Corrigendum: Beneficial effect of heat-killed Lactiplantibacillus plantarum L-137 on skin functions in healthy participants: A randomized, placebo-controlled, double-blind study.

[This corrects the article DOI: 10.3389/fmed.2022.912280.].

Beneficial Effect of Heat-Killed Lactiplantibacillus plantarum L-137 on Skin Functions in Healthy Participants: A Randomized, Placebo-Controlled, Double-Blind Study.

To determine whether consuming heat-killed Lactiplantibacillus plantarum L-137 (HK L-137) influences skin functions, we performed a randomized, placebo-controlled, double-blind study in healthy participants who were conscious of dry skin. A total of 80 healthy participants (20 men, 60 women; mean age, 47.3 years) were assigned to receive a tablet containing HK L-137 or a placebo tablet daily for 12 weeks. Every 4 weeks, the skin water content and transepidermal water loss (TEWL) were measured at the forearm and face, and participants completed two skin-related questionnaires, the Dermatology Life Quality Index and a self-evaluation. The HK L-137 group tended to show greater increases from baseline of water content at the forearm and larger decreases of TEWL at the face. The total scores of both questionnaires improved significantly more in the HK L-137 group. Water content and TEWL improved significantly in participants in the HK L-137 group who were above the median age of study participants or had relatively dry skin. These findings suggest that daily HK L-137 intake can improve dry skin, thereby contributing to skin satisfaction.

Heat-killed Lactobacillus plantarum L-137 attenuates obesity and associated metabolic abnormalities in C57BL/6†J mice on a high-fat diet.

Heat-killed Lactobacillus plantarum L-137 (HK L-137) has anti-allergic, antitumor, and antiviral effects in mice, as well as an anti-inflammatory effect in rats with metabolic syndrome through regulation of immunity. To evaluate the influence of HK L-137 on chronic inflammation in mice with diet-induced obesity, C57BL/6 J mice were fed a normal diet (16% of energy as fat) or a high-fat diet (62% of energy as fat) with or without 0.002% HK L-137 for 4 to 20 weeks. It was found that HK L-137 supplementation alleviated weight gain and elevation of plasma glucose, cholesterol, alanine aminotransferase, and aspartate transaminase levels in mice with diet-induced obesity. Expression of several inflammation-related genes, including F4/80, CD11c, and IL-1ß, in the epididymal adipose tissue of these mice was significantly downregulated by HK L-137. In addition, plasma levels of lipopolysaccharide-binding protein, a marker of endotoxemia, tended to be decreased by administration of HK L-137. These findings suggest that HK L-137 supplementation ameliorates obesity-induced metabolic abnormalities and adipose tissue inflammation, possibly through improvement of intestinal permeability.

Proinflammatory cytokine interleukin-1ß suppresses cold-induced thermogenesis in adipocytes.

In this study, we investigated the effects of interleukin-1ß (IL-1ß), a typical proinflammatory cytokine on the ß-adrenoreceptor-stimulated induction of uncoupling protein 1 (UCP1) expression in adipocytes. IL-1ß mRNA expression levels were upregulated in white adipose tissues of obese mice and in RAW264.7 macrophages under conditions designed to mimic obese adipose tissue. Isoproterenol-stimulated induction of UCP1 mRNA expression was significantly inhibited in C3H10T1/2 adipocytes by conditioned medium from lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages in comparison with control conditioned medium. This inhibition was significantly attenuated in the presence of recombinant IL-1 receptor antagonist and IL-1ß antibody, suggesting that activated macrophage-derived IL-1ß is an important cytokine for inhibition of ß-adrenoreceptor-stimulated UCP1 induction in adipocytes. IL-1ß suppressed isoproterenol-induced UCP1 mRNA expression in C3H10T1/2 adipocytes, and this effect was partially but significantly abrogated by inhibition of extracellular signal-regulated kinase (ERK). IL-1ß also suppressed the isoproterenol-induced activation of the UCP1 promoter and transcription factors binding to the cAMP response element. Moreover, intraperitoneal administration of IL-1ß suppressed cold-induced UCP1 expression in adipose tissues. These findings suggest that IL-1ß upregulated in obese adipose tissues suppresses ß-adrenoreceptor-stimulated induction of UCP1 expression through ERK activation in adipocytes.