ArticleCellular and molecular life sciences : CMLS2026
Cathelicidin-Ka, the first frog-derived TLR2 and TLR4 agonist, induces macrophage activation and promotes inflammation.
Article in Cellular and molecular life sciences : CMLS, 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
11 authors.
Funding
Abstract
TLR-targeted immunotherapy represents a promising strategy for combating infectious diseases by initiating or enhancing protective antimicrobial immunity. Here, we identified the first frog-derived TLR2 and TLR4 agonist, Cathelicidin-Ka (Cath-Ka), from the skin of Kaloula pulchra. The presence of Cath-Ka significantly enhanced proliferation, cytokine production, polarization, chemotaxis, phagocytosis, and intracellular bacterial killing of macrophages and peritoneal cells by targeting TLR2 and TLR4, rather than other pattern recognition receptors, and subsequently activated the downstream MyD88-MAPKs pathway. Cath-Ka also promoted macrophage polarization towards the M1 rather than M2 phenotype, and its intraperitoneal injection significantly promoted the chemotaxis of pro-inflammatory monocytes/macrophages into the peritoneal cavity. Finally, the mutant of Cath-Ka with amination at C-terminus had stronger effects on macrophage function modulation than the original peptide. These findings suggest that Cath-Ka and its amidated mutant are promising candidates for the treatment of TLR2 and TLR4-related diseases, including infections.
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.