# Inhibition of Porphyromonas gingivalis-Induced Respiratory Inflammation by an Alkaline Extract of Sasa senanensis Leaves

**Authors:** Asako Takagi, Akira Hasuike, Noriaki Kamio, Ryo Sakai, Yukihiro Karahashi, Kozue Sugimoto, Yurika Nakajima, Misaki Horiuchi, Kazuki Toeda, Hiroshi Sakagami, Shuichi Sato, Kenichi Imai

PMC · DOI: 10.3390/pathogens15020135 · Pathogens · 2026-01-26

## TL;DR

A leaf extract from Sasa senanensis reduces inflammation caused by a periodontal bacterium in respiratory tissues, both in human cells and mice.

## Contribution

The study demonstrates the anti-inflammatory effects of an alkaline leaf extract against P. gingivalis-induced respiratory inflammation.

## Key findings

- SE reduced IL-6 and IL-8 mRNA and cytokine secretion in human bronchial epithelial cells.
- SE inhibited NF-κB and MAPK pathways, including p38 and JNK, in a dose-dependent manner.
- In mice, SE lowered lung cytokine levels and NF-κB activity after P. gingivalis exposure.

## Abstract

Periodontal pathogens, including Porphyromonas gingivalis (P. gingivalis), are implicated in respiratory inflammatory conditions, and aspirated oral bacterial components may contribute to airway inflammation. This association has prompted the exploration of innovative therapeutic strategies in addition to conventional oral hygiene practices. We evaluated the anti-inflammatory efficacy of an alkaline extract of Sasa senanensis leaves (SE) against heat-inactivated P. gingivalis-induced inflammation in respiratory tissues. In human bronchial epithelial cells (BEAS-2B), SE reduced interleukin (IL)-6 and IL-8 mRNA expression and cytokine secretion in a dose-dependent manner. Moreover, SE attenuated nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs), including p38 and c-Jun N-terminal kinase (JNK), indicating broad anti-inflammatory actions. In mice, SE administration decreased early lung cytokine levels and reduced NF-κB activity following intratracheal challenge with heat-inactivated P. gingivalis. Together, these in vitro and in vivo findings indicate that SE suppresses proinflammatory signaling triggered by P. gingivalis components and may serve as a natural adjunct to mitigate bacteria-associated airway inflammatory responses.

## Linked entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569], CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], CRK (CRK proto-oncogene, adaptor protein) [NCBI Gene 1398], MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 5599]
- **Species:** Porphyromonas gingivalis (taxon 837), Sasa senanensis (taxon 387750), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** NFKBIA (NFKB inhibitor alpha) [NCBI Gene 4792] {aka EDAID2, IKBA, MAD-3, NFKBI}, RELA (RELA proto-oncogene, NF-kB subunit) [NCBI Gene 5970] {aka AIF3BL3, CMCU, NFKB3, p65}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}
- **Diseases:** chronic condition (MESH:D002908), infectious (MESH:D003141), proinflammatory cytokine (MESH:D000080424), LCCs (MESH:C562602), aspiration pneumonia (MESH:D011015), infection (MESH:D007239), cytotoxic (MESH:D064420), neutrophil (MESH:C564275), bacterial colonization (MESH:D015179), respiratory inflammatory (MESH:D012131), oral cancer (MESH:D009062), Pneumonia (MESH:D011014), chronic bronchitis (MESH:D029481), lung (MESH:D008171), respiratory tract infection (MESH:D012141), injury to (MESH:D014947), Periodontitis (MESH:D010518), inflammation (MESH:D007249), respiratory diseases (MESH:D012140)
- **Chemicals:** polyvinylidene fluoride (MESH:C024865), DMSO (MESH:D004121), lignin (MESH:D008031), CO2 (MESH:D002245), LPS (MESH:D008070), p-coumaric acid (MESH:C495469), U0126 (MESH:C113580), Lipofectamine 2000 (MESH:C086724), carbohydrate (MESH:D002241), Alkaline (-), curcumin (MESH:D003474), penicillin (MESH:D010406), BAY11-7082 (MESH:C434003), drinking water (MESH:D060766), resveratrol (MESH:D000077185), vitamin C (MESH:D001205), sodium dodecyl sulfate (MESH:D012967), Chlorophyllin (MESH:C007020), nitric oxide (MESH:D009569), hydroxyl radical (MESH:D017665), SP600125 (MESH:C432165), hemin (MESH:D006427), water (MESH:D014867), isoflurane (MESH:D007530), Iron (MESH:D007501), prostaglandin E2 (MESH:D015232), polysaccharide (MESH:D011134), N2 (MESH:D009584), SB203580 (MESH:C093642), streptomycin (MESH:D013307), polyacrylamide (MESH:C016679), menadione (MESH:D024483), sugar (MESH:D000073893), cynaropicrin (MESH:C075687)
- **Species:** Cricetinae (hamsters, subfamily) [taxon 10026], Homo sapiens (human, species) [taxon 9606], Porphyromonas gingivalis (species) [taxon 837], Orthomyxoviridae (family) [taxon 11308], Human immunodeficiency virus 1 (no rank) [taxon 11676], Mus musculus (house mouse, species) [taxon 10090], Sasa senanensis (species) [taxon 387750]
- **Cell lines:** 3C — Homo sapiens (Human), Hepatoblastoma, Cancer cell line (CVCL_1098), BEAS-2B — Homo sapiens (Human), Transformed cell line (CVCL_0168)

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12943373/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC12943373/full.md

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Source: https://tomesphere.com/paper/PMC12943373