ArticleBMC cancer2026
Lipopolysaccharide suppresses lung metastasis by activating CD8
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundInflammation plays a dual role in tumor progression, and its overall effect depends on the complex interactions between the nature of the stimuli and the dynamic changes within the tumor microenvironment. Lipopolysaccharide (LPS) is a bacterial endotoxin whose immune effects on tumors may be either promoting or inhibiting, depending on the dose and timing. This study investigates the effects of LPS on tumor cells, fibroblasts, and immune cells in a mouse model of lung metastasis.
methodsTo investigate the effects of LPS on tumor progression, we employed C57BL/6 immune-competent mice, immune-compromised nude mice and immune-deficient NOD-SCID mice. We assessed metastasis through in vivo experiments, while in vitro studies were conducted to evaluate the proliferation of tumor cells in the presence of LPS and LPS-treated fibroblasts. Additionally, we analyzed immune cell infiltration and the role of specific immune cell populations, such as CD8+ T cells, macrophages, and dendritic cells, in mediating the effects of LPS.
resultsLPS treatment significantly suppressed metastasis in immune-competent C57BL/6 mice but had no effect in immune-compromised nude mice, and even promoted metastasis in severely immune-deficient NOD-SCID mice. In vitro, LPS inhibited tumor cell proliferation. However, when tumor cells were co-cultured with LPS-treated fibroblasts, their growth was promoted compared to those co-cultured with untreated fibroblasts. In vivo, LPS enhanced the infiltration of mature macrophages, neutrophils, and CD8+ T cells while reducing M2 macrophages in the tumor microenvironment. Depletion of CD8+ T cells, macrophages, or dendritic cells individually abolished the protective effect of LPS, demonstrating their essential roles. Furthermore, LPS boosted the cytotoxicity of CD8+ T cells against tumor targets.
conclusionLPS exerts a dual influence on tumors: overall LPS suppresses metastasis by activating cell-mediated immunity, specifically cytotoxic CD8+ T cells, despite promoting effect via inflamed fibroblasts.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.