Evidence map›Paper›PMID 39329771›Full record

ReviewCells2024

The Battle of LPS Clearance in Host Defense vs. Inflammatory Signaling.

Pankaj Kumar, Evan A Schroder, Murugesan V S Rajaram, Edward N Harris, Latha P Ganesan

Abstract readReview
In one paragraph

Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed.

  1. Review
  2. Article
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  6. Review
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  15. Review
  16. International journal of molecular sciences · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Pankaj KumarDepartment of Internal Medicine, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.ORCID 0000-0002-4146-0543
Evan A SchroderDepartment of Biochemistry, University of Nebraska, Lincoln, NE 68588, USA.ORCID 0000-0001-7342-5796
Murugesan V S RajaramDepartment of Microbial Infection and Immunity, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.
Edward N HarrisDepartment of Biochemistry, University of Nebraska, Lincoln, NE 68588, USA.ORCID 0000-0001-7045-1040
Latha P GanesanDepartment of Internal Medicine, College of Medicine, The Ohio State University, Columbus, OH 43210, USA.ORCID 0000-0002-4236-6620

Funding

Molecular mechanism of cardiac inflammation and dysfunction in Pseudomonas aeruginosa infectionR01AI146252 · NIAID · OHIO STATE UNIVERSITY · PI RAJARAM, MURUGESAN · 2019 to 2023
$2.2M
Host protective immune functions of Stabilin receptors in liverR56AI170880 · NIAID · OHIO STATE UNIVERSITY · PI GANESAN, LATHA PRABHA · 2023 to 2023
$373k
NIAID NIH HHS AI170880NIAID NIH HHS R01 AI146252NIAID NIH HHS R56 AI170880
6 · The paper itself

Abstract

Lipopolysaccharide (LPS) in blood circulation causes endotoxemia and is linked to various disease conditions. Current treatments focus on preventing LPS from interacting with its receptor Toll-like receptor 4 (TLR4) and reducing inflammation. However, our body has a natural defense mechanism: reticuloendothelial cells in the liver rapidly degrade and inactivate much of the circulating LPS within minutes. But this LPS clearance mechanism is not perfect. Excessive LPS that escape this clearance mechanism cause systemic inflammatory damage through TLR4. Despite its importance, the role of reticuloendothelial cells in LPS elimination is not well-studied, especially regarding the specific cells, receptors, and mechanisms involved. This gap hampers the development of effective therapies for endotoxemia and related diseases. This review consolidates the current understanding of LPS clearance, narrates known and explores potential mechanisms, and discusses the relationship between LPS clearance and LPS signaling. It also aims to highlight key insights that can guide the development of strategies to reduce circulating LPS by way of bolstering host defense mechanisms. Ultimately, we seek to provide a foundation for future research that could lead to innovative approaches for enhancing the body's natural ability to clear LPS and thereby lower the risk of endotoxin-related inflammatory diseases, including sepsis.

Indexed as

InflammationLipopolysaccharidesSignal TransductionAnimalsEndotoxemiaHumansToll-Like Receptor 4LipopolysaccharidesToll-Like Receptor 4clearanceendotoxemiaendotoxin associated diseasesKupffer cellsliverLPSLSECsscavenger receptorssepsissignaling

Identifiers

PMID39329771
PMCPMC11430141

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.