Rationale. Sarcoidosis is a multi-organ granulomatous disease of unknown etiology. A combination of environmental factors and genetic susceptibility are suggested in the etiology of sarcoidosis. This disease is usually diagnosed in adults between 47 and 51 years old, and rarely has been reported in children. We hypothesized that children have strong lung repair mechanisms after inflammatory insult that prevent sarcoidosis development. To understand the effect of age in repair response, we evaluated two different age population in a mouse model. Methods. Eight-week-old and 74-week old C57BI/6 male mice were divided into 4 groups (n=8 mice in each group): young control, young challenged, old control, and old challenged. After anesthetized, mice were challenged to noninfectious microparticles intratracheally a total of 4 times: 50 µL for first installation and 20 µL for 3 more within 2 weeks, followed by 2 weeks of daily saline injection. After the first 2 weeks, half of the mice in each group were euthanized. Lungs were harvested and fixed. H&E and immunohistochemistry was performed in lung section. Histopathology was semi-quantitatively counts of granuloma in the lung by a lung pathologist. At week 4, the remaining of the mice underwent the same procedure. Results. After 2 weeks both young and old mice revealed significant granulomatous reaction in the lung parenchyma with a mean of 67.5% and 75% respectively. After 4 weeks, lung parenchyma in young mice showed 1-3% of parenchymal inflammation. The older mice had persistent granulomatous inflammation with a mean score of 85%, and patchy areas of inflammation throughout the parenchyma at week 4 (Fig. 1). Conclusion. Young mice were able to reach almost complete resolution of the granulomatous inflammation within 4 weeks. This reflects the preserved repair mechanisms after insult at a young age. Among the older mice, the persistent granulomatous reaction may suggest that sarcoidosis is basically a failure to fully recover from inflammation after antigen exposure.
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