Changes in the Phenotype and Metabolism of Peritoneal Macrophages in Mucin-2 Knockout Mice and Partial Restoration of Their Functions In Vitro After L-Fucose Treatment.

In the development of inflammatory bowel disease (IBD), peritoneal macrophages contribute to the resident intestinal macrophage pool. Previous studies have demonstrated that oral administration of L-fucose exerts an immunomodulatory effect and repolarizes the peritoneal macrophages in vivo in mice. In this study, we analyzed the phenotype and metabolic profile of the peritoneal macrophages from mice, as well as the effect of L-fucose on the metabolic and morphological characteristics of these macrophages in vitro.

Sheaths are diverse and abundant cell surface layers in archaea.

Prokaryotic cells employ multiple protective layers crucial for defense, structural integrity, and cellular interactions in the environment. Archaea often feature an S-layer, with some species possessing additional and remarkably resistant sheaths. The archaeal sheath has been studied in Methanothrix and Methanospirillum, revealing a complex structure consisting of amyloid proteins organized into rings.

The application of explants, crypts, and organoids as models in intestinal barrier research.

models are of great importance in advancing our understanding of human diseases, especially complex disorders with unknown etiologies like inflammatory bowel diseases (IBD). One of the key IBD features is the increased intestinal permeability. The disruption of the intestinal barrier can occur due to a destructive inflammatory response involving intestinal cell death.

Stable coexistence between an archaeal virus and the dominant methanogen of the human gut.

The human gut virome, which is mainly composed of bacteriophages, also includes viruses infecting archaea, yet their role remains poorly understood due to lack of isolates. Here, we characterize a temperate archaeal virus (MSTV1) infecting Methanobrevibacter smithii, the dominant methanogenic archaeon of the human gut. The MSTV1 genome is integrated in the host chromosome as a provirus which is sporadically induced, resulting in virion release.