Anatomical relationships between type II pneumonocytes and alveolar septal gaps in the human lung.

Abstract

This report describes a relationship between type II pneumonocytes and breaks in continuity in the alveolar septum of the human lung. Breaks in continuity of the septum are defined as gaps in the connective tissue matrix of the alveolar septum, with or without discontinuity of the accompanying alveolar epithelium. Septal connective tissue gaps accompanied by epithelial discontinuity are recognized as interalveolar pores of Kohn. When the discontinuity is confined to the connective tissue matrix, epithelial continuity may be maintained by either a single or a double layer of type I epithelium, by a type II cell, or by both type I and type II epithelial cells. Alveolar septal gaps were studied by electron microscopy on random sections in 26 adult human lung specimens and by serially sectioning and montaging the entire circumference of one alveolus to a depth of 103 microns (approximately one-half a normal alveolus) from one of the specimens. Fixation was by way of the airways in most specimens, but by vascular perfusion in the serially sectioned specimen and in seven others. In lungs studied by random sections, we found that the incidence of septal connective tissue gaps with epithelial continuity per specimen correlated with the incidence of pores (r = .468, P less than .016), and also with the incidence of type II cells (r = .422, P less than .025) in the specimen. Five percent of all type II cells observed in the random sections in the 26 specimens (103/1,955) occupied septal gaps, and 2.5% (49/1,955) were located at the rim of a pore. In contrast, in the single serially sectioned montaged alveolus, 69% of all type II cells occupied some type of septal gap, with 24% of all type II cells forming part of the rim of a pore. Over half of all pores in this alveolus were associated with a type II cell. We concluded that a relationship between the incidence of type II cells and gaps in the alveolar septum could be demonstrated on random sections in normal human lungs, which was much more obvious in a single serially sectioned hemialveolus. Serial section techniques of whole alveoli may be necessary to establish relationships that may not be apparent on random sections and that require the study of whole cells in continuity with their environment in order to be identified. The findings may be significant in suggesting a possible role of the type II cell in alveolar septal repair.