ArticleInfection and immunity1999
Effects of cytokines and endotoxin on the intracellular growth of bacteria.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed.
- Dual-Action Sutures: Chlorhexidine and Dexamethasone for Infection Control and Inflammation Suppression.Molecules (Basel, Switzerland) · 2026Article
- Natural and synthetic chemicals acting as enhancers of bacterial pathogenic success within the human host.Frontiers in cellular and infection microbiology · 2026Review
- Article
- Harnessing Epigenetics: Innovative Approaches in Diagnosing and Combating Viral Acute Respiratory Infections.Pathogens (Basel, Switzerland) · 2025Review
- Resolvin D1 alleviates lipopolysaccharide-inducedBioImpacts : BI · 2025Article
- Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis.Critical care (London, England) · 2024Review
- The influence of steroid type on outcomes in patients with acute respiratory distress syndrome.Journal of intensive care · 2023Article
- Microbiome and Human Health: Current Understanding, Engineering, and Enabling Technologies.Chemical reviews · 2023Review
- A cooperativity between virus and bacteria during respiratory infections.Frontiers in microbiology · 2023Review
- Composition and diversity analysis of the lung microbiome in patients with suspected ventilator-associated pneumonia.Critical care (London, England) · 2022Article
- Inborn errors of immunity and related microbiome.Frontiers in immunology · 2022Review
- Immunomonitoring of Monocyte and Neutrophil Function in Critically Ill Patients: From Sepsis and/or Trauma to COVID-19.Journal of clinical medicine · 2021Review
- Lipopolysaccharide from biofilm-formingJournal of medical microbiology · 2021Article
- Effects of Anti-Cytokine Antibodies on Gut Barrier Function.Mediators of inflammation · 2019Review
- HMGB1 Antagonist, Box A, Reduces TLR4, RAGE, and Inflammatory Cytokines in the Cornea of P. aeruginosa-Infected Mice.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2018Article
- Protective effect of early low-dose hydrocortisone on ventilator-associated pneumonia in the cancer patients: a propensity score analysis.Annals of intensive care · 2017Article
- A nonsense mutation in TLR5 is associated with survival and reduced IL-10 and TNF-α levels in human melioidosis.PLoS neglected tropical diseases · 2017Article
- Article
- The respiratory tract microbiome and lung inflammation: a two-way street.Mucosal immunology · 2017Review
- The Microbiome and the Respiratory Tract.Annual review of physiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with unresolving acute respiratory distress syndrome (ARDS) have persistently elevated levels of proinflammatory cytokines in the lungs and circulation and increased rates of bacterial infections. Phagocytic cells hyperactivated with lipopolysaccharide (LPS), which induces high levels of proinflammatory cytokines in monocytic cells, are inefficient in killing ingested bacteria despite having intact phagocytic activity. On the other hand, phagocytic cells that are activated with an analogue of LPS that does not induce the expression of proinflammatory cytokines effectively ingest and kill bacteria. We hypothesized that in the presence of high concentrations of proinflammatory cytokines, bacteria may adapt and utilize cytokines to their growth advantage. To test our hypothesis, we primed a human monocytic cell line (U937) with escalating concentrations of the proinflammatory cytokines tumor necrosis factor alpha, interleukin-1beta (IL-1beta), and IL-6 and with LPS. These cells were then exposed to fresh isolates of three common nosocomial pathogens: Staphylococcus aureus, Pseudomonas aeruginosa, and an Acinetobacter sp. In human monocytes primed with lower concentrations of proinflammatory cytokines (10 to 250 pg) or LPS (1 and 10 ng), intracellular bacterial growth decreased. However, when human monocytes were primed with higher concentrations of proinflammatory cytokines (1 to 10 ng) or LPS (1 to 10 micrograms), intracellular growth of the tested bacteria increased significantly (P <0.0001). These results were reproduced with peripheral blood monocytes obtained from normal healthy volunteers. The specificity of the cytokine activity was demonstrated by neutralizing the cytokines with specific antibodies. Our findings provide a possible mechanism to explain the frequent development of bacterial infections in patients with an intense and protracted inflammatory response.
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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.