I'm thinking about supplementing cellulose, especially when going out to eat. Seems like a good way to protect against LPS.
Effect of dietary cellulose supplementation on gut barrier function and apoptosis in a murine model of endotoxemia
Some quotes from the study:
Previously, we have demonstrated a novel link between the diet-induced alteration of the gut microbiome with cellulose and improved outcomes in sepsis. As compared to mice receiving basal fiber (BF) diet, mice that were fed a non-fermentable high fiber (HF) diet demonstrated significant improvement in survival and decreased organ injury in both cecal-ligation and puncture (CLP) and endotoxin sepsis models.
LPS injection induced an approximately 10-fold increase in the intestinal permeability of BF diet mice as compared to control at 24h (1151 ± 196 vs. 111 ± 15 ng/ml; P = 0.005). In contrast, mice that were fed HF diet demonstrated a significant reduction in LPS-induced intestinal permeability as compared to BF fed mice (523 ± 94 vs. 1151 ± 196 ng/ml; P = 0.02) (Fig 3). Taken together, we have shown that mice on the HF diet subjected to endotoxin demonstrated a decrease in cecal permeability as compared to mice on BF diet with relative preservation of the intestinal architecture in both groups.
To understand the contribution of tight junction proteins in the amelioration of the intestinal barrier dysfunction, we next measured the protein expression of claudins and occludin by immunoblotting. As shown in Fig 4, LPS administration demonstrated a significant decrease in the protein expression of both claudin-1 and occludin in BF fed mice after LPS exposure as compared to BC mice (P ≤ 0.05). Similarly, the protein expression of claudin 1 and occludin was higher in HF diet mice when compared to BF diet mice after LPS administration (P ≤ 0.05).
We then confirmed the anti-apoptotic action of HF diet by evaluating its effect on another marker of apoptosis DNA fragmentation. Using the TUNEL assay, we noted that in comparison to BC mice, BF diet mice demonstrated a significant increase in the apoptotic cell population at 24 h after LPS administration (4.7 ± 0.56 vs. 1.4 ± 0.14%; P = 0.0033). In contrast, there was a minimal increase in the intestinal apoptotic rate in HF diet-fed mice (2.2 ± 0.15 vs. 0.7± 0.07%; P = 0.4). The number of apoptotic cells is comparable in BF and HF diet mice at 72 h post-LPS administration (Fig 5C). Taken together, these findings suggest that the use of HF diet in mice is associated with a reduction in LPS-mediated intestinal apoptosis and associated intestinal permeability as compared to mice on BF diet.
In conclusion, our findings suggest that the use of the HF diet can be a simple and effective tool that can decrease gut permeability by its effect on the tight junction proteins and decreasing LPS mediated apoptosis and increasing intestinal epithelial proliferation. Understanding the intricate relationship between the epithelial barrier, gut microbiota, and diet will open up additional therapeutic avenues for the treatment of gut dysfunction in critical illness. Future work involves mechanistic microbiota studies to transplant Akkermansia in gnotobiotic mice to quantify the modulatory role of the gut microbiome on the gut barrier function.
Effect of dietary cellulose supplementation on gut barrier function and apoptosis in a murine model of endotoxemia
Some quotes from the study:
Previously, we have demonstrated a novel link between the diet-induced alteration of the gut microbiome with cellulose and improved outcomes in sepsis. As compared to mice receiving basal fiber (BF) diet, mice that were fed a non-fermentable high fiber (HF) diet demonstrated significant improvement in survival and decreased organ injury in both cecal-ligation and puncture (CLP) and endotoxin sepsis models.
LPS injection induced an approximately 10-fold increase in the intestinal permeability of BF diet mice as compared to control at 24h (1151 ± 196 vs. 111 ± 15 ng/ml; P = 0.005). In contrast, mice that were fed HF diet demonstrated a significant reduction in LPS-induced intestinal permeability as compared to BF fed mice (523 ± 94 vs. 1151 ± 196 ng/ml; P = 0.02) (Fig 3). Taken together, we have shown that mice on the HF diet subjected to endotoxin demonstrated a decrease in cecal permeability as compared to mice on BF diet with relative preservation of the intestinal architecture in both groups.
To understand the contribution of tight junction proteins in the amelioration of the intestinal barrier dysfunction, we next measured the protein expression of claudins and occludin by immunoblotting. As shown in Fig 4, LPS administration demonstrated a significant decrease in the protein expression of both claudin-1 and occludin in BF fed mice after LPS exposure as compared to BC mice (P ≤ 0.05). Similarly, the protein expression of claudin 1 and occludin was higher in HF diet mice when compared to BF diet mice after LPS administration (P ≤ 0.05).
We then confirmed the anti-apoptotic action of HF diet by evaluating its effect on another marker of apoptosis DNA fragmentation. Using the TUNEL assay, we noted that in comparison to BC mice, BF diet mice demonstrated a significant increase in the apoptotic cell population at 24 h after LPS administration (4.7 ± 0.56 vs. 1.4 ± 0.14%; P = 0.0033). In contrast, there was a minimal increase in the intestinal apoptotic rate in HF diet-fed mice (2.2 ± 0.15 vs. 0.7± 0.07%; P = 0.4). The number of apoptotic cells is comparable in BF and HF diet mice at 72 h post-LPS administration (Fig 5C). Taken together, these findings suggest that the use of HF diet in mice is associated with a reduction in LPS-mediated intestinal apoptosis and associated intestinal permeability as compared to mice on BF diet.
In conclusion, our findings suggest that the use of the HF diet can be a simple and effective tool that can decrease gut permeability by its effect on the tight junction proteins and decreasing LPS mediated apoptosis and increasing intestinal epithelial proliferation. Understanding the intricate relationship between the epithelial barrier, gut microbiota, and diet will open up additional therapeutic avenues for the treatment of gut dysfunction in critical illness. Future work involves mechanistic microbiota studies to transplant Akkermansia in gnotobiotic mice to quantify the modulatory role of the gut microbiome on the gut barrier function.
