Marina Gomes Machado

Centre National de la Recherche Scientifique

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

François Trottein

Center for Infection and Immunity of Lille

Mauro M. Teixeira

Universidade Federal de Minas Gerais

Valentin Sencio

Center for Infection and Immunity of Lille

Luciana P. Tavares

Brigham and Women's Hospital

Patricia Muñóz

Hospital General Universitario Gregorio Marañón

Lirlândia P. Sousa

Universidade Federal de Minas Gerais

Lucie Deruyter

Center for Infection and Immunity of Lille

Celso Martins Queiroz‐Junior

Universidade Federal de Minas Gerais

Marta Bodro

Hospital Clínic de Barcelona

Séverine Heumel

Center for Infection and Immunity of Lille

Cooperative Institutions

Universitat de Barcelona

Hospital General Universitario Gregorio Marañón

Instituto de Salud Carlos III

Centro de Investigación Biomédica en Red

Hospital Clínic de Barcelona

Marqués de Valdecilla University Hospital

Universidad Complutense de Madrid

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer

Inserm

Hospital Universitario Puerta de Hierro Majadahonda

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

CN1 TREATMENTS FOR METASTATIC MELANOMA: SYNTHESIS OF EVIDENCE FROM RANDOMIZED TRIALS

Value in Health (2006)

TR Einarson Pauline Po Yee Lui Robert Cashin Marina Gomes Machado Patricia K. Corey‐Lisle

10.1016/s1098-3015(10)63203-2

Cite

Citations (1)

Shotgun metagenomics and systemic targeted metabolomics highlight indole-3-propionic acid as a protective gut microbial metabolite against influenza infection

Gut Microbes (2024)

Séverine Heumel Vinícius de Rezende Rodovalho Charlotte Urien Florian Specque Patrícia Brito Rodrigues

The gut-to-lung axis is critical during respiratory infections, including influenza A virus (IAV) infection. In the present study, we used high-resolution shotgun metagenomics and targeted metabolomic analysis to characterize influenza-associated changes in the composition and metabolism of the mouse gut microbiota. We observed several taxonomic-level changes on day (D)7 post-infection, including a marked reduction in the abundance of members of the Lactobacillaceae and Bifidobacteriaceae families, and an increase in the abundance of Akkermansia muciniphila. On D14, perturbation persisted in some species. Functional scale analysis of metagenomic data revealed transient changes in several metabolic pathways, particularly those leading to the production of short-chain fatty acids (SCFAs), polyamines, and tryptophan metabolites. Quantitative targeted metabolomics analysis of the serum revealed changes in specific classes of gut microbiota metabolites, including SCFAs, trimethylamine, polyamines, and indole-containing tryptophan metabolites. A marked decrease in indole-3-propionic acid (IPA) blood level was observed on D7. Changes in microbiota-associated metabolites correlated with changes in taxon abundance and disease marker levels. In particular, IPA was positively correlated with some Lactobacillaceae and Bifidobacteriaceae species (Limosilactobacillus reuteri, Lactobacillus animalis) and negatively correlated with Bacteroidales bacterium M7, viral load, and inflammation markers. IPA supplementation in diseased animals reduced viral load and lowered local (lung) and systemic inflammation. Treatment of mice with antibiotics targeting IPA-producing bacteria before infection enhanced viral load and lung inflammation, an effect inhibited by IPA supplementation. The results of this integrated metagenomic-metabolomic analysis highlighted IPA as an important contributor to influenza outcomes and a potential biomarker of disease severity.

Metabolome

Akkermansia muciniphila

10.1080/19490976.2024.2325067

Cite

Citations (9)

Oral decontamination with colistin plus neomycin in solid organ transplant recipients colonized by multidrug-resistant Enterobacterales: a multicentre, randomized, controlled, open-label, parallel-group clinical trial

Clinical Microbiology and Infection (2020)

María Carmen Fariñas Claudia González-Rico Marta Fernández-Martínez Jesús Fortün Rosa Escudero-Sánchez

Colistin

Neomycin

10.1016/j.cmi.2020.12.016

Cite

Citations (26)

Molecular characterization of multidrug resistant Enterobacterales strains isolated from liver and kidney transplant recipients in Spain

Scientific Reports (2021)

