways (Wu et al, 2025). For example, Lactobacilli have an immunomodulatory capacity associated with a reduction in excessive skin inflammation (Delanghe et al, 2021). Their influence on the immune system is mediated by bacterial metabolites and cell wall-associated or excreted microbe-associated molecular patterns (MAMPs). Lactobacilli acting as immune modulators associated with a reduction in excessive skin inflammation exert their influence on the immune system by secreting many bacterial metabolites, a type of postbiotic (this is a term I introduced in 2019; Maguire and Maguire, 2019), along with the cell wall-associated MAMPs that are not released but integrated into the cell of the bacterium. In addition, Lactobacilli can also enhance the skin barrier function, which is often disrupted as a result of infection, trauma, or in inflammatory skin diseases such as eczema and psoriasis. Lebeer et al (2022) found that the Lactobacillis species L. crispatus, L. iners, L. gasseri, and L. jensenii, all still belonging to the genus Lactobacillus strictu sensu, have a broader human adaptation to stratified epithelium than merely the human vaginal epithelial cells, based on their association with healthy skin. In other words, Lactobacilli colonize the skin just as they do in other epithelial tissues. However, these colonies of bacteria on the skin can be disrupted by a number of extrinsic and intrinsic factors, such as harsh chemicals and aging. For example, aged skin contains significantly fewer L. crispatus (a beneficial symbiont) than young skin. Let’s now breiefly look at how symbiotic bacteria benefit the skin through quorum sensing and the release of post-biotic molecules, including molecules that will inhibit pathogenic bacteria such as certain strains of Staphlacoccus aureus.

Quorum Sensing and Post-Biotic Release

Mechanisms of quorum sensing is different for gram-positive versus gram-negative bacteria. Regardless, quorum sensing molecules (AIP or QS molecules) can work within species or on other species to control growth. This is an important means by which symbiotic bacteria, such as B. subtilis, can inhibit pathogenic bacteria such as S. aureus.

As bacteria grow, they secrete and sense signaling molecule in the surrounding environment. By detecting variations in the concentration of these signal molecules, bacteria can modulate the expression of related genes, thereby regulating associated behaviors. Consequently, interfering in bacterial QS signaling to either promote or inhibit the development of lactic acid bacteria (LAB) biofilms holds substantial significance in terms of enhancing skin immunity, promoting skin health.

Quorum sensing allows bacteria to communicate and coordinate collective behaviors by sensing population density through chemical signals, or autoinducers. While primarily species-specific, interspecies communication also occurs when different bacteria produce or detect shared autoinducers like autoinducer-2 (AI-2), a “universal” signal molecule used by many species. This interspecies communication can lead to either cooperation or competition, influencing functions such as biofilm formation, virulence, and resistance against other microbes.

For example, colonization of the skin by Staphylococcus aureus is associated with exacerbation of atopic dermatitis (AD). Proteases and phenol-soluble modulin α (PSMα) secreted by S. aureus leads to endogenous epidermal proteolysis and skin barrier damage that promotes inflammation (Williams et al, 2019). Other species of bacteria residing on normal skin can produce autoinducing peptides that inhibit the S. aureus agr system, in turn decreasing PSMα expression. A number of bacteria types, such as Bacillus subtilis (it secretes lactic acid), can quorum sense (Spacacan et al, 2020) and react to the S. aureus overcolonization by inhibiting the S. aureus through disruption of their QS system (Leistikow et al, 2024).

Quorum-sensing systems in the skin can be divided into two paradigmatic classes: LuxI/LuxR–type quorum-sensing systems in Gram-negative bacteria and oligopeptide/two-component–type quorum-sensing circuits in Gram-positive bacteria. All of this is very complicated, relaizing that bacteria have elaborate chemical signaling systems that enable them to communicate within and between species is only recently been explored and the field is emerging quickly. Based on our current knowledge, I’ve developed two new products, MB-2 and MB-3, using symbiotic, live bacteria known to perform QS or interfere with QS in other bacteria strains and promote skin benefits, including reduced inflammation and barrier function rebuild.

