Chlamydia pneumoniae-immunoglobulin E antibody responses in serum from children with asthma.
Chlamydia pneumoniae
asthma
immunoglobulin E
interferon-gamma
Journal
Pathogens and disease
ISSN: 2049-632X
Titre abrégé: Pathog Dis
Pays: United States
ID NLM: 101595366
Informations de publication
Date de publication:
17 01 2023
17 01 2023
Historique:
received:
16
05
2023
revised:
19
06
2023
accepted:
03
07
2023
medline:
21
7
2023
pubmed:
5
7
2023
entrez:
5
7
2023
Statut:
ppublish
Résumé
Chlamydia pneumoniae is an obligate intracellular bacterium that causes respiratory infections in humans. An association between persistent C. pneumoniae infection and asthma pathogenesis has been described. It is unknown whether specific immunoglobulin E (IgE) is a marker of persistent immune activation responses. Therefore, the association between C. pneumoniae-specific-IgE antibodies (Abs) and interferon (IFN)-gamma produced by C. pneumoniae-stimulated peripheral blood mononuclear cells (PBMC) was examined. Blood was collected and serum separated. PBMC from 63 children with or without stable asthma (N = 45 and 18, respectively) were infected or not infected with C. pneumoniae AR-39 and cultured for up to 7 days. Supernatants were collected, and IFN-gamma levels measured (ELISA). Serum C. pneumoniae-IgE Abs were detected by immunoblotting. C. pneumoniae-IgE Abs were detected in asthmatics (27%), compared with non-asthmatics (11%) (P = NS). IFN-gamma responses were more prevalent among asthmatics who had positive C. pneumoniae-IgE Abs (60%) compared with asthmatics without C. pneumoniae-IgE Abs (20%) (P = 0.1432). IFN-gamma responses in C. pneumoniae-stimulated PBMC from children with asthma were more frequent in children who had specific anti-C. pneumoniae-IgE Abs compared to those who did not. This immune response may reflect persistent infection, which may contribute to ongoing asthma symptoms.
Identifiants
pubmed: 37403376
pii: 7219311
doi: 10.1093/femspd/ftad015
pii:
doi:
Substances chimiques
Immunoglobulin E
37341-29-0
Antibodies, Bacterial
0
Antibodies, Protozoan
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of FEMS.