Translocation Pathway of the Intratracheally Instilled Ultrafine Particles from the Lung into the Blood Circulation in the Mouse

TLDR

Ultrafine particles can translocate from the lung into systemic circulation, yet the anatomical mechanisms at the alveolar wall remain unclear. The study examined the translocation pathway of intratracheally instilled ultrafine carbon black in mice. The authors used intratracheal instillation of ultrafine carbon black in mice to trace its movement into the bloodstream. Electron microscopy revealed that intratracheally instilled ultrafine carbon black accumulates in large gaps between alveolar epithelial cells and occasionally penetrates the basement membrane, indicating that inhaled UFPs can cross the air–blood barrier via these gaps.

Abstract

Recently, it has been demonstrated that ultrafine particles (UFPs) are able to translocate from the lung into the systemic circulation. Precise mechanisms of the anatomical translocation (crossing the air–blood barrier) of inhaled UFPs at the alveolar wall are not fully understood. In this study, we examined the translocation pathway of the intratracheally instilled ultrafine carbon black (UFCB) from the lung into the blood circulation in mouse. Electron microscopy demonstrated accumulation of intratracheally instilled UFCB in the large-sized gaps developing between the cytoplasmic processes of the alveolar epithelial cells, possibly as a result of shrinkage of cytoplasm, by receiving stimulus/signals generated and released following UFCB attachment on the alveolar epithelial cells. Occasional penetration of the accumulated UFCB into the alveolar basement membrane, exposing to the air space, was observed at the gap. These results suggest that inhaled UFPs may, in part, pass the air-blood barrier through the large-sized gap formed between the alveolar epithelial cells.