Haemophilus influenzae and Moraxella catarrhalis in sputum of severe asthma with inflammasome and neutrophil activation.


Journal

Allergy
ISSN: 1398-9995
Titre abrégé: Allergy
Pays: Denmark
ID NLM: 7804028

Informations de publication

Date de publication:
11 2023
Historique:
revised: 19 04 2023
received: 28 12 2022
accepted: 24 04 2023
medline: 13 11 2023
pubmed: 8 6 2023
entrez: 8 6 2023
Statut: ppublish

Résumé

Because of altered airway microbiome in asthma, we analysed the bacterial species in sputum of patients with severe asthma. Whole genome sequencing was performed on induced sputum from non-smoking (SAn) and current or ex-smoker (SAs/ex) severe asthma patients, mild/moderate asthma (MMA) and healthy controls (HC). Data were analysed by asthma severity, inflammatory status and transcriptome-associated clusters (TACs). α-diversity at the species level was lower in SAn and SAs/ex, with an increase in Haemophilus influenzae and Moraxella catarrhalis, and Haemophilus influenzae and Tropheryma whipplei, respectively, compared to HC. In neutrophilic asthma, there was greater abundance of Haemophilus influenzae and Moraxella catarrhalis and in eosinophilic asthma, Tropheryma whipplei was increased. There was a reduction in α-diversity in TAC1 and TAC2 that expressed high levels of Haemophilus influenzae and Tropheryma whipplei, and Haemophilus influenzae and Moraxella catarrhalis, respectively, compared to HC. Sputum neutrophils correlated positively with Moraxella catarrhalis and negatively with Prevotella, Neisseria and Veillonella species and Haemophilus parainfluenzae. Sputum eosinophils correlated positively with Tropheryma whipplei which correlated with pack-years of smoking. α- and β-diversities were stable at one year. Haemophilus influenzae and Moraxella catarrhalis were more abundant in severe neutrophilic asthma and TAC2 linked to inflammasome and neutrophil activation, while Haemophilus influenzae and Tropheryma whipplei were highest in SAs/ex and in TAC1 associated with highest expression of IL-13 type 2 and ILC2 signatures with the abundance of Tropheryma whipplei correlating positively with sputum eosinophils. Whether these bacterial species drive the inflammatory response in asthma needs evaluation.

Sections du résumé

BACKGROUND
Because of altered airway microbiome in asthma, we analysed the bacterial species in sputum of patients with severe asthma.
METHODS
Whole genome sequencing was performed on induced sputum from non-smoking (SAn) and current or ex-smoker (SAs/ex) severe asthma patients, mild/moderate asthma (MMA) and healthy controls (HC). Data were analysed by asthma severity, inflammatory status and transcriptome-associated clusters (TACs).
RESULTS
α-diversity at the species level was lower in SAn and SAs/ex, with an increase in Haemophilus influenzae and Moraxella catarrhalis, and Haemophilus influenzae and Tropheryma whipplei, respectively, compared to HC. In neutrophilic asthma, there was greater abundance of Haemophilus influenzae and Moraxella catarrhalis and in eosinophilic asthma, Tropheryma whipplei was increased. There was a reduction in α-diversity in TAC1 and TAC2 that expressed high levels of Haemophilus influenzae and Tropheryma whipplei, and Haemophilus influenzae and Moraxella catarrhalis, respectively, compared to HC. Sputum neutrophils correlated positively with Moraxella catarrhalis and negatively with Prevotella, Neisseria and Veillonella species and Haemophilus parainfluenzae. Sputum eosinophils correlated positively with Tropheryma whipplei which correlated with pack-years of smoking. α- and β-diversities were stable at one year.
CONCLUSIONS
Haemophilus influenzae and Moraxella catarrhalis were more abundant in severe neutrophilic asthma and TAC2 linked to inflammasome and neutrophil activation, while Haemophilus influenzae and Tropheryma whipplei were highest in SAs/ex and in TAC1 associated with highest expression of IL-13 type 2 and ILC2 signatures with the abundance of Tropheryma whipplei correlating positively with sputum eosinophils. Whether these bacterial species drive the inflammatory response in asthma needs evaluation.

