ReviewInternational journal of molecular sciences2011
The role of reactive-oxygen-species in microbial persistence and inflammation.
Review in International journal of molecular sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
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
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 246 citations in OpenAlex.
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- Medical Gas Plasma Inactivates Adenoviruses via Capsid Oxidation.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Epigenetic regulation by HDAC11-driven STAT3 activation promotes pro-inflammatory cytokine production and endothelial dysfunction upon bacterial infection in diabetes.Cell communication and signaling : CCS · 2026Article
- Aquamin, a marine derived multi-mineral, attenuates toll-like receptor-mediated inflammatory responses in macrophages.Frontiers in immunology · 2026Article
- The emerging role of the microbiome in bladder cancer: prognostic implications and treatment response.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Review
- The impacts of chronic infections on shaping cellular senescence.Immunity & ageing : I & A · 2025Review
- Atypical Mitochondrial Phenotype of Colonic CD4+ and CD8+ T Cells During Experimental Chronic Colitis.Biomedicines · 2025Article
- Are Black Phosphorus Hydrogels Antimicrobial Without Photonic Activation?Molecules (Basel, Switzerland) · 2025Article
- MvfR ShapesCells · 2025Article
- A 5-HT-mediated urethral defense against urinary tract infections.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From Inflammation to Infertility: How Oxidative Stress and Infections Disrupt Male Reproductive Health.Metabolites · 2025Review
- A comprehensive analysis of the uterine microbiome in endometrial cancer patients - identification ofFrontiers in cellular and infection microbiology · 2025Article
- Pathogen-induced mitochondrial dysfunction: mechanistic insights, immune crosstalk, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Microenvironmental host-microbe interactions in chronic inflammatory skin diseases.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2024Review
- Tumor-targeting bacteria as immune stimulants - the future of cancer immunotherapy?Critical reviews in microbiology · 2024Review
49 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms of chronic infections caused by opportunistic pathogens are of keen interest to both researchers and health professionals globally. Typically, chronic infectious disease can be characterized by an elevation in immune response, a process that can often lead to further destruction. Reactive-Oxygen-Species (ROS) have been strongly implicated in the aforementioned detrimental response by host that results in self-damage. Unlike excessive ROS production resulting in robust cellular death typically induced by acute infection or inflammation, lower levels of ROS produced by host cells are increasingly recognized to play a critical physiological role for regulating a variety of homeostatic cellular functions including growth, apoptosis, immune response, and microbial colonization. Sources of cellular ROS stimulation can include "danger-signal-molecules" such as extracellular ATP (eATP) released by stressed, infected, or dying cells. Particularly, eATP-P2X(7) receptor mediated ROS production has been lately found to be a key modulator for controlling chronic infection and inflammation. There is growing evidence that persistent microbes can alter host cell ROS production and modulate eATP-induced ROS for maintaining long-term carriage. Though these processes have yet to be fully understood, exploring potential positive traits of these "injurious" molecules could illuminate how opportunistic pathogens maintain persistence through physiological regulation of ROS signaling.
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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.