ArticleAntimicrobial agents and chemotherapy1995
Interleukin-1 (IL-1)-induced resistance to bacterial infection: role of the type I IL-1 receptor.
Article in Antimicrobial agents and chemotherapy, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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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.
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Who cites it
3 citing papers in PubMed, 24 citations in OpenAlex.
- Succinate and inosine coordinate innate immune response to bacterial infection.PLoS pathogens · 2022Article
- Interleukin-23-mediated inflammation in Pseudomonas aeruginosa pulmonary infection.Infection and immunity · 2012Article
- Natural pathogens of laboratory mice, rats, and rabbits and their effects on research.Clinical microbiology reviews · 1998Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pretreatment with a low dose of recombinant human interleukin-1 beta (IL-1) (3 to 30 micrograms/kg) 24 h before a lethal Pseudomonas aeruginosa infection prolongs survival in neutropenic mice. We investigated the role of the type I IL-1 receptor (IL-1RI) and IL-1RII in this IL-1-induced protection by using a specific IL-1 receptor antagonist (IL-1-Ra), which blocks effects mainly via IL-1RI. Pretreatment with IL-1Ra before IL-1 partially blocked the IL-1-induced enhanced survival, whereas pretreatment with a specific neutralizing monoclonal antibody to IL-1RI (35F5) eliminated the IL-1 induced protection. The nonapeptide fragment 163-171 of recombinant human IL-1 beta, which possesses the immunoadjuvant but not the inflammatory effect of the entire molecule via a non-receptor-mediated signal transduction process, did not reproduce the IL-1-induced protection. IL-1-induced protection was associated with reduced serum aspartate aminotransferase and alanine aminotransferase concentrations in conjunction with ameliorated histopathology of the liver. These findings may be due to reduced cytokine production and cytokine sensitivity of target cells after infection. We conclude that the IL-1-induced nonspecific resistance to infection is mediated by cells bearing IL-1RI and is associated with a reduction of liver damage.
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Registered trials
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