Interspecies Quorum Sensing Fosters Both Competition and Collaboration

To be clear, quorum sensing between different bacterial species occurs as well. For example, some species cannot produce their own autoinducers, but have receptors for the autoinducer molecules of other species, allowing them to sense and respond to others in their environment. Like human behavior, bacteria behavior operates on a continuum of individualism and collectivism. This quality can breed conflict, but also collaboration and interspecies quorum sensing can take both forms. In other words, the good guys, the symbiotic bacteria, can work together through quorum sensing among themselves (intraspecies quorum sensing) to inhibit the bad guys, the pathogenic bacteria, through interspecies quorum sensing. The good guys can be fighting some bacterial species, such as S. aureus, that use quorum sensing to enhance each other’s virulence.

Let’s now look at the five symbiotic bacteria that are contained in MB-2 and MB-3

Lactobacillus plantarum

Lactobacillus plantarum treatment reduced wound bacterial load, neutrophils, apoptotic and necrotic cells, modified IL-8 production and induced wound healing (Peral et al, 2010). When topically applied to a disease skin model for acne, L. plantarum induced a significant reduction in viability of virulent bacteria phylotypes, lipid production, and modulated inflammatory markers (Podrini et al, 2023).  Further, L. plantarum whole cultures promote tissue repair, and this bacterium may also improve the healing of diabetic wounds in rats through the regulation of inflammatory cytokines (Ishi et al, 2023). In a study of 23 subjects, topical L. plantarum in a cream formulation was found to benefit skin aging properties, including TEWL, barrier function, and wrinkles (Elvebakken et al, 2023).

 Lactobacillus crispatus

An oily suspension containing Lactobacillus crispatus and Lacticaseibacillus paracasei was found to benefit Seborrheic dermatitis (Truglio et al, 2024). In a study of 29 women with topical application of L. crispatus, the density of the sub-epidermal zone significantly increased vs baseline by 11% and of the dermis by 6% (+5% vs placebo). As I mentioned in the introduction,, studies of live Lactobacillus crispatus (LBC) demonstrated benefit to the skin when compared to inactivated LBC biomass, stimulating collagen in vitro. Moreover, the live LBC was stable in formulations not containing antimicrobial preservatives and was found to improve dermis density and wrinkle appearance in vivo.

Bacillus subtilis

Topical application of live Bacillus subtilis has been found to reduce the number of pathogenic bacteria in skin, including S. aureus (Moskovicz et al, 2021; Piewngam et al, 2023). Topical application also helps to reduce acne breakouts (Ma’or et al, 2023). B. subtilis is being developed for drug delivery for a number of reasons (Montgomery et al, 2024). It may have advantages over other candidate bacteria as a platform for drug delivery to the skin because of its safety profile and genetic tractability. It is found in the skin microflora and is metabolically active on the skin. It is nonpathogenic and has natural antimicrobial properties against pathogenic staphylococci and fungi. B. subtilis has generally regarded as safe status from the FDA, and multiple B. subtilis probiotic products as well as a genetically modified strain of B. subtilis are currently commercially available. Further, an important characteristic of B. subtilis is that it is commonly used in biotechnology for the production of proteins, vitamins, and antibiotics because of its efficient protein secretion system, and ease of cultivation, factors that mean it can work well when topically applied to the skin as a probiotic.

Bacillus coagulans

LactoSporin, a metabolite of Bacillus coagulens, cream topically applied for 10 weeks resulted in a significant reduction in visibility of wrinkles around crow’s feet, nasolabial folds, frown lines, and facial fine lines compared to baseline and placebo by dermatological and Antera imaging assessments (Majeed et al, 2023). . Optimal conditions for growth include a temperature range of 30–50°C and a pH level of 5.5–6.5, matching the surface of the skin. This bacterium exhibits weak adhesion to epithelial cells, which prevents long-term colonization, but allows temporary colonization and yielding positive effects.

