Journal: Nature Microbiology

Article Title: Weaning drives microbiome-mediated epigenetic regulation to shape immune memory in mice

doi: 10.1038/s41564-026-02295-6

Figure Lengend Snippet: a , Time-course analysis of Cd74 methylation and expression in GF colonic organoids treated with a low dose of IFNγ (0.1 ng ml −1 ) demonstrates rapid demethylation and concomitant gene activation. Data are presented as mean ± s.e.m. of 2 independent experiments. b , DNA demethylase TET3 mediates IFNγ-induced epigenetic reprogramming of Cd74 . Shown is the Cd74 locus with its genomic location, ATAC-seq peaks from sorted Lgr5-GFP + ISCs ( GSE83394 ), the microbial-induced DMR (dashed box) and the positions of primer sets used to assess STATs and TETs binding by ChIP–qPCR. Compared with a non-DMR control region (ChIP-1), STAT3 and TET3 showed an IFNγ-dependent increase in binding at the DMR/enhancer (ChIP-2 and ChIP-3). c , Combined treatment with IFNγ and the hypomethylation agent DAC synergistically enhanced IFNγ-induced demethylation and transcriptional activation. In contrast, treatment with TNF, sodium butyrate (NaB) or LPS alone did not alter Cd74 methylation. d , Experimental design for testing transcriptional memory in organoids with (primed) or without (naïve) previous IFNγ exposure. Pretreated organoids were rested for 7 days without IFNγ and then restimulated with IFNγ or TNF. Memory was indicated by faster and stronger induction of Cd74 expression. e , Before restimulation, organoids exposed to IFNγ for 3 passages (primed) showed nearly complete loss of Cd74 methylation. f , IFNγ (left) or TNF (right) restimulation of primed organoids accelerated and enhanced Cd74 expression compared to naïve organoids. g , Experimental design to determine whether microbiota drive methylation-dependent transcriptional memory of epithelial MHC-II. h , Methylation of MHC-II genes in organoids derived from adult GF, SPF and GF→ SPF (converted at weaning) mice at 15 weeks of age, with methylation assessed after passage 2. i , IFNγ stimulation induced methylation-dependent, memory-like transcriptional activation of the MHC-II genes Cd74 , H2-Eb1 , H2-Aa and Ciita in SPF and GF→ SPF organoids, measured by RT–qPCR. In b , c , e , f , h and i , all data are presented as mean ± s.e.m. of at least 3 independent experiments. In b , c , e and h , P values were calculated using unpaired (two-tailed) t -test.

Article Snippet: For single-agent treatment, organoids were treated for 48 h with 0.1 ng ml −1 IFNγ, 5 ng ml −1 TNF (R&D Systems, 410-MT-010), 2.5 μg ml −1 LPS (Thermo Fisher, 00-4976-03), 2 mM sodium butyrate (Sigma-Aldrich, 303410) or 0.08 μM DAC (Sigma-Aldrich, A3656).

Techniques: Methylation, Expressing, Activation Assay, Binding Assay, ChIP-qPCR, Control, Derivative Assay, Quantitative RT-PCR, Two Tailed Test

Journal: Brain, Behavior, & Immunity - Health

Article Title: Endotoxin-induced inflammation promotes, via the adrenomedullary system, a hyperglycemic and anti-inflammatory reflex

doi: 10.1016/j.bbih.2026.101183

Figure Lengend Snippet: Glycemic, Corticosterone, and TNF responses after administration of different doses of LPS . A, LPS-induced hyperglycemia is only observable 30 min after administering 100 μg/kg doses. B, Circulating Corticosterone in response to LPS has an earlier onset when higher doses are used. C, Plasmatic TNF response to LPS is proportional to the administered LPS dose and only detectable 50 min after LPS administration. Data are expressed as the mean ± SEM of 7 subjects per group. P values comparing the control group (no LPS) were calculated using repeated measures two-way ANOVA.

Article Snippet: For TNF measurements, MaxiSorp plates were sensitized with rat TNFα mouse recombinant monoclonal antibody (R&D Systems, MAB510R) used as the capture antibody and a goat polyclonal biotinylated antibody (R&D Systems, BAF510) was used as the detection antibody with the signal provided by Streptavidin-biotin (Jackson Immunoresearch, 016-030-084) revealed with TMB and hydrogen peroxide in acetate/citrate buffers.

Techniques: Control

Journal: Brain, Behavior, & Immunity - Health

Article Title: Endotoxin-induced inflammation promotes, via the adrenomedullary system, a hyperglycemic and anti-inflammatory reflex

doi: 10.1016/j.bbih.2026.101183

Figure Lengend Snippet: Indomethacin administration prevents LPS-induced hyperglycemia and enhances the TNF response. A. Indomethacin administration prevents LPS-induced hyperglycemia. B. LPS-induced corticosterone secretion is not modified by prostaglandin inhibition. C. TNF response to LPS is exacerbated by indomethacin. Data are expressed as mean ± SEM of 7 subjects per group. P values comparing the control group (no LPS) were calculated using repeated measures two-way ANOVA in figures A&B and by one-way ANOVA for figure C, where all groups are compared.

Article Snippet: For TNF measurements, MaxiSorp plates were sensitized with rat TNFα mouse recombinant monoclonal antibody (R&D Systems, MAB510R) used as the capture antibody and a goat polyclonal biotinylated antibody (R&D Systems, BAF510) was used as the detection antibody with the signal provided by Streptavidin-biotin (Jackson Immunoresearch, 016-030-084) revealed with TMB and hydrogen peroxide in acetate/citrate buffers.

