ReviewArchives of microbiology2026
Divergent mechanistic pathways of diarrheagenic bacterial infections at the host-microbiota interface: a review.
Review in Archives of microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Article
- The BaeS/BaeR two-component system enhancesFrontiers in cellular and infection microbiology · 2026Article
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
Bacterial diarrheal diseases continue to constitute a major burden on global public health, particularly within pediatric populations in low-resource settings. While clinically unified by the symptomology of diarrhea, the primary causative agents; Enterotoxigenic Escherichia coli (ETEC), Shigella species, Salmonella enterica, and Clostridioides difficile employ fundamentally distinct molecular strategies to subvert intestinal homeostasis. This review presents a comparative analysis of these ecosystem engineers, proposing that their pathogenicity is defined by their unique management of the host-microbiota metabolic and signaling conflict. We advance beyond the traditional host-pathogen dyad to explore a mechanistic triangle, integrating recent findings that the microbiota acts as a dynamic third player imposing colonization resistance via secondary bile acids and nutrient competition (proline), or conversely, providing metabolic fuel (formate, tetrathionate) for pathogen expansion. We synthesize advanced molecular insights from including the energetics of the Shigella T3SS sorting platform (Spa47); the multilayered "effector-immunity arms race" involving the Shigella effectors OspC1 and OspD3 in manipulating necroptosis; novel Salmonella T3SS-2 targets such as LMO4 and SteA-mediated ER contact sites; and the receptor diversity of C. difficile TcdB variants. Finally, we map these mechanisms to next-generation therapeutic vulnerabilities, highlighting the transition from broad-spectrum antibiotics to precision bacteriophage biocontrol (LPEK22, LPST94) and AI-discovered lysins (DeepLysin) as the future of intervention.
Indexed as
Identifiers
42007992What OpenQuestion 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 OpenQuestion graph.