Marta Fernández-Martínez Claudia González-Rico Mónica Gozalo-Margüello Francesc Marco Irene Gracia-Ahufinger

Abstract The objective of this study was to analyse the mechanisms of resistance to carbapenems and other extended-spectrum-β-lactams and to determine the genetic relatedness of multidrug-resistant Enterobacterales (MDR-E) causing colonization or infection in solid-organ transplantation (SOT) recipients. Prospective cohort study in kidney (n = 142), liver (n = 98) or kidney/pancreas (n = 7) transplant recipients between 2014 and 2018 in seven Spanish hospitals. We included 531 MDR-E isolates from rectal swabs obtained before transplantation and weekly for 4–6 weeks after the procedure and 10 MDR-E from clinical samples related to an infection. Overall, 46.2% Escherichia coli , 35.3% Klebsiella pneumoniae , 6.5% Enterobacter cloacae , 6.3% Citrobacter freundii and 5.7% other species were isolated. The number of patients with MDR-E colonization post-transplantation (176; 71.3%) was 2.5-fold the number of patients colonized pre-transplantation (71; 28.7%). Extended-spectrum β-lactamases (ESBLs) and carbapenemases were detected in 78.0% and 21.1% of MDR-E isolates respectively. In nine of the 247 (3.6%) transplant patients, the microorganism causing an infection was the same strain previously cultured from surveillance rectal swabs. In our study we have observed a low rate of MDR-E infection in colonized patients 4–6 weeks post-transplantation. E. coli producing bla CTX-M-G1 and K. pneumoniae harbouring bla OXA-48 alone or with bla CTX-M-G1 were the most prevalent MDR-E colonization strains in SOT recipients.

Enterobacter cloacae

Citrobacter freundii

Citrobacter

10.1038/s41598-021-90382-5

Cite

Citations (12)

Avaliação do papel da proteína anexina A1 e do seu receptor FPR2 em um modelo murino de pneumonia pneumocócica

Marina Gomes Machado

A pneumonia pneumococica e a principal causa de pneumonia adquirida na comunidade e e responsavel por altas taxas de mortalidade. A infeccao pulmonar pela bacteria Streptococcus pneumoniae caracteriza-se por um intenso infiltrado neutrofilico, que e importante para a eliminacao bacteriana, mas tambem pode causar dano tecidual. Assim sendo, imunomoduladores como a anexina A1 (AnxA1), podem ser alvos terapeuticos interessantes. A AnxA1 e um mediador pro-resolutivo, mimetizado pelo peptideo sintetico Ac226, que ao se ligar ao receptor FPR2 induz a apoptose de neutrofilos seguido da remocao destas celulas pelo processo de eferocitose, dentre varios outros efeitos imunomoduladores. Portanto, o objetivo desse estudo foi avaliar o papel da AnxA1 e do receptor FPR2 na resposta inflamatoria causada pela pneumonia pneumococica. Para tal, camundongos selvagens (WT) e deficientes (KO) para AnxA1 ou FPR2/3 foram infectados por via intranasal com 5x104 CFU de S. pneumoniae e eutanasiados em diferentes tempos apos a infeccao para a avaliacao de parâmetros inflamatorios e de funcao pulmonar. Alem disso, animais selvagens foram infectados com um inoculo maior - 105 CFU de S. pneumoniae intranasal - e tratados com 6mg/Kg de Ac2-26 e eutanasiados para avaliacao de parâmetros inflamatorios. Foi observado que animais AnxA1 KO foram mais susceptiveis a infeccao, apresentando uma resposta inflamatoria mais intensa, maior carga bacteriana e funcao pulmonar reduzida quando comparados aos animais WT. De modo semelhante, os animais FPR2/3 KO apresentaram parâmetros similares aos observados nos animais AnxA1 KO, com inflamacao mais intensa, carga bacteriana elevada, piora da funcao pulmonar e reducao da sobrevivencia quando comparados com animais WT. De modo coerente, os animais tratados com Ac2-26 apresentaram reducao dos parâmetros inflamatorios e das contagens bacterianas. Portanto, a deficiencia de AnxA1 ou de FPR2/3 contribuiu para a intensificacao da resposta inflamatoria desencadeada por S. pneumoniae nos pulmoes. Neste sentido, a administracao de Ac2-26 teve um importante papel no controle da inflamacao e da proliferacao bacteriana. Assim, a modulacao da resposta inflamatoria parece ser benefica em casos de pneumonia pneumococica grave e o tratamento com o peptideomimetico da AnxA1 pode ser uma estrategia terapeutica importante para o tratamento de doencas cuja inflamacao e exacerbada.

