Alginate/κ-Carrageenan-Based Edible Films Incorporated with Clove Essential Oil: Physico-Chemical Characterization and Antioxidant-Antimicrobial Activity.

This study aimed to enhance the properties of CaCl2 crosslinked sodium alginate/k-carrageenan (SA/KC) incorporated with clove essential oil (CEO). An evaluation of the modification effects on physicochemical, morphological, antioxidant, and antibacterial properties was performed. The properties were observed at various SA/KC ratios (10/0 to 1.5/1), CEO (1.5% to 3%), and CaCl2 (0% to 2%). The surface morphology was improved by addition of KC and CaCl2. The Fourier transform infrared (FTIR) result showed insignificant alteration of film chemical structure. The X-ray diffraction (XRD) result confirmed the increased crystallinity index of the film by CaCl2 addition. On physicochemical properties, a higher proportion of SA/KC showed the declined tensile strength, meanwhile both elongation at break and water solubility were increased. The incorporated CEO film reduced both tensile strength and water solubility; however, the elongation at break was significantly increased. The presence of Ca2+ ions remarkably increased the tensile strength despite decreased water solubility. Overall, the addition of KC and CaCl2 helped in repairing the mechanical properties and flexibility. CEO incorporation showed the effectiveness of profiling the antioxidant and antimicrobial activity indicated by high 2,2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity up to 90.32% and inhibition zone of E. coli growth up to 113.14 mm2.

IL-10 signaling in dendritic cells controls IL-1ß-mediated IFNγ secretion by human CD4+ T cells: relevance to inflammatory bowel disease.

Uncontrolled interferon γ (IFNγ)-mediated T-cell responses to commensal microbiota are a driver of inflammatory bowel disease (IBD). Interleukin-10 (IL-10) is crucial for controlling these T-cell responses, but the precise mechanism of inhibition remains unclear. A better understanding of how IL-10 exerts its suppressive function may allow identification of individuals with suboptimal IL-10 function among the heterogeneous population of IBD patients. Using cells from patients with an IL10RA deficiency or STAT3 mutations, we demonstrate that IL-10 signaling in monocyte-derived dendritic cells (moDCs), but not T cells, is essential for controlling IFNγ-secreting CD4+ T cells. Deficiency in IL-10 signaling dramatically increased IL-1ß release by moDCs. IL-1ß boosted IFNγ secretion by CD4+ T cells either directly or indirectly by stimulating moDCs to secrete IL-12. As predicted a signature of IL-10 dysfunction was observed in a subgroup of pediatric IBD patients having higher IL-1ß expression in activated immune cells and macroscopically affected intestinal tissue. In agreement, reduced IL10RA expression was detected in peripheral blood mononuclear cells and a subgroup of pediatric IBD patients exhibited diminished IL-10 responsiveness. Our data unveil an important mechanism by which IL-10 controls IFNγ-secreting CD4+ T cells in humans and identifies IL-1ß as a potential classifier for a subgroup of IBD patients.