SynthesisBMC infectious diseases2025
Pathogenic mechanisms and resistance profiles of microbial pulmonary infections in lung cancer: a systematic review.
Synthesis in BMC infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- RNA modifications shape innate immunity and cellular adaptation during bacterial respiratory infection.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary infections caused by microorganisms in lung cancer patients contribute to disease progression and treatment challenges. This systematic review aims to explore the clinical and pathophysiological characteristics of microbial pulmonary infections in lung cancer.
methodsA systematic literature search was conducted across Embase, PubMed/MEDLINE, Scopus, and Web of Science, covering studies published between January 1, 2015 and February 1, 2025, without restrictions on population or language. We included original studies reporting findings in human, animal, cell, or in silico models that examined non-viral microbial pulmonary infections in the context of lung cancer, with a focus on pathogen profiles, antimicrobial resistance, and associated molecular mechanisms. Evidence synthesis was narrative.
resultsA total of 8,879 records were identified, with 37 studies included comprising 14 human, 14 in vitro, 8 in vivo and one in silico studies. Of the 14 human studies, 8 studies reported microbial strain prevalence in 2,598 lung cancer patients. The most common pathogens included Klebsiella pneumoniae (21.1%), Pseudomonas aeruginosa (17.0%), Staphylococcus spp. (16.1%), Streptococcus spp. (14.1%), Candida spp. (12.4%), Haemophilus influenzae (7.9%), Enterobacter spp. (7.7%), and Aspergillus spp. (3.1%). Antibiotic sensitivity varied, with K. pneumoniae showing complete sensitivity to tigecycline and S. pneumoniae exhibiting low clindamycin sensitivity (~6%). Mechanistic studies identified key molecular pathways, including PD-1/PD-L1, NF-κB, and TLR4/MyD88, linking microbial pulmonary infections to lung cancer progression.
conclusionPulmonary infections play a significant role in lung cancer pathogenesis, particularly infections caused by K. pneumoniae and P. aeruginosa, potentially by triggering immune evasion and inflammatory signaling pathways.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.