[1.1] - Staphylococcal bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine.
- Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain.
-This aberrant pain signalling resulted from histamine receptor H1-mediated sensitization of visceral afferents.
- Injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with #Irritable bowel syndrome induced local oedema and mast cell activation.
[1.3] [#Atopic Dermatitis] [#Staphylococcus epidermidis] - increased abundance of S. aureus with depletion of S. epidermidis and #Corynebacterium spp. among AD patients.
- S. epidermidis, a commensal present on non–inflamed skin, appears to be S. aureus best antagonist.
- less severe flares of AD had higher counts of S. epidermidis whereas the more severe flares were associated with S. aureus
[1.4] [#Atopic Dermatitis] - samples where S. aureus was highly abundant, lower abundances of S. hominis and Cutibacterium acnes were observed. M. osloensis and M. luteus were more abundant in AD.
- The flexures exhibited lower alpha-diversity and were colonized by S. aureus, accompanied by S. epidermidis in lesions. Malassezia species were absent on the neck in AD.
[1.5] [#Atopic Dermatitis] - S. aureus, a dominant species among the family of Staphylococcae, can be 100 times more abundant in AD skin compared to normal healthy skin.
- AD is associated with a depletion in the coagulase-negative staphylococcal species (CoNS), such as S. epidermidis, S. hominis, and other skin commensal bacterial communities, including Streptococcus salivarius, Propionibacterium, Streptococcus, Acinetobacter, Corynebacterium, Prevotella and Proteobacteria.
- AD patients exhibit abundant S. aureus in their gut microbiota
[1.7] [#Systemic lupus erythematosus] - after Staphylococcus aureus was epicutaneously applied on NfkbizΔK5 mice, NfkbizΔK5 mice developed SLE-associated autoantibodies, anti-dsDNA antibodies, anti-Sm antibodies, and glomerulonephritis with IgG deposition.
- This staphylococcal skin colonization promoted caspase-mediated keratinocyte apoptosis and neutrophil activation, inducing the interleukin-23 (IL-23)/IL-17 immune response by activating dendritic cells and T cells.
- the subcutaneous administration of anti–IL-23p19 and anti–IL-17A antibodies alleviated the systemic autoimmune response.
[1.8] - widespread class of #Bacillus lipopeptides, the fengycins, eliminates S. aureus by inhibiting S. aureus quorum sensing—a process through which bacteria respond to their population density by altering gene regulation.
- consumption of #Probiotic#Bacillus bacteria comprehensively abolished colonization by the dangerous pathogen Staphylococcus aureus in a rural Thai population.
[1.9] [#Natural Skin Microbiome] - upon injury, adaptive responses to the microbiota directly promote sensory neuron regeneration.
- At homeostasis, tissue-resident commensal-specific T cells colocalize with sensory nerve fibers within the dermis, express a transcriptional program associated with neuronal interaction and repair, and promote axon growth and local nerve regeneration following injury.
[#Epigallocatechingallat] - Epigallocatechin gallate (ECGC) exert strong antimicrobial properties, binding to the Staphylococcus aureus peptidoglycan and destroying the osmotic protection of the cell wall.
[1.14] [#Cutaneous T cell lymphomas] [#Bacteriophage] - #Endolysin strongly inhibits proliferation of S. aureus isolated from CTCL skin and significantly decreases S. aureus bacterial cell counts in a dose-dependent manner.
- #Endolysin inhibits the patient-derived S. aureus induction of Interferon-gamma (IFNγ) and IFNγ-inducible chemokine CXCL10 in healthy skin.
- #Endolysin strongly inhibits the effects of S. aureus on activation (reduced CD25 and STAT5 phosphorylation) and proliferation (reduced Ki67) of malignant T cells and cell lines in the presence of non-malignant T cells.
- Staphylococcus aureus (S. aureus) is suspected to fuel disease activity in cutaneous T cell lymphomas (CTCL).
[1.15] [#Atopic Dermatitis] - Patients with AD exhibit decreased expression of #Antimicrobial peptides (AMPs) which is linked to increased colonization by Staphylococcus aureus.
[#Atopic Dermatitis] [#Ceramides] - The lesional skin of AD patients shows higher prevalence of S.aureus (up to 70%) than nonlesional skin of the same patients (39%)
- The enzyme ceramidase secreted by S. aureus lowers lipid and fatty acid levels and makes the skin permeable to allergens.
- Lower fatty acid levels also lead to decreased formation of phospholipid hydrolysis products in sebum and sweat, which increase skin surface pH and further promote S. aureus growth.
- Alpha toxin secreted by S. aureus is cytotoxic to keratinocytes and alters the integrity of E-cadherin, compromising barrier function
- #Cutibacterium acnes secretes a lipase that converts triacylglycerols contained in sebum to #Propionic acid, which contributes to the acidification of the skin surface; a factor that limits the growth of S. aureus