Toll-like receptors 2 and 4, and bacterial proteins in IgG4-related sialadenitis, other types of chronic sialadenitis and sialolithiasis.

Immunoglobulin G4 Porphyromonas gingivalis head and neck lipopolysaccharide salivary gland submandibular gland

Journal

Journal of oral microbiology
ISSN: 2000-2297
Titre abrégé: J Oral Microbiol
Pays: United States
ID NLM: 101551049

Informations de publication

Date de publication:
2024
Historique:
medline: 26 7 2024
pubmed: 26 7 2024
entrez: 26 7 2024
Statut: epublish

Résumé

The association of chronic sclerosing sialadenitis and IgG4-related disease (IgG4-RD) has resulted in the more frequent identification of IgG4-positivity in submandibular gland inflammations, also uncovering IgG4 overexpression in nonspecific inflammations. These findings lead us to hypothesise that IgG4-positive sialadenitis represents a continuous inflammatory process overlapping histologically with IgG4-RD, possibly differing in aetiology. However, the antigen underlying IgG4 overexpression in IgG4-positive sialadenitis and IgG4-RD remains unknown. Here, we investigated toll-like receptor (TLR) - mediated bacterial inflammation in submandibular gland tissues of patients with IgG4-positive and IgG4-negative chronic inflammatory lesions of the submandibular gland ( We observed TLR2- and TLR4-immunopositivity in 64 (98%) samples. However, TLR2 and TLR4 staining intensity was significantly stronger in the IgG4-positive group. LPS- and gingipain R1 immunopositivity were observed in 56 (86%) and 58 (89%) samples, respectively. LPS-positivity localised exclusively in mast cell-like cells, while gingipain R1-positivity remained scarce. A stronger TLR2 or TLR4 expression in IgG4-positive sialadenitis may indicate a tissue-related factor underlying this form of chronic sialadenitis. LPS- and

Sections du résumé

Background UNASSIGNED
The association of chronic sclerosing sialadenitis and IgG4-related disease (IgG4-RD) has resulted in the more frequent identification of IgG4-positivity in submandibular gland inflammations, also uncovering IgG4 overexpression in nonspecific inflammations. These findings lead us to hypothesise that IgG4-positive sialadenitis represents a continuous inflammatory process overlapping histologically with IgG4-RD, possibly differing in aetiology. However, the antigen underlying IgG4 overexpression in IgG4-positive sialadenitis and IgG4-RD remains unknown.
Materials and methods UNASSIGNED
Here, we investigated toll-like receptor (TLR) - mediated bacterial inflammation in submandibular gland tissues of patients with IgG4-positive and IgG4-negative chronic inflammatory lesions of the submandibular gland (
Results UNASSIGNED
We observed TLR2- and TLR4-immunopositivity in 64 (98%) samples. However, TLR2 and TLR4 staining intensity was significantly stronger in the IgG4-positive group. LPS- and gingipain R1 immunopositivity were observed in 56 (86%) and 58 (89%) samples, respectively. LPS-positivity localised exclusively in mast cell-like cells, while gingipain R1-positivity remained scarce.
Conclusions UNASSIGNED
A stronger TLR2 or TLR4 expression in IgG4-positive sialadenitis may indicate a tissue-related factor underlying this form of chronic sialadenitis. LPS- and

Identifiants

pubmed: 39055281
doi: 10.1080/20002297.2024.2382633
pii: 2382633
pmc: PMC11271128
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2382633

Informations de copyright

© 2024 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

Déclaration de conflit d'intérêts

No potential conflict of interest was reported by the author(s).

Auteurs

Elin Waltimo (E)

Department of Oral and Maxillofacial Diseases, University of Helsinki, Helsinki, Finland.

Mine Eray (M)

Department of Pathology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.

Antti Mäkitie (A)

Department of Otorhinolaryngology - Head and Neck Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Research Program in Systems Oncology, Faculty of Medicine, Helsinki, Helsinki, Finland.

Caj Haglund (C)

Research Programmes Unit, Translational Cancer Medicine, University of Helsinki, Helsinki, Finland.
Department of Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.

Timo Atula (T)

Department of Otorhinolaryngology - Head and Neck Surgery, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.

Jaana Hagström (J)

Department of Oral and Maxillofacial Diseases, University of Helsinki, Helsinki, Finland.
Department of Pathology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Research Programmes Unit, Translational Cancer Medicine, University of Helsinki, Helsinki, Finland.
Department of Oral Pathology and Radiology, University of Turku, Turku, Finland.

Classifications MeSH