Lactoccus lactis

Various strains of L. lactis have recently been reported to induce anti-inflammatory activity in vitro (Luerce et al, 2014). Administration of L. lactis LB 1022 improved clinical AD symptoms, decreased serum IgE and suppressed the Th2 cytokines secretion, such as IL4, IL-13, and TSLP in blood, which are factors found to be elevated by AD. Similarily, oral L. lactis LB 1022 may have a protective effect against AD by reducing high IgE serum levels and Th2-related responses that arise from an imbalance in the gut microbiota. Topical application of L. lactis is likely to have similar effects on AD, but given the likely lower colonization levels when topically applied, requires more frequent dosing to achieve similar positive results. It is also possible that L. lactis ferments glycans on the surface of the skin, thus producing beneficial lactic acid that may then be fermented into beneficial short chain fatty acids which then regulate the immune system and reduce inflammation.

Summary

As you can read here in the studies I’ve mentioned, there is much accumulating evidence for the benefits of the 5 types of symbiotic bacteria that I’ve chosen to include in our NeoGenesis MB-2 and MB-3 products. Working with a number of dermatologists in the USA, we’ve had remarkable postive results in compromised, inflammatory skin conditions where MB-2 (bacteria in an occlusive base) serves those conditions with interupted barrier function, such as atopic dermatitis and MB-3 (in a non-occlusive oil base) serves those conditions with a more intact barrier and oily and pustule-prone skin.

Epithelial Barrier Dysfunction in Noncommunicable and Communicable Diseases

The modern world’s dramatic increase in the number and types of chemicals in which man is exposed, a major part of of someone’s exposome, responsible for about 90% of diseases (not genetics), is causing a dramatic rise in noncommunicable and communicable diseases. Over 350 000 chemicals and mixtures of chemicals have been registered for production and use, up to three times as many as previously estimated, and an underestimate of the true number of chemical types that have been produced and commercialized. As the skin and other epithelial tissues are compromised and exposed to communicable diseases, skin and epithelial transmitted diseases are on the rise. For example, the shingles virus can enter through the skin or the epithelial tissue in our respiratory tract, and having shingles can even lead to increased risk of dementia (2nd Ref). Further, a compromised skin epithelial barrier caused by environmental factors such as mechanical trauma, exposure to exogenous proteases in microorganisms and our food, detergents, and air pollution can activate the innate and adaptive immune systems, inducing keratinocytes to release pro-inflammatory cytokines and chemokines and enhancing the antigen presentation by intradermal Langerhans cells (LCs) and dermal DCs and activating T-cells. In turn, for example, activation of T2 type T-cells leads to IL-4, IL-5, and IL-13 secretion, provoking skin barrier alteration, immune cell infiltration into skin, and itch as observed in atopic dermatitis. 

The first essential step to skin immunity is the epithelial barrier, as infection and resulting inflammation are impossible without first breaching it. Epithelia, coated with a sugary glycocalyx, not only comprise our skin but also the mucosal membranes that line our organs. Their ability to secrete squalene, mucus, lipids, and antimicrobials help protect against pathogen invasion. Additionally, epithelia can prevent inflammation by physically shoving out cells infested with toxins, allergens, antigens, pathogens, or other damage by seamlessly extruding them. This is a strategy employed by not only epithelia, but also our hair does the same as it sheds. Given that chronic inflammation could stem from a defective epithelial barrier, the current approach of treating only the inflammation will only partially mitigate symptoms of a more central problem, ongoing wound healing and disrupted barrier.

Scientists now understand that in patients with allergic disease, regardless of tissue location, the homeostatic balance of the epithelial tissue barrier is skewed toward loss of differentiation, reduced junctional integrity, and impaired innate defense and a hyperactive adaptive (trained immunity) immune system. Importantly, epithelial dysfunction characterized by these traits appears to pre-date a predisposition to immunological responses against a range of antigens or allergens, and development of allergic disease.

From the disease perspective, trained immunity is beneficial, as it improves the host’s defense against subsequent infection from pathogens. However, it can also be detrimental and result in overly active immune responses or chronic inflammation.  Even the innate immune system has some memory, given evidence that components in House Dust Mite extract activate and likely train macrophages to produce high amounts of CCL17, IL-6, and cysteinyl leukotrienes following re-exposure to HDM through the TNF-α and PGE2 pathways. Thus, an activated immune system, one that has memory and is primed to react, can lead to sensitivities that may be triggered by an overabundance of chemicals in the environment, and those sensitivities heightened by a disrupted barrier.

