Our goal in this study was to determine the potential for dietary fibers to prevent gut inflammation in IL-10-deficient (IL-10(-/-)) mice. C57BL/6J wild-type (WT) mice (n = 90) and IL-10(-/-) mice (n = 185) were assigned to a control diet or diets supplemented with PROMITOR soluble corn fiber (SCF), STA-LITE III polydextrose (PDX), Biogum (BG), Pullulan (PI-20), PROMITOR resistant starch-75 (RS-75), SCF&BG, RS-75&BG, and inulin (4 g fiber/100 g diet). On d 47, spleen, mesenteric lymph nodes (MLN), duodenum, jejunum, ileum, and colon were macroscopically and histologically evaluated. The spleen and Peyer's patches (PP) were collected for isolating mononuclear cells and measuring the percentages of regulatory T cells (Treg) and cytokines produced by CD4(+) T cells (i.e. IFNγ and IL-10). Dietary supplementation with RS-75, SCF, RS-75&BG, and inulin ameliorated disease activity on d 47. Dietary RS-75 and inulin supplementation decreased ileal and colonic inflammatory lesions. RS-75, SCF, and inulin decreased IFNγ production by effector CD4(+) T cells from PP and RS-75 increased the IL-10-expressing cells in spleen of WT mice. Dietary SCF, PDX, BG, PI-20, and RS-75 upregulated colonic PPARγ expression in WT mice and SCF upregulated Supressor of cytokine signaling 3 in IL-10(-/-) mice. These data suggest that soluble fibers and resistant starch influence Treg cells, IFNγ, and colonic PPARγ expression to suppress gut inflammation.
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http://dx.doi.org/10.3945/jn.111.139022 | DOI Listing |
Cancer Cell
December 2024
Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Electronic address:
Disseminated cancer cells in the peritoneal fluid often colonize omental fat-associated lymphoid clusters but the mechanisms are unclear. Here, we identify that innate-like B cells accumulate in the omentum of mice and women with early-stage ovarian cancer concomitantly with the extrusion of chromatin fibers by neutrophils called neutrophil extracellular traps (NETs). Studies using genetically modified NET-deficient mice, pharmacologic inhibition of NETs, and adoptive B cell transfer show that NETs induce expression of the chemoattractant CXCL13 in the pre-metastatic omentum, stimulating recruitment of peritoneal innate-like B cells that in turn promote expansion of regulatory T cells and omental metastasis through producing interleukin (IL)-10.
View Article and Find Full Text PDFEcotoxicol Environ Saf
January 2025
NHC Key Laboratory of Radiobiology, School of Public Health, Jilin University, Changchun, Jilin 130021, PR China. Electronic address:
Exposure of PM2.5 can cause different degrees of lung injury, which is referred with inflammatory response. Some evidences showed that low-dose radiation (LDR) induces hormesis in immune, however, it is unknown if LDR ameliorates the PM2.
View Article and Find Full Text PDFCytokine
January 2025
Department of Cardiology, the First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, Jiangsu Province, China. Electronic address:
Aims: Angiogenesis is tightly controlled by growth factors and cytokines in pathophysiological settings. Despite the importance of Interleukin 29 (IL-29), a newly identified cytokine of type III interferon family, its role in angiogenesis remains unknown. We aimed to elucidate IL-29's impact on angiogenesis under both and physiological and pathological conditions.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Brigham and Women's Hospital; Harvard Medical School, Boston, MA, USA.
Background: Previously, we found that germline C3 deletion protected cognition and hippocampal synapses in aged APP/PS1dE9 mice, despite increasing Aß plaques. Here, we crossed our C3 inducible conditional mouse model to APP knockin mice to determine whether global C3 lowering in an adult amyloid mouse model would be protective.
Methods: C3;Rosa26-Cre-ERT2 (C3iKO) mice were crossed to C3;APP mice to generate APP;C3iKO mice, which received 75 mg/kg tamoxifen (TAM; n = 16) or corn oil (CO; n = 15) for 5 days at 3.
Alzheimers Dement
December 2024
Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Background: One of the major outstanding questions in the field of Alzheimer's disease (AD) research is the underlying mechanism by which APOE ε4, the strongest genetic risk factor for AD, contributes to disease pathogenesis. Current therapies targeting amyloid-beta plaques show modest effect in non-APOE4 male AD patients, and greatly increase the risk for amyloid-related imaging abnormalities - edema/effusion (ARIA-E) in APOE ε4 carriers. We made an important discovery that APOE4 neutrophil-microglia interactions drive cognitive impairment in a sex-dependent manner.
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