Due to structural and functional divergence, the different isoforms of SAA play distinctive roles in health and disease.[9, 39] For example, in murine experimental autoimmune encephalomyelitis, hepatic SAA1 and SAA2 are first activated to prime systemic response, followed by an increase in SAA3 of central nervous system.[23] In our model, L. intestinalis‐mediated anti‐inflammation primarily involves downregulation of SAA1 and SAA2 but not SAA3. Here, SAA1 is linked to experimental autoimmune encephalomyelitis.