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Jiang et al. Microbiome Res Rep 2024;3:47 https://dx.doi.org/10.20517/mrr.2024.12 Page 11 of 20

DSS (mice) ATCC BAA-835 Immunity Reduce the infiltration of pro-inflammatory [21]
macrophages and CTL in the spleen and intestinal
lymph nodes of mice with colitis
AOM/DSS (mice) ATCC BAA-835 Immunity Increase the number of CTL in MLN and inhibit the [21]
expression of PD-1 on pro-inflammatory macrophages
of MLN and splenic, and reduce the proportion of
+
PD-1 CTL
DSS (mice) Unclear Trp metabolism Increase the expression of AhR-targeted genes such [87]
as IL-10 and CYP1A1
Caco-2 cells ATCC BAA-835 5-HT Promote the expression of 5-HT synthesis rate- [88]
limiting enzyme Tph1 in RIN-14B cells and reduce the
expression of SERT in Caco-2 cells through the direct
interaction with TLR2
Amuc_2172 AOM/DSS (mice) ATCC BAA-835 Immunity Acetylate the Lys14 site on histone H3 of the HSP70 [4]
gene to promote HSP70 secretion and activate CTLs
CT26 bearing (mice)
min +
Apc / (mice)
Amuc_2109 DSS (mice) Unclear Gut microbiota Reshape the intestinal microbiota and inhibit the [89]
and immunity expression of the pro-inflammatory factors and NLRP3
P9 HFD (mice) ATCC-BAA- Immunity Stimulate the expression of IL-6 and promote the [90]
835 secretion of GLP-1 through ICAM2
Akk/A. Muciniphila: Akkermansia muciniphila; DSS: dextran sulfate sodium salt; Tregs: regulatory T cells; SCFA: short chain fatty acid; NOD:
nucleotide-binding oligomerization domain; RegIIIγ: regenerating islet-derived protein IIIγ; TLR: Toll-like receptor; HFD: high-fat diet; BA: bile
acids; APAP: acetaminophen; CMC: carboxymethyl cellulose; P80: polysorbate 80; Lyz1: lysozyme 1; CTL: cytotoxic T lymphocyte; AOM:
azoxymethane; MLN: mesenteric lymph nodes; PD-1: programmed death 1; TNF-α: tumor necrosis factor-α; AmEVs: extracellular vesicles of Akk;
IL-6: interleukin-6; EV: extracellular vesicles; ZO: zonula occludens; AMPK: adenylate-activated protein kinase; CRC: colorectal cancer; PBMC:
peripheral blood mononuclear cell; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; Trp: tryptophan; AhR: aryl hydrocarbon
receptor; 5-HT: 5-hydroxy tryptamine; Tph1: tryptophan hydroxylase 1; HSP70: heat shock protein 70; NLRP3: NOD-like receptor thermal protein
domain associated protein 3; P9: protein 9; GLP-1: glucagon-like peptide-1; ICAM2: intercellular adhesion molecule-2.

The effect of living Akk
The development of intestinal diseases is often accompanied by dysbiosis and disturbance of the intestinal
[91]
microbiota . Studies have shown that intestinal probiotics tend to alleviate intestinal diseases by regulating
intestinal homeostasis, inhibiting the growth of harmful bacteria, and promoting the reproduction of
beneficial bacteria. Akk gavage has been found to increase the production of the metabolite SCFAs such as
acetate and propionate, restore the damaged intestinal microbiota, and alleviate colonic inflammation in
mice [29,30] . In addition, Akk inhibits the growth of Salmonella pullorum, thereby reducing colonic mucosal
damage . Moreover, Akk was able to interact with other intestinal bacteria to regulate intestinal immune
[92]
function and alleviate colonic inflammation. In DSS-induced colitis mice, gavage of Lactobacillus pentosus
significantly increased the abundance of Akk and made Akk the dominant bacterium in the colon, which
[79]
reduced colonic inflammation . In another study, the administration of Akk to DSS-induced colitis mice
increased the abundance of Clostridia, Firmicutes, Ruminococcaceae, and Akkermansia, and inhibited
Bacteroidetes, further demonstrating that Akk reshapes the gut microbial community . Additional studies
[30]
have observed that Akk induces gut microbiota remodeling and controls islet autoimmunity in non-obese
diabetic mice, potentially reducing the incidence of diabetes . Akk promoted mucus production and the
[53]
expression of the antimicrobial peptide RegIIIγ, decreased the abundance of Ruminococcus and the levels of
serum endotoxin, as well as islet TLR expression, thus inhibiting the development of diabetes. It was also
found that the combination of Akk and quercetin could drive protective effects against obesity and NAFLD
[80]
through modulation of the gut microbiota . In addition, recent studies have discovered the potential
mechanism of Akk regulating intestinal microbial composition. Firstly, Akk can support the growth of
butyrate producers by degrading mucin and producing acetate and propionate [93,94] . Secondly, Akk can use
the vitamin B12 produced by other bacteria to produce propionate . Furthermore, another study has
[95]
shown that Akk can produce sulfatase, thus producing cysteine by hydrogen sulfide, which may alleviate the
toxicity caused by sulfate-reducing bacteria in the host . Taken together, the regulation of intestinal
[96]