Modulation of allergic contact dermatitis via gut microbiota modified by diet, vitamins, probiotics, prebiotics, and antibiotics

Abstract

Allergic contact dermatitis is one of the most common recorded occupational diseases. There are many different substances that the skin comes into contact with on a daily basis and that can cause ACD, e.g., preservatives, surfactants, and antimicrobial agents. The development of a mouse model of ACD has provided insight into the immune mechanisms involved. Drugs used in the treatment of skin diseases have many side effects. Therefore, alternative methods of suppressing the immune response to reduce the symptoms of skin diseases are being sought. In recent years, high hopes have been placed on dietary modulation and supplementation to affect the intestinal microbial composition and promote anti-inflammatory responses. In addition, other studies have shown the crucial role of intestinal microbiota in many immune-mediated diseases. Recognition and characterization of pro- and anti-inflammatory nutrients and supplements may be crucial to support the treatment of diseases such as atopic dermatitis, acne vulgaris, psoriasis, and allergic contact dermatitis.

Effect of Bacillus subtilis and Bacillus coagulans spores on induced allergic contact dermatitis in dogs

“…The symptoms of dogs receiving probiotics, similar to those in the prednisolone plus probiotic group, decreased more quickly and favourably compared to the control group. Various studies investigated the effects of probiotics on the treatment of dermatitis (Kiecka et al., 2023 ; Lolou & Panayiotidis, 2019 ). Previously, Lactobacillus casei (Chapat et al., 2004 ), Lactobacillus acidophilus (Shah et al., 2012 ) and Bifidobacterium longum 51A (Ribeiro et al., 2021 ) were reported as effective probiotics that could regulate the mice immune responses and used in the management of allergic contact dermatitis.…”

Impact of proton pump inhibitors on the onset of gastrointestinal immune‐related adverse events during immunotherapy

“…These cytokines, including TNFα and IL-10, may shift the threshold of immune subsets activation within the tumor micro-environment, thereby resulting in augmented adaptive immune responses. 19 The exact mechanism of PPI exposure and increased risk of GI irAEs remains unknown, but if these data will be confirmed by larger prospective cohorts with GM analysis, the clinicians should use PPIs more carefully and only if strictly indicated. In fact, there is a high percentage of inappropriate PPI prescription.…”

“…The compositional and functional alterations in GM lead to intestinal barrier breakage with an increased translocation of toxins and inflammatory factors that may be able to alter dynamically the immunological profile in a pro‐inflammatory direction. These cytokines, including TNFα and IL‐10, may shift the threshold of immune subsets activation within the tumor micro‐environment, thereby resulting in augmented adaptive immune responses 19 . The exact mechanism of PPI exposure and increased risk of GI irAEs remains unknown, but if these data will be confirmed by larger prospective cohorts with GM analysis, the clinicians should use PPIs more carefully and only if strictly indicated.…”

A review of the long-term use of proton pump inhibitors and risk of celiac disease in the context of HLA-DQ2 and HLA-DQ8 genetic predisposition

“…In the stomach where H pylori is abundant, PPIs can cause PPI-induced gastric bacterial overgrowth. [26] Individuals taking PPIs will experience greater pH changes and are subsequently more prone to further overgrowth of Streptococcus, Lactobacillus, and other bacteria, leading to impaired bile acid creation, bloating, nausea, and diarrhea. [27] In the proximal duodenum, PPI users have been shown to have an increase in the variation and quantity of the microbiome.…”

“…[11] The concept of bacterial translocation is important when considering the long-term effects of PPIs and the weakened barrier functions that result from decreased levels of gastric acid. [26] Translocation is the process by which bacteria from the gastrointestinal tract progress into other organs and regions of the body by various mechanisms. [34] Pathogen associated molecular patterns from these bacteria are then recognized by pattern recognition receptors of the immune system, which can initiate several signaling pathways as well as carcinogenesis.…”