ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2011
Morphine, but not trauma, sensitizes to systemic Acinetobacter baumannii infection.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
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- Impact of recently initiated medications on the incidence of urinary tract infections in patients with type 2 diabetes: an observational case-control study.Therapeutic advances in drug safety · 2025Article
- Humoral response induced after intranasal vaccination with heat inactivatedFrontiers in immunology · 2025Article
- Blocking IL-17A prevents oxycodone-induced depression-like effects and elevation of IL-6 levels in the ventral tegmental area and reduces oxycodone-derived physical dependence in rats.Brain, behavior, and immunity · 2024Article
- Insights into the Current and Possible Future Use of Opioid Antagonists in Relation to Opioid-Induced Constipation and Dysbiosis.Molecules (Basel, Switzerland) · 2023Review
- Dynamic Gene Clusters Mediating Carbapenem-ResistantAntibiotics (Basel, Switzerland) · 2022Article
- Opioid-Mediated HIV-1 Immunopathogenesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- Opioid use potentiates the virulence of hospital-acquired infection, increases systemic bacterial dissemination and exacerbates gut dysbiosis in a murine model ofGut microbes · 2020Article
- Host Innate Immune Responses toFrontiers in cellular and infection microbiology · 2020Review
- Sequence similarity searches for morphine biosynthesis enzymes in bacteria yield putative targets for understanding associations between infection and opiate administration.Journal of medical microbiology · 2019Article
- A potential role for the gut microbiome in substance use disorders.Psychopharmacology · 2019Review
- Acute intraperitoneal infection with a hypervirulent Acinetobacter baumannii isolate in mice.Scientific reports · 2019Article
- Part I: Minimum Quality Threshold in Preclinical Sepsis Studies (MQTiPSS) for Study Design and Humane Modeling Endpoints.Shock (Augusta, Ga.) · 2019Review
- A Porcine Wound Model ofAdvances in wound care · 2019Article
- The Role of Opioid Receptors in Immune System Function.Frontiers in immunology · 2019Review
- Thioredoxin-A is a virulence factor and mediator of the type IV pilus system in Acinetobacter baumannii.PloS one · 2019Article
- Association between rs2275913 single-nucleotide polymorphism of the interleukin-17A gene and perioperative analgesic use in cosmetic orthognathic surgery.Neuropsychopharmacology reports · 2018Article
- Update of the Scientific Opinion on opium alkaloids in poppy seeds.EFSA journal. European Food Safety Authority · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Acinetobacter baumannii is an important nosocomial pathogen in civilian intensive care units. Recently the incidence has increased in wounded military personnel. Morphine is documented in numerous animal studies to be immunosuppressive and to sensitize to infection. The hypotheses were tested that morphine, administered for analgesia in the battlefield, predisposes to Acinetobacter infection, and that the opioid may have an additive or synergistic effect with trauma. To test these hypotheses, an intraperitoneal infection model was established in mice using several Acinetobacter strains. Morphine administered for 48 h by implantation of a slow-release morphine pellet increased mortality compared to animals receiving a placebo pellet, an effect that was blocked by the mu-opioid receptor antagonist, naltrexone. Acinetobacter burdens in the blood, spleens, livers, and lungs of morphine-treated mice, were significantly higher than those in placebo-treated animals, confirming that mortality was due to potentiated growth of the bacteria. There were also elevated levels of pro-inflammatory cytokines in morphine-treated versus placebo-treated mice. Morphine caused a reduction in the total number of cells in the peritoneal cavity, a decrease in the percentage and total numbers of neutrophils, and a decrease in the total number of macrophages. Morphine treatment also suppressed levels of the neutrophil-inducing molecules, IL-17A and KC/CXCL1. However, IL-17A(-/-) mice given morphine were not sensitized to Acintobacter infection to a greater degree than similarly treated wild-type mice. Trauma alone did not sensitize to Acinetobacter infection, and there was no additive effect between morphine and trauma. These results support the hypothesis that morphine potentiates Acinetobacter infection.
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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.