Related Experiment Video
Updated: May 7, 2026
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
Reduced number and morphofunctional change of alveolar macrophages in MafB gene-targeted mice
Michiko Sato-Nishiwaki1, Yasuko Aida, Shuichi Abe
1Department of Cardiology, Pulmonology and Nephrology, School of Medicine, Yamagata University, Yamagata City, Yamagata, Japan.
Abstract:
Alveolar macrophages (AMs) play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). We previously demonstrated that the transcription factor, MafB, increased in the AMs of mice exposed to cigarette smoke, and in those of human patients with COPD. The aim of this study was to evaluate the role of MafB in AMs using newly established transgenic (TG) mice that specifically express dominant negative (DN) MafB in macrophages under the control of macrophage scavenger receptor (MSR) enhancer-promoter. We performed cell differential analyses in bronchoalveolar lavage cells, morphological analyses with electron microscopy, and flow cytometry-based analyses of surface markers and a phagocytic capacity assay in macrophages. AM number in the TG mice was significantly decreased compared with wild-type (WT) mice. Morphologically, the high electron density area in the nucleus increased, the shape of pseudopods on the AMs was altered, and actin filament was less localized in the pseudopods of AMs of TG mice, compared with WT mice. The expression of surface markers, F4/80 and CD11b, on peritoneal macrophages in TG mice was reduced compared with WT mice, while those on AMs remained unchanged. Phagocytic capacity was decreased in AMs from TG mice, compared with WT mice. In conclusion, MafB regulates the phenotype of macrophages with respect to the number of alveolar macrophages, the nuclear compartment, cellular shape, surface marker expression, and phagocytic function. MSR-DN MafB TG mice may present a useful model to clarify the precise role of MafB in macrophages.
Insights
MafB, a transcription factor, influences alveolar macrophage (AM) number, nuclear structure, and phagocytic function in chronic obstructive pulmonary disease (COPD). This study used novel transgenic mice to investigate MafB
Area of Science:
- * Pulmonary immunology and cell biology.
- * Investigating macrophage function in respiratory diseases.
Background:
- * Alveolar macrophages (AMs) are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD).
- * The transcription factor MafB is elevated in AMs of mice exposed to cigarette smoke and in human COPD patients.
Purpose of the Study:
- * To elucidate the role of MafB in AMs.
- * To establish and characterize novel transgenic (TG) mice expressing dominant-negative (DN) MafB in macrophages.
Main Methods:
- * Generation of macrophage scavenger receptor (MSR)-DN MafB TG mice.
- * Analysis of bronchoalveolar lavage cells, including differential counts.
- * Morphological assessment via electron microscopy.
- * Flow cytometry for surface marker expression (F4/80, CD11b) and phagocytic capacity assays.
Main Results:
- * TG mice exhibited significantly decreased AM numbers compared to wild-type (WT) mice.
- * AMs in TG mice showed nuclear alterations, altered pseudopod shape, and reduced actin localization.
- * Peritoneal macrophages in TG mice had reduced F4/80 and CD11b expression, but AMs did not.
- * Phagocytic capacity of AMs was significantly decreased in TG mice.
Conclusions:
- * MafB plays a regulatory role in macrophage phenotype, affecting AM number, nuclear morphology, cell shape, surface marker expression, and phagocytic function.
- * The MSR-DN MafB TG mouse model is a valuable tool for further research into MafB's function in macrophages.
