PMID- 37375559
OWN - NLM
STAT- MEDLINE
DCOM- 20230629
LR  - 20230701
IS  - 2072-6643 (Electronic)
IS  - 2072-6643 (Linking)
VI  - 15
IP  - 12
DP  - 2023 Jun 7
TI  - Lactiplantibacillus plantarum OLL2712 Induces Autophagy via MYD88 and Strengthens 
      Tight Junction Integrity to Promote the Barrier Function in Intestinal Epithelial 
      Cells.
LID - 10.3390/nu15122655 [doi]
LID - 2655
AB  - Autophagy is an important system conserved in eukaryotes that maintains 
      homeostasis by degrading abnormal proteins. Autophagy incompetence in intestinal 
      epithelial cells causes the abnormal function of intestinal stem cells and other 
      cells and damages intestinal barrier function. The disruption of the intestinal 
      barrier causes chronic inflammation throughout the body, followed by impaired 
      glucose and lipid metabolism. Lactiplantibacillus plantarum OLL2712 (OLL2712) is 
      a lactic acid bacterium that induces interleukin-10 production from immune cells, 
      alleviates chronic inflammation, and improves glucose and lipid metabolism. In 
      this study, we hypothesized that OLL2712 exerts anti-inflammatory effects by 
      inducing autophagy and ameliorating intestinal barrier dysfunction, and we 
      investigated its autophagy-inducing activities and functions. Caco-2 cells 
      stimulated with OLL2712 for 24 h showed an increased number of autolysosomes per 
      cell, compared with unstimulated cells. Therefore, the permeability of 
      fluorescein isothiocyanate dextran 4000 (FD-4) was suppressed by inducing 
      autophagy. In contrast, mucin secretion in HT-29-MTX-E12 cells was also increased 
      by OLL2712 but not via autophagy induction. Finally, the signaling pathway 
      involved in autophagy induction by OLL2712 was found to be mediated by myeloid 
      differentiation factor 88 (MYD88). In conclusion, our findings suggest that 
      OLL2712 induces autophagy in intestinal epithelial cells via MYD88, and that 
      mucosal barrier function is strengthened by inducing autophagy.
FAU - Watanabe-Yasuoka, Yumiko
AU  - Watanabe-Yasuoka Y
AD  - Food Microbiology and Function Research Laboratories, Division of Research and 
      Development, Meiji Co., Ltd., Hachiouji, Tokyo 192-0919, Japan.
FAU - Gotou, Ayako
AU  - Gotou A
AD  - Food Microbiology and Function Research Laboratories, Division of Research and 
      Development, Meiji Co., Ltd., Hachiouji, Tokyo 192-0919, Japan.
FAU - Shimizu, Shigeomi
AU  - Shimizu S
AD  - Department of Pathological Cell Biology, Medical Research Institute, Tokyo 
      Medical and Dental University, Tokyo 113-8510, Japan.
FAU - Sashihara, Toshihiro
AU  - Sashihara T
AUID- ORCID: 0000-0001-7617-0987
AD  - Food Microbiology and Function Research Laboratories, Division of Research and 
      Development, Meiji Co., Ltd., Hachiouji, Tokyo 192-0919, Japan.
LA  - eng
PT  - Journal Article
DEP - 20230607
PL  - Switzerland
TA  - Nutrients
JT  - Nutrients
JID - 101521595
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Humans
MH  - *Myeloid Differentiation Factor 88/metabolism
MH  - *Tight Junctions/metabolism
MH  - Caco-2 Cells
MH  - Epithelial Cells/metabolism
MH  - Inflammation/metabolism
MH  - Autophagy
MH  - Glucose/metabolism
MH  - Intestinal Mucosa/metabolism
MH  - Permeability
PMC - PMC10300898
OTO - NOTNLM
OT  - autophagy
OT  - intestinal barrier
OT  - lactic acid bacteria
OT  - mucin 2
OT  - myeloid differentiation factor 88
COIS- Y.W.-Y., A.G., and T.S. are employees of Meiji Co., Ltd. Y.W.-Y., T.S., and S.S. 
      are the inventors of the pending patent WO2023/28754 A1.
EDAT- 2023/06/28 06:42
MHDA- 2023/06/29 06:42
PMCR- 2023/06/07
CRDT- 2023/06/28 01:34
PHST- 2023/05/24 00:00 [received]
PHST- 2023/06/03 00:00 [revised]
PHST- 2023/06/05 00:00 [accepted]
PHST- 2023/06/29 06:42 [medline]
PHST- 2023/06/28 06:42 [pubmed]
PHST- 2023/06/28 01:34 [entrez]
PHST- 2023/06/07 00:00 [pmc-release]
AID - nu15122655 [pii]
AID - nutrients-15-02655 [pii]
AID - 10.3390/nu15122655 [doi]
PST - epublish
SO  - Nutrients. 2023 Jun 7;15(12):2655. doi: 10.3390/nu15122655.