Evidence map›Paper›PMID 41408488›Full record

ReviewInflammopharmacology2026

SARS-CoV-2 infection and gut-lung axis: the potential role of rifaximin.

Taghreed N Almanaa, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Maii A Abdelnaby, Athanasios Alexiou, Marios Papadakis, Islam E Abo-ElFetoh, Gaber El-Saber Batiha

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Taghreed N AlmanaaDepartment of Botany and Microbiology, College of Science, King Saud University, 11451, Riyadh, Saudi Arabia.
Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ali I Al-GareebDepartment of Clinical Pharmacology and Medicine, Jabir Ibn Hayyan Medical University, Al-Ameer Qu./ Najaf - Iraq, Kufa, Po. Box 13, Iraq.
Maii A AbdelnabyHealth Affairs Directorate in Alexandria, Ministry of Health and Population, Alexandria, Egypt.
Athanasios AlexiouUniversity Centre for Research & Development, Chandigarh University, Chandigarh-Ludhiana Highway, Mohali, Punjab, India.
Marios PapadakisMedical Department, Faculty of Life Sciences, University of Thessaly, 3 Panepistimiou, 41500, Larissa, Greece. marios_papadakis@yahoo.gr.
Islam E Abo-ElFetohCentral Administration of Environmental Affairs, Preventive Sector, Ministry of Health and Population, 44511, Sharkia, Egypt. islamezzat546@gmail.com.
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, AlBeheira, 22511, Egypt. gabersaberbatiha@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), leading to global effects. COVID-19 causes pulmonary and extra-pulmonary manifestations. One of the most common extra-pulmonary manifestations is gastrointestinal (GI) manifestation. Enteric COVID-19 triggers changes in the diversity of gut microbiota (dysbiosis). Dysbiosis of gut flora increases gut permeability, resulting in secondary bacterial infections, systemic inflammation, and injury of the peripheral organs. Dysbiosis may affect the immune system and pulmonary response to the SARS-CoV-2 invasion, suggesting a link between the lungs and gut through the gut-lung axis. Intestinal inflammation caused by SARS-CoV-2 infection induces leaky gut with subsequent transmission of toxins and antigens to the systemic circulation, causing further worsening of the septic condition in COVID-19 patients. Therefore, the anti-inflammatory agents' interruption of the gut-lung axis may reduce respiratory complications due to intestinal inflammation in COVID-19. Rifaximin (RXM) is a semi-synthetic antibacterial drug derived from natural rifamycin that acts locally within GI by inhibiting bacterial RNA polymerase and reducing the bacterial population and associated intestinal inflammation. RXM inhibits bacterial adherence to the intestinal epithelial lining and translocation across this GI lining. RXM has anti-inflammatory effects by inhibiting the release of pro-inflammatory cytokines and modulating the gut pregnane X receptor (PXR). RXM acts as a prebiotic in maintaining the growth of gut microbiota and may prevent the development of COVID-19-induced dysbiosis. Therefore, RXM could be effective in managing COVID-19 and associated inflammatory complications. Therefore, this review aims to discuss the potential role of RXM in managing COVID-19.

Indexed as

COVID-19COVID-19 Drug TreatmentGastrointestinal MicrobiomeLungRifaximinAnimalsDysbiosisHumansSARS-CoV-2RifaximinCOVID-19DysbiosisGut microbiotaPro-inflammatory cytokinesRifaximinSARS-CoV-2

Identifiers

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.