Evidence map›Paper›PMID 35314399›Full record

ArticleCellular and molecular gastroenterology and hepatology2022

Interleukin 1β Blockade Reduces Intestinal Inflammation in a Murine Model of Tumor Necrosis Factor-Independent Ulcerative Colitis.

Marina Liso, Giulio Verna, Elisabetta Cavalcanti, Stefania De Santis, Raffaele Armentano, Angela Tafaro, Antonio Lippolis, Pietro Campiglia, Antonio Gasbarrini, Mauro Mastronardi and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
8.0field-weighted citation impact, top 2% of its field
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

36 citing papers in PubMed, 46 citations in OpenAlex.

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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

14 authors at 7 institutions in 2 countries.

Marina LisoNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy.
Giulio VernaDepartment of Pharmacy, University of Salerno, Fisciano (SA), Italy; Digestive Health Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.
Elisabetta CavalcantiNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy.
Stefania De SantisDepartment of Pharmacy-Drug Science, University of Bari Aldo Moro, Bari, Italy.
Raffaele ArmentanoNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy.
Angela TafaroNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy.
Antonio LippolisNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy.
Pietro CampigliaDepartment of Pharmacy, University of Salerno, Fisciano (SA), Italy.
Antonio GasbarriniDigestive Disease Center-Unità Operativa Complessa di Medicina Interna e Gastroenterologia, Dipartimento di Scienze Mediche e Chirurgiche, Fondazione Policlinico Universitario "A. Gemelli" Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Roma, Italy.
Mauro MastronardiNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy.
Theresa Torres PizarroDigestive Health Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA; Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.
Fabio CominelliDigestive Health Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA; Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.
Loris Riccardo LopetusoDigestive Disease Center-Unità Operativa Complessa di Medicina Interna e Gastroenterologia, Dipartimento di Scienze Mediche e Chirurgiche, Fondazione Policlinico Universitario "A. Gemelli" Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Roma, Italy; Department of Medicine and Ageing Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy; Center for Advanced Studies and Technology, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Marcello ChieppaNational Institute of Gastroenterology "S. de Bellis," Research Hospital, Castellana Grotte (BA), Italy; Dietetics and Clinical Nutrition Laboratory, Department of Public Health, Experimental and Forensic Medicine, University of Pavia, Pavia, Italy; Department of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, via Monteroni, Lecce, Italy. Electronic address: marcello.chieppa@unisalento.it.
Gastroenterology Hospital "Saverio de Bellis" · ITCase Western Reserve University · USUniversity of Salerno · ITAgostino Gemelli University Polyclinic · ITUniversity of Bari Aldo Moro · ITUniversity of Chieti-Pescara · ITUniversity of Salento · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsInflammatory bowel diseases are multifactorial diseases commonly treated with either immunomodulatory drugs or anti-tumor necrosis factor (TNF). Currently, failure to respond to anti-TNF therapy (assessed no earlier than 8-12 weeks after starting treatment) occurs in 20%-40% of patients enrolled in clinical trials and in 10%-20% in clinical practice. Murine models of inflammatory bowel disease provide important tools to better understand disease mechanism(s). In this context and among the numerous models available, Winnie-TNF-knockout (KO) mice recently were reported to show characteristics of ulcerative colitis (UC) that are independent of TNF, and with increased interleukin (IL)1β production.

methodsHerein, the efficacy of recombinant IL1-receptor antagonist (anakinra) administration was evaluated in Winnie-TNF-KO mice, used as a UC model of primary anti-TNF nonresponders.

resultsWe analyzed gut mucosal biopsy specimens and circulating cytokine profiles of a cohort of 30 UC patients; approximately 75% of primary nonresponders were characterized by abundant IL1β in both the serum and local intestinal tissues. In Winnie-TNF-KO mice, administration of anakinra efficiently reduced the histologic score of the distal colon, which represents the most common site of inflammation in Winnie mice. Furthermore, among lamina propria and mesenteric lymph node-derived T cells, interferon γ-expressing CD8

conclusionsOur study provides new insight and alternative approaches to treat UC patients, and points to anti-IL1 strategies (ie, anakinra) that may be a more effective therapeutic option for primary nonresponders to anti-TNF therapy.

Indexed as

Colitis, UlcerativeInflammatory Bowel DiseasesAnimalsCD8-Positive T-LymphocytesDisease Models, AnimalHumansInflammationInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinIntestinal MucosaMiceMice, KnockoutTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsInterleukin-1betaInterleukin 1 Receptor Antagonist ProteinTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsCytokinesTNFUlcerative Colitis

Identifiers

PMID35314399
PMCPMC9120241
OpenAlexW4221137129

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.