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At least 181 records · Page 10Linked to original sources
PubMed2026

Integrated Multi-omics Profiling of 2,4-dinitrochlorobenzene (DNCB)-induced Atopic Dermatitis in Mice Reveals a Coordinated Network of Barrier Dysfunction, Immune Activation, and Metabolic Reprogramming.

Atopic dermatitis (AD) is caused by a combination of epidermal barrier defect and immune imbalance. However, the molecular networks between these structural abnormalities and metabolic variations are unclear. This study aim of this research was to examine the concurrent molecular alterations in skin barrier damage and metabolic disorders in an AD-like mouse model by a multi-omics strategy. A 2,4-dinitrochlorobenzene (DNCB)-induced AD-like mouse model was established and the skin tissues were examined through the combination of transcriptomic, quantitative proteomic, and metabolomic analyses. Cross-omics correlation and network analyses were performed to identify consistently abnormal molecular pathways and crucial regulatory molecules. DNCB treatment caused severe epidermal hyperplasia, and prominent infiltration of CD3⁺ T cells, F4/80⁺ macrophages, and mast cells. Transcriptomic and proteomic analysis indicated significant disruption in keratinocyte differentiation, extracellular matrix organization, and cornified envelope formation pathways. Combined analysis detected 171 molecules which were simultaneously altered at both mRNA and protein levels, and network analysis identified FLG2 and KRT6B as central barrier-related molecules. Pathway enrichment analysis consistently showed the participation of AMPK and PPAR signaling pathways. Metabolomic analysis also revealed coordinated changes in lipid and amino acid metabolism which were closely associated with cornified envelope-associated genes and collagen-modifying enzymes. These findings indicate a close relationship between barrier, immune and metabolic regulation in DNCB-induced dermatitis and provide a multi-omics resource for future mechanistic studies of atopic skin inflammation.

Animals↗
PubMed1986

Immune dysfunction in rabbits associated with chronic administration of enemas and rectal insemination.

NZ rabbits were treated with various combinations of enemas and intrarectal insemination (1 or 3 ml of semen a week) to investigate the effects of intestinal uptake and immunogenicity of seminal components and of an unrelated antigen, bovine serum albumin (BSA), given simultaneously. For 5 months the treatment was limited to enemas and/or semen, and total immunoglobulins and antisperm and antilymphocyte antibodies were determined. Then, without interruption of the treatments, the animals received two courses of three consecutive daily intrarectal administrations of BSA, and the humoral response was determined 7 days after each course of administration. Only 1 of 18 intrarectally inseminated animals responded with production of antisperm antibodies; none had antilymphocyte antibodies. Total immunoglobulins, however, were significantly increased in animals receiving enemas alone (p less than 0.02) or followed by insemination (p less than 0.05). The humoral response to BSA was significantly (p less than 0.01) enhanced by prior administration of enemas but was moderately reduced by simultaneous administration of semen, in a dose-related fashion.

Animals↗
PubMed1998

Endometriosis: abnormal endometrium and dysfunctional immune response.

This review highlights recent studies that illuminate the role of the immune system in endometriosis. The findings are discussed in the framework of a model which proposes that endometriosis reflects an immunological selection process. Endometrial cells, which are inherently resistant to apoptosis and immune-mediated elimination, acquire the capacity to utilize the products of an activated immune system to establish ectopic foci of disease. Cyclical inflammatory/immune cell stimulation that fails to eliminate ectopic endometrial implants results in progressive immunological derangement and associated pathophysiological changes which are characteristic of the disease.

Endometriosis↗
PubMed1989

Immune dysfunction in primary biliary cirrhosis. II. Increased production of prostaglandin E.

In a previous study we observed that after in vitro treatment with indomethacin, lymphocyte response to phytohaemagglutinin (PHA) in primary biliary cirrhosis (PBC) patients was higher than that of controls. We know that indomethacin also inhibits prostanoid production, and thus in the present work we directly measured prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) production by mononuclear cells and monocytes from 12 PBC patients, 11 control subjects, and three control disease patients (alcoholic cirrhosis, AC). PHA-stimulated enriched monocytes from PBC patients produced approximately threefold more PGE2 (after 48 h of culture) than did normal and AC monocytes (P less than 0.05). TXB2 production was similar in all groups studied. We also made cultures in which PBC-purified lymphocytes proliferated better than PBC mononuclear cells (i.e. lymphocytes plus monocytes). Thus, a monocyte population producing PGE2 could be responsible, at least in part, for the hyporesponsiveness to PHA observed in PBC patients.

Humans↗