Strain-Dependent Augmentation of Tight-Junction Barrier Function in Human Primary Epidermal Keratinocytes by Lactobacillus and Bifidobacterium Lysates

Abstract

In this study, we investigated whether probiotic lysates can modify the tight-junction function of human primary keratinocytes. The keratinocytes were grown on cell culture inserts and treated with lysates from Bifidobacterium longum, Lactobacillus plantarum, Lactobacillus reuteri, Lactobacillus fermentum, or Lactobacillus rhamnosus GG. With the exception of L. fermentum (which decreased cell viability), all strains markedly enhanced tight-junction barrier function within 24 h, as assessed by measurements of transepithelial electrical resistance (TEER). However, B. longum and L. rhamnosus GG were the most efficacious, producing dose-dependent increases in resistance that were maintained for 4 days. These increases in TEER correlated with elevated expression of tight-junction protein components. Neutralization of Toll-like receptor 2 abolished both the increase in TEER and expression of tight-junction proteins induced by B. longum, but not L. rhamnosus GG. These data suggest that some bacterial strains increase tight-junction function via modulation of protein components but the different pathways involved may vary depending on the bacterial strain.

Gleaning Insights from Fecal Microbiota Transplantation and Probiotic Studies for the Rational Design of Combination Microbial Therapies

“…Similarly, both Bifidobacterium longum and LGG have been shown to induce the upregulation of claudin-1, ZO-1, and occludin protein levels in keratinocytes (185). Intriguingly, the in vitro increase in keratinocyte transepithelial electrical resistance (TER) induced by a B. longum lysate, but not by an L. rhamnosus GG lysate, was abrogated in the presence of a TLR2-neutralizing antibody, suggesting that these bacteria act on different pathways to influence tight junction molecule expression (185). An in vivo infectious model recently demonstrated that a defined mixture of 33 probiotic bacterial strains pre- vented the Salmonella enterica serovar Typhimurium-induced disruption of ZO-1 and claudin-1 in mice and ameliorated disease severity (191).…”

“…The probiotic yeast S. boulardii increases the expression of ZO-1 in T84 cells (186) and has been associated with decreased intestinal permeability in numerous studies (155,(187)(188)(189)(190). Similarly, both Bifidobacterium longum and LGG have been shown to induce the upregulation of claudin-1, ZO-1, and occludin protein levels in keratinocytes (185). Intriguingly, the in vitro increase in keratinocyte transepithelial electrical resistance (TER) induced by a B. longum lysate, but not by an L. rhamnosus GG lysate, was abrogated in the presence of a TLR2-neutralizing antibody, suggesting that these bacteria act on different pathways to influence tight junction molecule expression (185).…”

“…Some studies suggest that butyrate, an SCFA whose level increases with probiotic administration, decreases intestinal permeability through the induction of AMP-activated protein kinase activity and the increased assembly of tight junctions in Caco-2 monolayers (184). Junctional complex expression is also influenced by innate immune functions of epithelial cells, such as by TLR recognition of microbial ligands (185).…”

Bacterial Derivatives of Lactococcus lactis and Ectoin for Atopic Dermatitis: Dermal Compatibility and Cosmetic Acceptability

“…Likewise, administering during pregnancy and early infancy can reduce the risk of eczema developing [20]. More recently, topical application of probiotics and bacterial composites such as the cellular wall, its metabolites and dead bacteria has also been shown to produce certain immunity responses in the skin and to improve and reinforce the skin barrier [23][24][25].In cases of AD selective defects exist in the expression of the multiple genes which codify the corneal layer of the skin, including the filaggrin or the loricrin which only show 2% of the normal level, with structural alterations and a reduction in the corneocytes and the intercellular lipids. As a result, the whole process of terminal differentiation of the keratinocytes (cytoplasmic compaction, cornification and the release of lipids) necessary for the establishment of the barrier function is defective [37].…”

“…Similarly, non-viable bacterial derivatives have been shown to exert antimicrobial and immunomodulating action and can elicit certain immune responses on the skin and improve skin barrier functions [23]. It has been found that the application of lysates of probiotic bacteria, such as the Lactobacillus or Bifidobacterium species, on in vitro models increase the barrier function through the modulation of tight-junction protein components and decrease skin reactivity, the release of cytokines and signs of inflammation [24,25]. In addition, trials in healthy volunteers have shown that topical application of bacterial lysates in the form of a cream strengthens the barrier function and decreases skin dryness [25].…”