From Cell Biology to Tissue Engineering


Ultrastructural evidence of the evolutional process in malakoplakia

Yeon Seung Jung1, Dong Yong Chung2, Eun Jin Kim2 and Nam Hoon Cho1

1Department of Pathology, Yonsei University College of Medicine and 2Electron Microscope Core, Yonsei Biomedical Research Institute, Yonsei University College of Medicine, Seoul, Korea

Offprint requests to: Nam Hoon Cho, Department of Pathology, Yonsei University College of Medicine, 250 Seongsanno, Seodaemun-gu, Seoul, 120-152, Korea. e-mail: cho1988@yuhs.ac

Summary. Context. Malakoplakia can be caused by incomplete digestion of Escherichia coli by lysosomes, leading to recurrent urinary tract infections and consequential mass-forming events that mimic tumors. Objectives. By using ultrastructural findings, we aimed to specify the process of phagolysosome to evoke malakoplakia. Design. We observed a series of processes to form a peculiar Michaelis-Gutmann (MG) body in three patients with malakoplakia and compared with xanthogranulomatous pyelonephritis. Results. The ultrastructural findings were realigned according to the sequence of events as pre-phagosomal, phagosomal, and post-phagosomal stages. For the mature MG body, numerous lysosomal aggregates targeting pathogens and subsequent incomplete digestion are prerequisite factors for the pre-phagosomal stage. Scattered lamellated residue is late evidence of the pre-phagosomal stage. Phagosomes can be formed by the fusion of multiple pathogens and multiple lysosomes. We utilized transmission and scanning electron microscopy to speculate on the process of phagolysosomal formation. Conclusion. The recognition of E. coli captured by phagosomes or partially damaged by lysosomal attack within the cell was recorded for the first time. Furthermore, SEM observation was performed on human tissue. Histol Histopathol 35, 177-184 (2020)

Key words: Malakoplakia, Michaelis-Gutmann body, E. coli, Xanthogranulomatous pyelonephritis, Transmission electron microscope, Scanning electron microscope

DOI: 10.14670/HH-18-150