Host–pathogen
LN DCs shelter antibiotic-tolerant Salmonella
Open access · cc by · source: Europe PMC
Slow-growing Salmonella in cecum lymph-node dendritic cells survive ciprofloxacin therapy.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Multiple empirical papers in this library examine host–pathogen with mechanistic biological findings.
Evidence for the claim as stated.
Gut lumen clears in 3 h, but 50–1,000 bacteria persist in cLN up to 10 days with slowed killing after the first 2 h.
Evidence for the claim as stated.
Systems and scales differ across host–pathogen studies (species, tissues, methods), so mechanisms should not be over-generalised.
Evidence for the claim as stated.
After high-dose ciprofloxacin, Salmonella Typhimurium was cleared from the mouse gut lumen in 3 hours, but 50–1,000 bacteria persisted in cecal lymph-node dendritic cells up to 10 days, with killing slowing after the first 2 hours. Flow/isolation of LN DC populations is how those shelters were assigned; the mouse model does not invent a new antibiotic.
Evidence for the claim as stated.
Flow is counting different objects. Salmonella work counts persistent bacteria inside LN DCs (50–1,000, lumen clear at 3 h); hESC work counts CXCR4+ DE-like cells under 1.5% O2; TB work profiles PD-1+ T cells in 35 human lungs. Those gates are not one 'immune panel'.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
Systems and scales differ across host–pathogen studies (species, tissues, methods), so mechanisms should not be over-generalised.
- Supports · PD-1 blockade reactivates TB via TNF
- Supports · How does malaria’s blood-stage transcriptome unfold?
Flow is counting different objects. Salmonella work counts persistent bacteria inside LN DCs (50–1,000, lumen clear at 3 h); hESC work counts CXCR4+ DE-like cells under 1.5% O2; TB work profiles PD-1+ T cells in 35 human lungs. Those gates are not one 'immune panel'.
- Supports · What marks definitive endoderm progenitors in hESCs?
- Supports · PD-1 blockade reactivates TB via TNF
Study at a glance
- Design
- Animal / in-vitro — S. Typhimurium–infected mice treated with high-dose ciprofloxacin; residual bacteria localized to cLN DCs
- N
- Mouse infection/antibiotic kinetics study; infection dose 5×10⁷ cfu — no single analytic N in stored text
- Population
- Mice infected with Salmonella Typhimurium
- Outcome
- Persistence of slow-growing bacteria in cecum lymph-node dendritic cells after ciprofloxacin
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
LN DCs shelter antibiotic-tolerant Salmonella
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
Pathogen cleared from gut lumen within 3 h.
Within 3 h of ciprofloxacin treatment, the pathogen was cleared from the gut lumen and pathogen spread to the spleen was prevented by the antibiotic ( and ).
50–1,000 viable bacteria remained up to 10 d.
After the first 2 h, the killing kinetics slowed down and 50–1,000 viable bacteria remained for up to 10 d (, ).
Key findings
Gut lumen clears in 3 h, but 50–1,000 bacteria persist in cLN up to 10 days with slowed killing after the first 2 h.
Methodology
Infected mice with S. Typhimurium, treated with high-dose ciprofloxacin, and localized surviving bacteria to cLN dendritic cells.
Limitations
Does not invent a new antibiotic; mouse model of persistence.
Related papers in this topic
Same topic cluster — not a recommendation engine.