ArticleThe American journal of pathology2012
Morphine decreases bacterial phagocytosis by inhibiting actin polymerization through cAMP-, Rac-1-, and p38 MAPK-dependent mechanisms.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03534102 (Can Simplified and More Detailed Instructions Affect Post-Operative Narcotic Consumption), which is not on this map. Cited by 34 papers.
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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.
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.
Can Simplified and More Detailed Instructions Affect Post-Operative Narcotic Consumption
Who cites it
34 citing papers in PubMed, 60 citations in OpenAlex.
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- Irisflorentin promotes bacterial phagocytosis and inhibits inflammatory responses in macrophages during bacterial infection.Heliyon · 2024Article
- Changes in Plasma Metabolic Signature upon Acute and Chronic Morphine Administration in Morphine-Tolerant Mice.Metabolites · 2023Article
- Morphine disrupts macrophage functions even during HIV infection.Journal of leukocyte biology · 2022Article
- PGE2 inhibits neutrophil phagocytosis through the EP2R-cAMP-PTEN pathway.Immunity, inflammation and disease · 2022Article
- Methamphetamine Dysregulates Macrophage Functions and Autophagy to Mediate HIV Neuropathogenesis.Biomedicines · 2022Article
- Opioid Modulation of the Gut-Brain Axis in Opioid-Associated Comorbidities.Cold Spring Harbor perspectives in medicine · 2021Review
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- Opioids Regulate the Immune System: Focusing on Macrophages and Their Organelles.Frontiers in pharmacology · 2021Review
- Ginsenoside Rb1 increases macrophage phagocytosis through p38 mitogen-activated protein kinase/Akt pathway.Journal of ginseng research · 2019Article
- Morphine Potentiates Dysbiotic Microbial and Metabolic Shifts in Acute SIV Infection.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Article
- Multi-omics Analysis of Liver Infiltrating Macrophages Following Ethanol Consumption.Scientific reports · 2019Article
- The Role of Opioid Receptors in Immune System Function.Frontiers in immunology · 2019Review
- The Effects of Opioids on HIV Neuropathogenesis.Frontiers in immunology · 2019Review
- Astrocyte EV-Induced lincRNA-Cox2 Regulates Microglial Phagocytosis: Implications for Morphine-Mediated Neurodegeneration.Molecular therapy. Nucleic acids · 2018Article
- Comparison of implant survivability in primary 1- to 2-level lumbar fusion amongst opioid abusers and non-opioid abusers.Journal of spine surgery (Hong Kong) · 2018Article
- Morphine reduces mouse microglial engulfment induced by lipopolysaccharide and interferon-γ via δ opioid receptor and p38 mitogen-activated protein kinase.Neurological research · 2018Article
- Immune-enhancing activity of C. militaris fermented with Pediococcus pentosaceus (GRC-ON89A) in CY-induced immunosuppressed model.BMC complementary and alternative medicine · 2018Article
- Morphine alters the circulating proteolytic profile in mice: functional consequences on cellular migration and invasion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Morphine increases the susceptibility to opportunistic infection by attenuating bacterial clearance through inhibition of Fcγ receptor (FcgR)-mediated phagocytosis. Mechanisms by which morphine inhibits this process remain to be investigated. Actin polymerization is essential for FcgR-mediated internalization; therefore, disruption of the signaling mechanisms involved in this process is detrimental to the phagocytic ability of macrophages. To our knowledge, this study is the first to propose the modulation of actin polymerization and upstream signaling effectors [cAMP, Rac1-GTP, and p38 mitogen-activated protein kinase (MAPK)] as key mechanisms by which morphine leads to inhibition of pathogen clearance. Our results indicate that long-term morphine treatment in vitro and in vivo, through activation of the μ-opioid receptor, leads to an increase in intracellular cAMP, activation of protein kinase A, and inhibition of Rac1-GTPase and p38 MAPK, thereby attenuating actin polymerization and reducing membrane ruffling. Furthermore, because of long-term morphine treatment, FcgR-mediated internalization of opsonized dextran beads is also reduced. Morphine's inhibition of Rac1-GTPase activation is abolished in J774 macrophages transfected with constitutively active pcDNA3-EGFP-Rac1-Q61L plasmid. Dibutyryl-cAMP inhibits, whereas H89 restores, activation of Rac-GTPase and abolishes morphine's inhibitory effect, implicating cAMP as the key effector in morphine's modulation of actin polymerization. These findings indicate that long-term morphine treatment, by increasing intracellular cAMP and activating protein kinase A, leads to inhibition of Rac1-GTPase and p38 MAPK, causing attenuation of actin polymerization, FcgR-mediated phagocytosis, and decreased bacterial clearance.
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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.