Source

Cite

Citations (0)

Mediators of Inflammation

Springer eBooks (2018)

Izabela Galvão Michelle A. Sugimoto Juliana P. Vago Marina Gomes Machado Lirlândia P. Sousa

Vascular permeability

Mediator

Platelet-activating factor

10.1007/978-3-319-77658-3_1

Cite

Citations (185)

The lung–gut axis during viral respiratory infections: the impact of gut dysbiosis on secondary disease outcomes

Mucosal Immunology (2021)

Valentin Sencio Marina Gomes Machado François Trottein

Bacteria that colonize the human gastrointestinal tract are essential for good health. The gut microbiota has a critical role in pulmonary immunity and host's defense against viral respiratory infections. The gut microbiota's composition and function can be profoundly affected in many disease settings, including acute infections, and these changes can aggravate the severity of the disease. Here, we discuss mechanisms by which the gut microbiota arms the lung to control viral respiratory infections. We summarize the impact of viral respiratory infections on the gut microbiota and discuss the potential mechanisms leading to alterations of gut microbiota's composition and functions. We also discuss the effects of gut microbial imbalance on disease outcomes, including gastrointestinal disorders and secondary bacterial infections. Lastly, we discuss the potential role of the lung–gut axis in coronavirus disease 2019.

Dysbiosis

Respiratory tract

10.1038/s41385-020-00361-8

Cite

Citations (221)

CXCR1/2 Antagonism Is Protective during Influenza and Post-Influenza Pneumococcal Infection

Frontiers in Immunology (2017)

Luciana P. Tavares Cristiana C. Garcia Marina Gomes Machado Celso Martins Queiroz‐Junior Adeline Barthélémy

Rationale: Influenza A infections are a leading cause of morbidity and mortality worldwide especially when associated with secondary pneumococcal infections. Inflammation is important to control pathogen proliferation but may also cause tissue injury and death. CXCR1/2 are chemokine receptors relevant for the recruitment of neutrophils. We investigated the role of CXCR1/2 during influenza, pneumococcal and post-influenza pneumococcal infections. Methods: Mice were infected with influenza A virus (IAV) or Streptococcus pneumoniae and then treated daily with the CXCR1/2 antagonist DF2162. To study secondary pneumococcal infection, mice were infected with a sublethal inoculum of IAV then infected with S. pneumoniae 14 days later. DF2162 was given in a therapeutic schedule from days 3 to 6 after influenza infection. Lethality, weight loss, inflammation, virus/bacteria counts and lung injury were assessed. Results: CXCL1 and CXCL2 were produced at high levels during IAV infection. DF2162 treatment decreased morbidity and this was associated with decreased infiltration of neutrophils in the lungs and reduced pulmonary damage and viral titers. During S. pneumoniae infection, DF2162 treatment decreased neutrophil recruitment, pulmonary damage and lethality rates, without affecting bacteria burden. Therapeutic treatment with DF2162 during sublethal IAV infection reduced the morbidity associated with virus infection and also decreased the magnitude of inflammation, lung damage and number of bacteria in the blood of mice subsequently infected with S. pneumoniae. Conclusion: Modulation of the inflammatory response by blocking CXCR1/2 improves disease outcome during respiratory influenza and pneumococcal infections, without compromising the ability of the murine host to deal with infection. Altogether, inhibition of CXCR1/2 may be a valid therapeutic strategy for treating lung infections caused by these pathogens, especially controlling secondary bacterial infection after influenza.

Pneumococcal infections

CXCL1

10.3389/fimmu.2017.01799

Cite

Citations (54)

Author Correction: Biofilm formation by multidrug resistant Enterobacteriaceae strains isolated from solid organ transplant recipients

Scientific Reports (2020)

José Ramos-Vivas Itziar Chapartegui-González Marta Fernández-Martínez Claudia González-Rico Jesús Fortün

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Solid organ

Enterobacteriaceae Infections

10.1038/s41598-020-60496-3