Evidence that epithelial barrier dysfunction explains the growing prevalence and exacerbations of inflammatory diseases such as eczema has grown through many studies performed world-wide. Diseases encompassed by the epithelial barrier theory share common features such as an increased prevalence after the 1960s that cannot be accounted soley by the emergence of improved diagnostic methods. They are indeed increasing in prevalence, i.e. the number of afflictions per 1,000 people.

Eepithelial barrier dysfunction enables the microbiome’s translocation from the skin’s surface to interepithelial and deeper subepithelial areas, doing in combination with allergens, toxins, pathogens, and pollutants. Thereafter, microbial dysbiosis and possible infection, characterized by colonization of opportunistic pathogenic bacteria and loss of the number and biodiversity of commensal bacteria results. Local inflammation, impaired tissue regeneration, and remodeling characterize the skin that suffers from impaired barrier. For example, commensal bacteria on the skin’s surface are important for epidermal lipid synthesis and improve barrier function. The skin’s microbiome is therefore critical to maintaining epidermal barrier function. The infiltration of inflammatory cells and inflammatory cytokines to affected tissues is part of the immune system’s response to erradicate invading bacteria, allergens, toxins, and pollutants away from the deep tissues. As Peter Elias, M.D. has written, “AD [atopic dermatitis] can be considered a disease of primary barrier failure, characterized by both a defective permeability (Proksch et al., 2006, and references therein) and antimicrobial function.” Further, inflammatory cells and inflammatory cytokines that migrate from the skin to other organs may play roles in the exacerbation of various inflammatory diseases in other organs. Thus, inflammation iniated in the skin may contribute to chronic inflammatory diseases in other tissues.

What Dr. Elias has been saying is that the permeability-barrier abnormality in AD is not merely an epiphenomenon but rather the “driver” of disease activity, an “outside–inside view of disease pathogenesis” (Elias and Feingold, 2001). The evidence for this is: (1) the extent of the permeability-barrier abnormality parallels severity of disease phenotype in AD, (2) both clinically uninvolved skin sites and skin cleared of inflammation for as long as 5 years continue to display significant barrier abnormalities, (3) topical artificial barrier therapy comprises effective ancillary therapy, and (4) specific replacement therapy, which targets the prominent lipid abnormalities that account for the barrier abnormality in AD, not only corrects the permeability-barrier abnormality but also comprises effective anti-inflammatory therapy for AD (Figure 1; Chamlin et al., 2002). Thus, inflammation in AD may begin with insults from without, i.e. the exposome.

That barrier insult can then activate epithelial cells in the skin, keratinocyes, which are non-professional immune cells, but do possess MHC-II molecules, that present antigens to professional immune cells, such as T-cells. Thus, with disrupted barriier, the keratinocytes can recognize antigens and present them to the immune system, leading to inflammation. More and more, scientists are discovering how epithelial cells are part of the immune system, regardless in which organ they exist. Key here is to protect barrier function in all of our epithelial tissues, including the skin.

So if inflammatory diseases such as eczema and psoriasis are environmentally triggered and lead to barrier dysfunction and resultant inflammation, what can we do?

First, calm the inflammation. It’s destructive and further degrades the epidermal barrier. S2RM technology (in NeoGenesis Recovery) is great for reducing inflammation, doing so in both the innate and adaptive immune systems.

Second, use a topical product that provides the 3 lipids and natural moisturizing factors that are needed to rebuild normal stratum corneum and barrier function. One product to use is NeoGenesis Barrier Renewal Cream (BRC).

Third, use a product that provides instantaneous barrier function and commensal bacteria. The instantaneous barrier allows the BRC to rebuld the natural barrier function over time, and the commensal bacteria help to rebuild the barrier through activation of lipid synthesis by skin cells. The commensal bacteria in Neogenesis MB-2 also help to reduce the Staphylococcus aureus infection often assicated with disrupted barrier function.

So remember, these inflammatory skin conditions are triggered by the environment. Therefore, their treatment and prevention means that if you change your environment, you can prevent or treat these diseases. Part of changing your environment is the careful choice of topical products to reduce inflammation and renormalize the structure and function of your skin.