Lacticaseibacillus paracasei KBL382 contributes to the immunomodulation in THP-1 cells
Gut microbiome imbalance can induce inflammatory responses via Toll-like receptor 2 (TLR2) signaling pathways. Lactobacillus spp., popularly applied as probiotics in both humans and animals, have come into the spotlight for their strong immunomodulatory effects. We aimed to evaluate the immunomodulatory potential of live or pasteurized Lacticaseibacillus paracasei (L. paracasei) KBL382, isolated from healthy Korean individuals, in an in vitro monocytic THP-1 cell model. Live L. paracasei KBL382 significantly increased TLR2 and MyD88 expressions and induced IRAK1 expression, irrespective of lipopolysaccharide (LPS) stimulation (p < 0.05). Under LPS stimulation, THP-1 cells treated with live L. paracasei KBL382 showed significantly increased interleukin (IL)-6 and IL-10 levels (p < 0.05). Pasteurized L. paracasei exhibited a decrease in IL-12 levels (p < 0.05). Moreover, live L. paracasei KBL382 also markedly elevated A20 and SOCS1 expressions, the critical negative regulators of inflammation, regardless of LPS stimulation (p < 0.05). The expression of IRAK3, another negative regulator of inflammation, was increased in THP-1 cells with live L. paracasei KBL382 under LPS stimulation (p < 0.05). Our findings demonstrate that L. paracasei KBL382 contributes to the immunomodulation in THP-1 cells by coordinating both positive and negative regulatory signaling. L. paracasei KBL382 could be used as a promising probiotic strain for attenuating chronic inflammation through the gut-immune axis mechanisms.
Authors
- Cheonghoon Lee (ORCID: https://orcid.org/0000-0002-6382-5611)
- M. -I. Kim
- Sung Jae Jang
- Min Jung Jo
- Gwangpyo Ko
- Woon-Ki Kim
- SungJun Park
- Seoung Bum Lee
Institutions
- Seoul National University (KR)
Publication Details
- Journal
- The Journal of Microbiology
- Published
- 2026-02-25
- DOI
- https://doi.org/10.71150/jm.2509016
- Primary Topic
- Probiotics and Fermented Foods
- Type
- article
- Field-Weighted Citation Impact
- 0.00