Changes in Skin Barrier Function in Neonates: Daily Variation and Impact of Bathing.

Background: The skin barrier function is an important predictor of neonatal barrier defects. This study aimed to investigate the daily changes in skin barrier function and the impact of bathing on skin barrier function in neonates.

Methods: We assessed the transepidermal water loss (TEWL) and stratum corneum hydration (SCH) on the forehead, cheek, volar forearm, and chest from days 2 to 7 and at 1 month after birth.

Macrophages Switch Their Phenotype by Regulating Maf Expression during Different Phases of Inflammation.

Macrophages manifest distinct phenotype according to the organs in which they reside. In addition, they flexibly switch their character in adaptation to the changing environment. However, the molecular basis that explains the conversion of the macrophage phenotype has so far been unexplored.

Intestinal CD169(+) macrophages initiate mucosal inflammation by secreting CCL8 that recruits inflammatory monocytes.

Lamina propria (LP) macrophages are constantly exposed to commensal bacteria, and are refractory to those antigens in an interleukin (IL)-10-dependent fashion. However, the mechanisms that discriminate hazardous invasion by bacteria from peaceful co-existence with them remain elusive. Here we show that CD169(+) macrophages reside not at the villus tip, but at the bottom-end of the LP microenvironment.

Vascular-resident CD169-positive monocytes and macrophages control neutrophil accumulation in the kidney with ischemia-reperfusion injury.

Monocytes and kidney-resident macrophages are considered to be involved in the pathogenesis of renal ischemia-reperfusion injury (IRI). Several subsets of monocytes and macrophages are localized in the injured tissue, but the pathologic roles of these cells are not fully understood. Here, we show that CD169(+) monocytes and macrophages have a critical role in preventing excessive inflammation in IRI by downregulating intercellular adhesion molecule-1 (ICAM-1) expression on vascular endothelial cells.