ArticleInfection and immunity1989
Stimulation by fibronectin of macrophage-mediated phagocytosis of Pseudomonas aeruginosa.
Article in Infection and immunity, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed, 14 citations in OpenAlex.
- Cell adhesion protein fibulin-7 and its C-terminal fragment negatively regulate monocyte and macrophage migration and functions in vitro and in vivo.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Mechanisms of nonopsonic phagocytosis of Pseudomonas aeruginosa.Infection and immunity · 1993Article
- S-layer-mediated association of Aeromonas salmonicida with murine macrophages.Infection and immunity · 1992Article
- Pseudomonas aeruginosa pili as ligands for nonopsonic phagocytosis by fibronectin-stimulated macrophages.Infection and immunity · 1989Article
- Fibronectin as an enhancer of nonopsonic phagocytosis of Pseudomonas aeruginosa by macrophages.Infection and immunity · 1989Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a previous investigation it was determined that Pseudomonas aeruginosa cells taken directly from a mouse in vivo growth system were significantly more susceptible to nonopsonic phagocytosis by macrophages than were similar cells after being washed in buffer (N. M. Kelly, J. L. Battershill, S. Kuo, J. P. Arbuthnott, and R. E. W. Hancock, Infect. Immun. 55:2841-2843, 1987). It was demonstrated that a phagocytosis-promoting factor was found in the supernatant obtained from chambers incubated in the peritoneal cavities of laboratory mice or rats. The phagocytosis-promoting factor was effective with both strains of P. aeruginosa tested, using both unelicited mouse peritoneal macrophages and the P388D1 mouse macrophage cell line as the phagocytic cells. Phagocytosis enhancement was observed with in vivo-grown bacteria and with bacteria grown in vitro on agar plates, but not with bacteria grown in vitro with rapid agitation. Supernatants from mice and rats were fractionated using a fast pressure liquid chromatography gel exclusion column. The phagocytosis-promoting factor copurified with fibronectin. Furthermore, antifibronectin sera negated the phagocytosis-promoting activities of in vivo chamber supernatant, while commercial bovine fibronectin was itself capable of promoting phagocytosis. The concentrations of fibronectin increased in both rat and mouse peritoneal chambers with time, coincident with the ability of chamber supernatants to promote phagocytosis. It was concluded that fibronectin was the phagocytosis-promoting factor of chamber supernatants. Bacterial presence in the peritoneal chambers was not required to elicit fibronectin uptake into the chambers.
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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.