Identifiants

pubmed: 37287344
doi: 10.1111/all.15776
doi:

Substances chimiques

Inflammasomes 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2906-2920

Subventions

Organisme : Innovative Medicines Initiative
ID : 115010

Investigateurs

L I Andersson (LI)
C Auffray (C)
Y E Badi (YE)
P Bakke (P)
A T Bansal (AT)
E H Bel (EH)
J Bigler (J)
B Billing (B)
H Bisgaard (H)
M J Boedigheimer (MJ)
K Bønnelykke (K)
J Brandsma (J)
P Brinkman (P)
E Bucchioni (E)
D Burg (D)
A Bush (A)
M Caruso (M)
R Chalekis (R)
P Chanez (P)
T Checa (T)
C H Compton (CH)
J Corfield (J)
D Cunoosamy (D)
B Dahlén (B)
S E Dahlén (SE)
B De Meulder (B)
V J Erpenbeck (VJ)
D Erzen (D)
K Fichtner (K)
L J Fleming (LJ)
E Formaggio (E)
S J Fowler (SJ)
U Frey (U)
M Gahlemann (M)
T Geiser (T)
V Goss (V)
Y Guo (Y)
S Hashimoto (S)
J Haughney (J)
G Hedlin (G)
P W Hekking (PW)
T Higenbottam (T)
J M Hohlfeld (JM)
C Holweg (C)
I Horváth (I)
A J James (AJ)
R G Knowles (RG)
J Kolmert (J)
J Konradsen (J)
N Krug (N)
N Lazarinis (N)
C-X Li (CX)
M J Loza (MJ)
R Lutter (R)
A Manta (A)
S Masefield (S)
J G Matthews (JG)
A Mazein (A)
Rjm Middelveld (R)
M Miralpeix (M)
C S Murray (CS)
J Musial (J)
S Mumby (S)
D Myles (D)
B Nordlund (B)
I Pandis (I)
S Pavlidis (S)
A Postle (A)
P Powel (P)
G Praticò (G)
M Puig Valls (M)
N Rao (N)
S Reinke (S)
A Roberts (A)
G Roberts (G)
A Rowe (A)
T Sandström (T)
Jpr Schofield (J)
W Seibold (W)
D E Shaw (DE)
R Sigmund (R)
F Singer (F)
P J Skipp (PJ)
M Smicker (M)
A R Sousa (AR)
M Sparreman-Mikus (M)
M Ström (M)
K Sun (K)
B Thornton (B)
M Uddin (M)
J Vestbo (J)
N H Vissing (NH)
S S Wagers (SS)
A Wheelock (A)
C E Wheelock (CE)
S J Wilson (SJ)
V Yasinska (V)

Informations de copyright

© 2023 The Authors. Allergy published by European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.

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Auteurs

Ali Versi (A)

National Heart & Lung Institute & Data Science Institute, Imperial College London, London, UK.

Fransiskus Xaverius Ivan (FX)

Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore City, Singapore.

Mahmoud I Abdel-Aziz (MI)

Department of Pulmonary Medicine, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.

Stewart Bates (S)

Respiratory Therapeutic Unit, GSK, Brentford, UK.

John Riley (J)

Respiratory Therapeutic Unit, GSK, Brentford, UK.

Frederic Baribaud (F)

Janssen Research and Development, High Wycombe, UK.

Nazanin Zounemat Kermani (NZ)

National Heart & Lung Institute & Data Science Institute, Imperial College London, London, UK.

Paolo Montuschi (P)

Department of Pharmacology, Catholic University of the Sacred Heart, Rome, Italy.

Sven-Erik Dahlen (SE)

Centre for Allergy Research, Karolinska Institute, Stockholm, Sweden.

Ratko Djukanovic (R)

Faculty of Medicine, Southampton University, Southampton, UK.
NIHR Southampton Respiratory Biomedical Research Unit, University Hospital Southampton, Southampton, UK.

Peter Sterk (P)

Department of Pulmonary Medicine, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.

Anke H Maitland-Van Der Zee (AH)

Department of Pulmonary Medicine, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands.

Sanjay H Chotirmall (SH)

Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore City, Singapore.
Department of Respiratory and Critical Care Medicine, Tan Tock Seng Hospital, Singapore City, Singapore.

Peter Howarth (P)

Faculty of Medicine, Southampton University, Southampton, UK.

Ian M Adcock (IM)

National Heart & Lung Institute & Data Science Institute, Imperial College London, London, UK.

Kian Fan Chung (KF)

National Heart & Lung Institute & Data Science Institute, Imperial College London, London, UK.

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