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Gutierrez et al. Microbiome Res Rep 2023;2:36 https://dx.doi.org/10.20517/mrr.2023.37 Page 13 of 23

Table 5. Literature review of strain-specific effects of Bifidobacterium species on immune modulation in the context of inflammation
Experimental
Bifidobacterium species Finding Body site Ref.
model
B. infantis Reduced pro-inflammatory cytokines & Colon TNBS colitis [176]
increased IL-10
B. breve CBT BR3 Reduced pro-inflammatory cytokines & Colon TNBS colitis [170]
increased IL-10
B. longum and B. animalis (probiotic cocktail) Reduced pro-inflammatory cytokines & Colon TNBS colitis [178]
increased IL-10
B. dentium ATCC 27678 Reduced pro-inflammatory cytokines & Serum and TNBS colitis [96]
increased IL-10 colon
Bifidobacterium animalis subspecies lactis CNCM- Reduced pro-inflammatory cytokines & Colon and T DNBS colitis [179]
I2494 increased IL-10 cells
B. longum Bif10 Reduced pro-inflammatory cytokines Serum and DSS colitis [171]
colon
B. breve Bif11 Reduced pro-inflammatory cytokines Serum and DSS colitis [171]
colon
B. longum Bif16 Reduced pro-inflammatory cytokines Serum and DSS colitis [171]
colon

Figure 3. Diagram outlining the major beneficial effects, especially in improving goblet cell function and in reducing inflammation, per
Bifidobacterium species in disease models. GABA: B. dentium-generated gamma-aminobutyric acid; NEC: necrotizing enterocolitis;
SCFAs: short-chain fatty acids.

When goblet cells undergo ER stress, they are unable to adequately synthesize and secrete MUC2, leading to
a reduction in goblet cell number and a thinning of the intestinal mucus layer. Several animal models have
shown that goblet cell ER stress or loss of mucus leads to intestinal inflammation (Winnie, MUC2 ,
-/-
-/-
AGR2 , glycan deficiency, etc.) [148-153] . These animal model phenotypes closely resemble the intestinal issues
observed in inflammatory bowel disease (IBD) patients, particularly in ulcerative colitis patients [138,154-157] .
Ulcerative colitis patients have decreased goblet cell numbers, truncated mucin glycosylation, reduced
mucus layer thickness, and limited mucus integrity [137,155-160] . Loss of both the thickness and integrity of the
mucus layer is thought to promote bacterial-epithelial interactions and drive inflammation [161-165] .