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. 2022 May 3;13:857418. doi: 10.3389/fmicb.2022.857418

Figure 1.

Figure 1

Postbiotics in mouse models of lung disease. (A) Short-chain fatty acids, major breakdown products of dietary fiber inhibit dendritic cell and Th2 responses, and augment regulatory T cell response, protecting mice against allergic airway inflammation. They also boost protective CD8+ T cell immunity against the influenza virus, and limit cytotoxic effects of neutrophils, leading to increased viral clearance and reduced immunopathology, respectively. Finally, they enhance the CCL20-Th17 axis to reduce tumor growth and metastasis. (B) Desaminotyrosine, derived from the metabolism of flavonoids augments type I interferon signaling in phagocytes and protects mice against influenza virus infection. (C) P-cresol sulfate, a product of L-tyrosine metabolism, inhibits the production of CCL20 and dendritic cell migration in the lungs, ultimately reducing allergic airway inflammation. (D) Imidazole propionate, derived from L-histidine, reduces the inflammasome activity and increases F-actin expression, leading to reduced pyroptosis and improved barrier integrity, respectively, and ultimately ameliorating cardiopulmonary injuries caused by radiation.