In support of a physiologic role for intestinal epithelial cell fusion, an appreciable baseline level of cell fusion was observed in non-DSS treated parabiotic pairs in both the colon (-DSS, 5.8±3.4%, n = 5) and DSI (-DSS, 15.0±3.2%, n = 5) (Figure 2E).
To rule out the possibility of surgically-induced inflammation that could potentially create an artificial baseline level of cell fusion within the intestinal epithelium, we repeated the parabiotic experiment by joining GFP and ROSA mice along with oral administration of an anti-inflammatory drug cocktail during and after the surgery (Figure 2A).
In these animals, the baseline level of cell fusion persisted and was unchanged relative to the untreated animals in both the colon (5-ASA treated: 5.3±2.0%, n = 5, P = 0.895) and DSI (5-ASA treated: 21.3±7.8%, n = 5, P = 0.477) (Figure 2E).
Together, these observations highlight the existence of an endogenous baseline level of epithelial cell fusion in the intestine, suggesting that the nature of rapidly self-renewing epithelium may sensitize or prime it for fusion with circulating BMDCs under certain microenvironmental conditions.
Currently, reports in other organ systems show that baseline levels of cell fusion are relatively non-detectable [11], [12], [33].
Here, we report considerable baseline levels of cell fusion in the intestine under homeostatic conditions, greater than that reported in other organ systems [1], [11], [22].
The homeostatic, or baseline, levels of cell fusion observed in both transplanted mice with suppressed inflammation and parabiotic mice may be due to the intrinsic proliferative nature of the intestinal crypt.
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