In an animal model, IUGR induced in late gestation produced alterations in alveolar function, corresponding to rapid development of alveoli during this time period (Maritz et al. 2001).
However, the effect of exogenous surfactant has not been studied directly on alveolar type II cells (ATII cells), a key cell type responsible for alveolar function and repair.
To investigate the phagocytosis function of alveolar macrophage, alveolar macrophages were isolated as described above.
Our hypothesis is that BMSCs support functions of alveolar epithelial type II cells and induce reforming the appropriate alveolar structure, which result in the recovery of function of alveolar tissue in the lung.
Moreover, to link the intracellular iron content to the function of alveolar macrophages, we assessed the phagocytosis of alveolar macrophages, and found that the alveolar macrophages from Ad-shHepc1-treated mice showed less phagocytic ability than those from the control animals.
We have studied especially the morphology and function of alveolar macrophages (AM), the morphology of alveolar type I and type II epithelial cells, and analyzed lung phospholipids.
Interestingly, although SP-B is synthesised by alveolar type II cells and bronchiolar epithelial cells, recent studies indicate that the function of alveolar and bronchiolar SP-B may differ (Lin et al, 1999b).
The major function of alveolar macrophages is uptake of inhaled microorganisms through phagocytosis.
Thalidomide treatment modulated pro-inflammatory function of alveolar macrophages by significantly (p < 0.05) decreasing their phagocytic potential in terms of phagocytic uptake and intracellular killing, spreading and hydrogen peroxide (H2O2) release.
This also leads to a relevant research question: does prenatal infection and subsequent inflammation influence the function of alveolar macrophages, the production of surfactant proteins, and local cytokine responses in the lung?
