Probiotics and the Potential of Genetic Modification as a Possible Treatment for Food Allergy.

Food allergy is a common condition that affects millions of people worldwide. It is caused by an abnormal immune response to harmless food antigens, which is influenced by genetics and environmental factors. Modulating the gut microbiota and immune system with probiotics or genetically modified probiotics confers health benefits to the host and offers a novel strategy for preventing and treating food allergy. This systematic review aims to summarize the current proof of the role of probiotics in food allergy and propose a promising future research direction of using probiotics as a possible strategy of treatment for food allergy.

The Potential Role of C-Reactive Protein in Metabolic-Dysfunction-Associated Fatty Liver Disease and Aging.

Nonalcoholic fatty liver disease (NAFLD), recently redefined as metabolic-dysfunction-associated fatty liver disease (MASLD), is liver-metabolism-associated steatohepatitis caused by nonalcoholic factors. NAFLD/MASLD is currently the most prevalent liver disease in the world, affecting one-fourth of the global population, and its prevalence increases with age. Current treatments are limited; one important reason hindering drug development is the insufficient understanding of the onset and pathogenesis of NAFLD/MASLD. C-reactive protein (CRP), a marker of inflammation, has been linked to NAFLD and aging in recent studies. As a conserved acute-phase protein, CRP is widely characterized for its host defense functions, but the link between CRP and NAFLD/MASLD remains unclear. Herein, we discuss the currently available evidence for the involvement of CRP in MASLD to identify areas where further research is needed. We hope this review can provide new insights into the development of aging-associated NAFLD biomarkers and suggest that modulation of CRP signaling is a potential therapeutic target.

Interaction of toxin-1 and T lymphocytes in toxic shock syndrome.

Toxic shock syndrome (TSS) is a potentially fatal illness caused by infection with the bacterium Staphylococcus aureus. TSS toxin-1 (TSST-1) contains a T-cell epitope with specificity for human V-beta-2. Binding of TSST-1 to the human major histocompatibility complex and T cell receptors activates T cells and triggers the secretion of high amounts of inflammatory cytokines, leading to TSS and potentially death. During this process, CD4+ T cells are inhibited by TSST-1, while regulatory T cells are increased. This suggests a protective immune response by the body in TSS. Thus, TSST-1 can trigger both, an inflammatory response that attacks the body and a protective response. In this review, we discuss the interaction between TSST-1 and T lymphocytes in TSS.