Techniques: Modification, Inhibition, Control

Journal: Brain, Behavior, & Immunity - Health

Article Title: Endotoxin-induced inflammation promotes, via the adrenomedullary system, a hyperglycemic and anti-inflammatory reflex

doi: 10.1016/j.bbih.2026.101183

Figure Lengend Snippet: β-adrenergic signaling is essential for LPS-induced hyperglycemia and mediates TNF suppression. A. The β-adrenergic antagonist propranolol inhibits LPS-induced glucose secretion; “x2” groups received a second dose of propranolol at minute 30 (indicated by a dark pink arrow), completely preventing the glucose increase. B. Corticosterone in response to LPS alone or in combination with propranolol; “x2” groups received a second dose at 30 min (also indicated by a dark pink arrow). C. TNF response to LPS alone or combined with a single or a double administration of propranolol. Data are expressed as mean ± SEM of 3–5 subjects per group, and P-values comparing the control group (no LPS) were calculated using repeated measures two-way ANOVA. For statistical interpretation, the following symbols were used: α indicates p < 0.05 with respect of group “Propranolol X2”, β indicates p < 0.05 with respect of groups "Propranolol X1 ″, "LPS + propranolol X2″, "Saline" and "Propranolol X2"; a indicates p < 0.05 with respect of groups "Propranolol X1″, "Propranolol X2″, and "Saline". (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: For TNF measurements, MaxiSorp plates were sensitized with rat TNFα mouse recombinant monoclonal antibody (R&D Systems, MAB510R) used as the capture antibody and a goat polyclonal biotinylated antibody (R&D Systems, BAF510) was used as the detection antibody with the signal provided by Streptavidin-biotin (Jackson Immunoresearch, 016-030-084) revealed with TMB and hydrogen peroxide in acetate/citrate buffers.

Techniques: Control, Saline

Journal: Brain, Behavior, & Immunity - Health

Article Title: Endotoxin-induced inflammation promotes, via the adrenomedullary system, a hyperglycemic and anti-inflammatory reflex

doi: 10.1016/j.bbih.2026.101183

Figure Lengend Snippet: The adrenal medulla mediates LPS-induced hyperglycemia, Corticosterone release, and TNF suppression. A. Glycemic responses after i.v. administration of 100 μg/kg of LPS via a remote canula in adrenal-medullectomized (AdMX) animals. B. Circulating corticosterone responses after remote i.v. administration of LPS in AdMX animals. C. Plasmatic TNF levels 50 min after LPS administration are higher in AdMX animals. D. Glycemic response to i.v. infusion of 50 ng/kg/min of adrenaline for 50 min. E. Corticosterone response to an i.v. bolus of 5 μg/kg ACTH. Data are expressed as mean ± SEM of 5 animals, P values were calculated using repeated measures two-way ANOVA ∗ indicates p < 0.05 and ∗∗ indicates p < 0.01 for both "AdMX LPS" and "AdMX Saline" groups for glycemia; + indicates p < 0.05 for "AdMX Saline" and ° p < 0.05 for "AdMX LPS".

Article Snippet: For TNF measurements, MaxiSorp plates were sensitized with rat TNFα mouse recombinant monoclonal antibody (R&D Systems, MAB510R) used as the capture antibody and a goat polyclonal biotinylated antibody (R&D Systems, BAF510) was used as the detection antibody with the signal provided by Streptavidin-biotin (Jackson Immunoresearch, 016-030-084) revealed with TMB and hydrogen peroxide in acetate/citrate buffers.

Techniques: Saline

Journal: Brain, Behavior, & Immunity - Health

Article Title: Endotoxin-induced inflammation promotes, via the adrenomedullary system, a hyperglycemic and anti-inflammatory reflex

doi: 10.1016/j.bbih.2026.101183

Figure Lengend Snippet: Hyperglycemia and TNF suppression are only recovered in AdMX animals that receive adrenaline. A. Glycemic responses after remote i.v. administration of LPS in adrenal-medullectomized (AdMX) animals with continuous infusion of adrenaline or noradrenaline. B. Corticosterone responses after remote i.v. administration of LPS in AdMX animals with constant infusion of adrenaline or noradrenaline. LPS infusion increases corticosterone, but Adrenaline and Noradrenaline cannot increase Corticosterone further. C. Circulating TNF response after remote i.v. administration of LPS in AdMX animals with continuous infusion of adrenaline or noradrenaline. Data are expressed as mean ± SEM of 4 subjects per group. P values were calculated using repeated measures two-way ANOVA for glycemia where ∗∗∗ indicates p < 0.001 with respect to both "AdMX LPS + inf-Sal" and "AdMX LPS + inf-Nadren" groups. One-way ANOVA compared groups with the same LPS doses in TNF and Corticosterone responses.

Article Snippet: For TNF measurements, MaxiSorp plates were sensitized with rat TNFα mouse recombinant monoclonal antibody (R&D Systems, MAB510R) used as the capture antibody and a goat polyclonal biotinylated antibody (R&D Systems, BAF510) was used as the detection antibody with the signal provided by Streptavidin-biotin (Jackson Immunoresearch, 016-030-084) revealed with TMB and hydrogen peroxide in acetate/citrate buffers.

Techniques: