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Article ; Online: Two Cases of

Satolli, Sara / Invernizzi, Federica / Danti, Federica Rachele / Reale, Chiara / Panteghini, Celeste / Nardocci, Nardo / Garavaglia, Barbara / Zorzi, Giovanna

Movement disorders clinical practice

2023 Volume 10, Issue 5, Page(s) 842–844

Language	English
Publishing date	2023-03-11
Publishing country	United States
Document type	Journal Article
ISSN	2330-1619
ISSN (online)	2330-1619
DOI	10.1002/mdc3.13705
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Article ; Online: The contribution of infection and the respiratory microbiome in acute exacerbations of idiopathic pulmonary fibrosis.

Invernizzi, Rachele / Molyneaux, Philip L

European respiratory review : an official journal of the European Respiratory Society

2019 Volume 28, Issue 152

Abstract: Idiopathic pulmonary fibrosis (IPF) arises in genetically susceptible individuals as a result of an aberrant wound-healing response following repetitive alveolar injury. The clinical course of the disease remains both variable and unpredictable with ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) arises in genetically susceptible individuals as a result of an aberrant wound-healing response following repetitive alveolar injury. The clinical course of the disease remains both variable and unpredictable with periods of more rapid decline, termed acute exacerbation of IPF (AE-IPF), often punctuating the disease trajectory. Exacerbations carry a significant morbidity and mortality, and their exact pathogenesis remains unclear. Given the emerging evidence that disruption and alteration in the lung microbiome plays a role in the pathogenesis and progression of IPF, this review discusses the current knowledge of the contribution of infection and the respiratory microbiome to AE-IPF.
MeSH term(s)	Animals ; Bacteria/pathogenicity ; Disease Progression ; Dysbiosis ; Host-Pathogen Interactions ; Humans ; Idiopathic Pulmonary Fibrosis/diagnosis ; Idiopathic Pulmonary Fibrosis/microbiology ; Lung/microbiology ; Microbiota ; Respiratory Tract Infections/diagnosis ; Respiratory Tract Infections/microbiology
Language	English
Publishing date	2019-07-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1077620-5
ISSN	1600-0617 ; 0905-9180
ISSN (online)	1600-0617
ISSN	0905-9180
DOI	10.1183/16000617.0045-2019
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Article ; Online: Respiratory microbiome and epithelial interactions shape immunity in the lungs.

Invernizzi, Rachele / Lloyd, Clare M / Molyneaux, Philip L

Immunology

2020 Volume 160, Issue 2, Page(s) 171–182

Abstract: The airway epithelium represents a physical barrier to the external environment acting as the first line of defence against potentially harmful environmental stimuli including microbes and allergens. However, lung epithelial cells are increasingly ... ...

Abstract	The airway epithelium represents a physical barrier to the external environment acting as the first line of defence against potentially harmful environmental stimuli including microbes and allergens. However, lung epithelial cells are increasingly recognized as active effectors of microbial defence, contributing to both innate and adaptive immune function in the lower respiratory tract. These cells express an ample repertoire of pattern recognition receptors with specificity for conserved microbial and host motifs. Modern molecular techniques have uncovered the complexity of the lower respiratory tract microbiome. The interaction between the microbiota and the airway epithelium is key to understanding how stable immune homeostasis is maintained. Loss of epithelial integrity following exposure to infection can result in the onset of inflammation in susceptible individuals and may culminate in lung disease. Here we discuss the current knowledge regarding the molecular and cellular mechanisms by which the pulmonary epithelium interacts with the lung microbiome in shaping immunity in the lung. Specifically, we focus on the interactions between the lung microbiome and the cells of the conducting airways in modulating immune cell regulation, and how defects in barrier structure and function may culminate in lung disease. Understanding these interactions is fundamental in the search for more effective therapies for respiratory diseases.
MeSH term(s)	Adaptive Immunity ; Airway Remodeling/immunology ; Epithelial Cells/immunology ; Homeostasis/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Lung/cytology ; Lung/immunology ; Lung/microbiology ; Lung Diseases/immunology ; Lung Diseases/microbiology ; Microbiota/immunology ; Respiratory Mucosa/immunology ; Respiratory Mucosa/microbiology
Keywords	covid19
Language	English
Publishing date	2020-04-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.13195
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Article: Pediatric Paroxysmal Exercise-Induced Neurological Symptoms: Clinical Spectrum and Diagnostic Algorithm.

Danti, Federica Rachele / Invernizzi, Federica / Moroni, Isabella / Garavaglia, Barbara / Nardocci, Nardo / Zorzi, Giovanna

Frontiers in neurology

2021 Volume 12, Page(s) 658178

Abstract: Paroxysmal exercise-induced neurological symptoms (PENS) encompass a wide spectrum of clinical phenomena commonly presenting during childhood and characteristically elicited by physical exercise. Interestingly, few shared pathogenetic mechanisms have ... ...

Abstract	Paroxysmal exercise-induced neurological symptoms (PENS) encompass a wide spectrum of clinical phenomena commonly presenting during childhood and characteristically elicited by physical exercise. Interestingly, few shared pathogenetic mechanisms have been identified beyond the well-known entity of paroxysmal exercise-induced dyskinesia, PENS could be part of more complex phenotypes including neuromuscular, neurodegenerative, and neurometabolic disease, epilepsies, and psychogenetic disorders. The wide and partially overlapping phenotypes and the genetic heterogeneity make the differential diagnosis frequently difficult and delayed; however, since some of these disorders may be treatable, a prompt diagnosis is mandatory. Therefore, an accurate characterization of these symptoms is pivotal for orienting more targeted biochemical, radiological, neurophysiological, and genetic investigations and finally treatment. In this article, we review the clinical, genetic, pathophysiologic, and therapeutic landscape of paroxysmal exercise induced neurological symptoms, focusing on phenomenology and differential diagnosis.
Language	English
Publishing date	2021-06-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564214-5
ISSN	1664-2295
ISSN	1664-2295
DOI	10.3389/fneur.2021.658178
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Article: Respiratory microbiome and epithelial interactions shape immunity in the lungs

Invernizzi, Rachele / Lloyd, Clare M / Molyneaux, Philip L

Immunology

Abstract	The airway epithelium represents a physical barrier to the external environment acting as the first line of defence against potentially harmful environmental stimuli including microbes and allergens. However, lung epithelial cells are increasingly recognized as active effectors of microbial defence, contributing to both innate and adaptive immune function in the lower respiratory tract. These cells express an ample repertoire of pattern recognition receptors with specificity for conserved microbial and host motifs. Modern molecular techniques have uncovered the complexity of the lower respiratory tract microbiome. The interaction between the microbiota and the airway epithelium is key to understanding how stable immune homeostasis is maintained. Loss of epithelial integrity following exposure to infection can result in the onset of inflammation in susceptible individuals and may culminate in lung disease. Here we discuss the current knowledge regarding the molecular and cellular mechanisms by which the pulmonary epithelium interacts with the lung microbiome in shaping immunity in the lung. Specifically, we focus on the interactions between the lung microbiome and the cells of the conducting airways in modulating immune cell regulation, and how defects in barrier structure and function may culminate in lung disease. Understanding these interactions is fundamental in the search for more effective therapies for respiratory diseases.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #11413
Database	COVID19

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Article: Autoantibodies are present in the bronchoalveolar lavage but not circulation in patients with fibrotic interstitial lung disease.

Boustani, Karim / Ghai, Poonam / Invernizzi, Rachele / Hewitt, Richard J / Maher, Toby M / Li, Quan-Zhen / Molyneaux, Philip L / Harker, James A

ERJ open research

2022 Volume 8, Issue 1

Abstract: Background: Fibrotic interstitial lung disease (fILD) has previously been associated with the presence of autoantibody. While studies have focused on systemic autoimmunity, the role of local autoantibodies in the airways remains unknown. We therefore ... ...

Abstract	Background: Fibrotic interstitial lung disease (fILD) has previously been associated with the presence of autoantibody. While studies have focused on systemic autoimmunity, the role of local autoantibodies in the airways remains unknown. We therefore extensively characterised the airway and peripheral autoantibody profiles in patients with fILD, and assessed association with disease severity and outcome. Methods: Bronchoalveolar lavage (BAL) fluid was collected from a cohort of fILD patients and total BAL antibody concentrations were quantified. An autoantigen microarray was used to measure IgG and IgA autoantibodies against 122 autoantigens in BAL from 40 idiopathic pulmonary fibrosis (IPF), 20 chronic hypersensitivity pneumonitis (CHP), 20 connective tissue disease-associated ILD (CTD-ILD) patients and 20 controls. Results: A subset of patients with fILD but not healthy controls had a local autoimmune signature in their BAL that was not present systemically, regardless of disease. The proportion of patients with IPF with a local autoantibody signature was comparable to that of CTD-ILD, which has a known autoimmune pathology, identifying a potentially novel subset of patients. The presence of an airway autoimmune signature was not associated with reduced survival probability or changes in lung function in the cohort as a whole. Patients with IPF had increased BAL total IgA and IgG Conclusion: Airway autoantibodies that are not present systemically identify a group of patients with fILD and the mechanisms by which these autoantibodies contribute to disease requires further investigation.
Language	English
Publishing date	2022-02-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2827830-6
ISSN	2312-0541
ISSN	2312-0541
DOI	10.1183/23120541.00481-2021
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Article ; Online: Computational prediction and experimental validation of

Demeter, Amanda / Jacomin, Anne-Claire / Gul, Lejla / Lister, Ashleigh / Lipscombe, James / Invernizzi, Rachele / Branchu, Priscilla / Macaulay, Iain / Nezis, Ioannis P / Kingsley, Robert A / Korcsmaros, Tamas / Hautefort, Isabelle

Frontiers in cellular and infection microbiology

2022 Volume 12, Page(s) 834895

Abstract: Macroautophagy is a ubiquitous homeostasis and health-promoting recycling process of eukaryotic cells, targeting misfolded proteins, damaged organelles and intracellular infectious agents. Some intracellular pathogens such ... ...

Abstract	Macroautophagy is a ubiquitous homeostasis and health-promoting recycling process of eukaryotic cells, targeting misfolded proteins, damaged organelles and intracellular infectious agents. Some intracellular pathogens such as
MeSH term(s)	Autophagy/physiology ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Epithelial Cells/metabolism ; Humans ; Salmonella Infections ; Salmonella typhimurium/genetics
Chemical Substances	Bacterial Proteins
Language	English
Publishing date	2022-08-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2022.834895
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Article ; Online: Linking microbial genes to plasma and stool metabolites uncovers host-microbial interactions underlying ulcerative colitis disease course.

Schirmer, Melanie / Stražar, Martin / Avila-Pacheco, Julian / Rojas-Tapias, Daniel F / Brown, Eric M / Temple, Emily / Deik, Amy / Bullock, Kevin / Jeanfavre, Sarah / Pierce, Kerry / Jin, Shen / Invernizzi, Rachele / Pust, Marie-Madlen / Costliow, Zach / Mack, David R / Griffiths, Anne M / Walters, Thomas / Boyle, Brendan M / Kugathasan, Subra /

Vlamakis, Hera / Hyams, Jeffrey / Denson, Lee / Clish, Clary B / Xavier, Ramnik J

Cell host & microbe

2024 Volume 32, Issue 2, Page(s) 209–226.e7

Abstract: Understanding the role of the microbiome in inflammatory diseases requires the identification of microbial effector molecules. We established an approach to link disease-associated microbes to microbial metabolites by integrating paired metagenomics, ... ...

Abstract	Understanding the role of the microbiome in inflammatory diseases requires the identification of microbial effector molecules. We established an approach to link disease-associated microbes to microbial metabolites by integrating paired metagenomics, stool and plasma metabolomics, and culturomics. We identified host-microbial interactions correlated with disease activity, inflammation, and the clinical course of ulcerative colitis (UC) in the Predicting Response to Standardized Colitis Therapy (PROTECT) pediatric inception cohort. In severe disease, metabolite changes included increased dipeptides and tauro-conjugated bile acids (BAs) and decreased amino-acid-conjugated BAs in stool, whereas in plasma polyamines (N-acetylputrescine and N1-acetylspermidine) increased. Using patient samples and Veillonella parvula as a model, we uncovered nitrate- and lactate-dependent metabolic pathways, experimentally linking V. parvula expansion to immunomodulatory tryptophan metabolite production. Additionally, V. parvula metabolizes immunosuppressive thiopurine drugs through xdhA xanthine dehydrogenase, potentially impairing the therapeutic response. Our findings demonstrate that the microbiome contributes to disease-associated metabolite changes, underscoring the importance of these interactions in disease pathology and treatment.
MeSH term(s)	Humans ; Child ; Colitis, Ulcerative/drug therapy ; Host Microbial Interactions ; Gastrointestinal Microbiome/genetics ; Disease Progression ; Genes, Microbial
Language	English
Publishing date	2024-01-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2023.12.013
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Article ; Online: Autoantibodies are present in the bronchoalveolar lavage but not circulation in patients with fibrotic interstitial lung disease

Karim Boustani / Poonam Ghai / Rachele Invernizzi / Richard J. Hewitt / Toby M. Maher / Quan-Zhen Li / Philip L. Molyneaux / James A. Harker

ERJ Open Research, Vol 8, Iss

2022 Volume 1

Abstract: Background Fibrotic interstitial lung disease (fILD) has previously been associated with the presence of autoantibody. While studies have focused on systemic autoimmunity, the role of local autoantibodies in the airways remains unknown. We therefore ... ...

Abstract	Background Fibrotic interstitial lung disease (fILD) has previously been associated with the presence of autoantibody. While studies have focused on systemic autoimmunity, the role of local autoantibodies in the airways remains unknown. We therefore extensively characterised the airway and peripheral autoantibody profiles in patients with fILD, and assessed association with disease severity and outcome. Methods Bronchoalveolar lavage (BAL) fluid was collected from a cohort of fILD patients and total BAL antibody concentrations were quantified. An autoantigen microarray was used to measure IgG and IgA autoantibodies against 122 autoantigens in BAL from 40 idiopathic pulmonary fibrosis (IPF), 20 chronic hypersensitivity pneumonitis (CHP), 20 connective tissue disease-associated ILD (CTD-ILD) patients and 20 controls. Results A subset of patients with fILD but not healthy controls had a local autoimmune signature in their BAL that was not present systemically, regardless of disease. The proportion of patients with IPF with a local autoantibody signature was comparable to that of CTD-ILD, which has a known autoimmune pathology, identifying a potentially novel subset of patients. The presence of an airway autoimmune signature was not associated with reduced survival probability or changes in lung function in the cohort as a whole. Patients with IPF had increased BAL total IgA and IgG1 while subjects with CHP had increased BAL IgA, IgG1 and IgG4. In patients with CHP, increased BAL total IgA was associated with reduced survival probability. Conclusion Airway autoantibodies that are not present systemically identify a group of patients with fILD and the mechanisms by which these autoantibodies contribute to disease requires further investigation.
Keywords	Medicine ; R
Subject code	610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	European Respiratory Society
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Computational prediction and experimental validation of Salmonella Typhimurium SopE-mediated fine-tuning of autophagy in intestinal epithelial cells

Amanda Demeter / Anne-Claire Jacomin / Lejla Gul / Ashleigh Lister / James Lipscombe / Rachele Invernizzi / Priscilla Branchu / Iain Macaulay / Ioannis P. Nezis / Robert A. Kingsley / Tamas Korcsmaros / Isabelle Hautefort

Frontiers in Cellular and Infection Microbiology, Vol

2022 Volume 12

Abstract	Macroautophagy is a ubiquitous homeostasis and health-promoting recycling process of eukaryotic cells, targeting misfolded proteins, damaged organelles and intracellular infectious agents. Some intracellular pathogens such as Salmonella enterica serovar Typhimurium hijack this process during pathogenesis. Here we investigate potential protein-protein interactions between host transcription factors and secreted effector proteins of Salmonella and their effect on host gene transcription. A systems-level analysis identified Salmonella effector proteins that had the potential to affect core autophagy gene regulation. The effect of a SPI-1 effector protein, SopE, that was predicted to interact with regulatory proteins of the autophagy process, was investigated to validate our approach. We then confirmed experimentally that SopE can directly bind to SP1, a host transcription factor, which modulates the expression of the autophagy gene MAP1LC3B. We also revealed that SopE might have a double role in the modulation of autophagy: Following initial increase of MAP1LC3B transcription triggered by Salmonella infection, subsequent decrease in MAP1LC3B transcription at 6h post-infection was SopE-dependent. SopE also played a role in modulation of the autophagy flux machinery, in particular MAP1LC3B and p62 autophagy proteins, depending on the level of autophagy already taking place. Upon typical infection of epithelial cells, the autophagic flux is increased. However, when autophagy was chemically induced prior to infection, SopE dampened the autophagic flux. The same was also observed when most of the intracellular Salmonella cells were not associated with the SCV (strain lacking sifA) regardless of the autophagy induction status before infection. We demonstrated how regulatory network analysis can be used to better characterise the impact of pathogenic effector proteins, in this case, Salmonella. This study complements previous work in which we had demonstrated that specific pathogen effectors can affect the autophagy ...
Keywords	Salmonella Typhimurium ; autophagy ; SopE ; network biology ; MAP1LC3B ; Host-microbe interactions ; Microbiology ; QR1-502
Subject code	570
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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