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ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025

Angiotensin-(1-7) treatment improves pneumonia and prevents sepsis caused by pneumococcal infection.

Eliza Mathias Melo, Izabela Galvão, Franciel Batista Felix, Fernanda Medeiros Vale Magalhães, Flavia Rago, Marina Gomes Machado, Fernando Roque Ascenção, Maria José Campagnole-Santos, Robson Augusto Souza Dos Santos, Geovanni Dantas Cassali and 1 more

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

11 authors.

Eliza Mathias MeloCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil. mathias.eliza@gmail.com.
Izabela GalvãoCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil.
Franciel Batista FelixCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Morfologia, Instituto de Ciências Biológicas, Belo Horizonte, MG, Brazil.
Fernanda Medeiros Vale MagalhãesCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil.
Flavia RagoCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil.
Marina Gomes MachadoCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil.
Fernando Roque AscençãoCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil.
Maria José Campagnole-SantosDepartamento de Fisiologia e Biofísica, Instituto Nacional de Ciência e Tecnologia em Nanobiofarmacêutica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Robson Augusto Souza Dos SantosDepartamento de Fisiologia e Biofísica, Instituto Nacional de Ciência e Tecnologia em Nanobiofarmacêutica, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Geovanni Dantas CassaliLaboratório de Patologia Comparada, Departamento de Patologia, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.
Mauro Martins TeixeiraCentro de Pesquisa e Desenvolvimento de Fármacos, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Pampulha, Belo Horizonte, MG, 31270-901, Brazil. mmtex@ufmg.br.

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 476071/2011-9Fundação de Amparo à Pesquisa do Estado de Minas Gerais PPM-00508-18
6 · The paper itself

Abstract

backgroundPneumonia caused by Streptococcus pneumoniae remains a major global health concern, leading to significant morbidity and mortality. Angiotensin-(1-7) [Ang-(1-7)] is an endogenous peptide with known anti-inflammatory and pro-resolving properties, but its therapeutic potential in bacterial pneumonia is not fully understood. PURPOSE: This study aimed to investigate whether Ang-(1-7) could reduce inflammation, improve bacterial clearance, and enhance survival in a murine model of pneumococcal pneumonia, alone or in combination with the antibiotic ceftriaxone.

methodsA mouse model of S. pneumoniae pneumonia was used to evaluate the effects of Ang-(1-7). Mice received Ang-(1-7) treatment after infection, either alone or combined with ceftriaxone. Outcomes included leukocyte infiltration, pulmonary edema, lung tissue damage, cytokine production (TNF-α, IL-6, CXCL-1), bacterial load in bronchoalveolar lavage and blood, survival analysis, bone marrow-derived macrophage phagocytosis assays, and expression of lung barrier-associated genes.

resultsAng-(1-7) reduced leukocyte infiltration, pulmonary edema, and lung tissue injury, and decreased pro-inflammatory cytokine levels. Treatment improved bacterial clearance in both lungs and bloodstream and increased survival in infected mice. Importantly, combining Ang-(1-7) with ceftriaxone further enhanced survival, even when treatment initiation was delayed. Mechanistically, Ang-(1-7) increased macrophage phagocytic activity and upregulated genes associated with lung barrier integrity.

conclusionAng-(1-7) decreased inflammation, improved bacterial clearance, and enhanced survival in severe pneumococcal pneumonia. Its combination with ceftriaxone produced additive benefits, supporting Ang-(1-7) as a promising adjuvant therapeutic strategy in this infectious condition.

Indexed as

Angiotensin IAnti-Inflammatory AgentsPeptide FragmentsPneumonia, PneumococcalSepsisAnimalsAnti-Bacterial AgentsBronchoalveolar Lavage FluidCeftriaxoneCytokinesFemaleLungMacrophagesMaleMiceMice, Inbred C57BLAngiotensin Iangiotensin I (1-7)Anti-Bacterial AgentsAnti-Inflammatory AgentsCeftriaxoneCytokinesPeptide FragmentsAngiotensin-(1-7)InfectionInflammationPhagocytosisSepsisStreptococcus pneumoniae

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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.