Aggregatibacter actinomycetemcomitans Outer Membrane Proteins 29 and 29 Paralogue Induce Evasion of Immune Response
( ) is abundant within the microbial dysbiotic community of some patients with periodontitis. outer membrane protein 29 (OMP29), a member of the OMPA family, mediates the invasion of to gingival epithelial cells (GECs). This study evaluated the effect of OMP29 and its paralogue OMP29 on the response...
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Published in | Frontiers in oral health Vol. 3; p. 835902 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
03.02.2022
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Subjects | |
Online Access | Get full text |
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Summary: | (
) is abundant within the microbial dysbiotic community of some patients with periodontitis.
outer membrane protein 29 (OMP29), a member of the OMPA family, mediates the invasion of
to gingival epithelial cells (GECs). This study evaluated the effect of OMP29 and its paralogue OMP29
on the response of GECs to
. The
or/and
deletion mutants AaΔ29, AaΔ29P, and AaΔ29Δ29P were constructed, and recombinant
OMP29
was obtained. Microarray analysis and the evaluation of
gene expression were performed to examine the response of GECs line OBA-09 to
and its mutants. The expression of
and its product CXCL-8 was examined in LPS-stimulated OBA-09 cells with
OMP29
. Proteomics analysis showed that the deletion of
led to overexpression of both OMP29
and another membrane protein OMP39, the expression of which was further increased in AaΔ29Δ29P. OBA-09 cells challenged with AaΔ29Δ29P exhibited a higher expression of
in comparison to wildtype
strain AaD7S or single-deletion mutants AaΔ29 or AaΔ29P. LPS-stimulated OBA-09 cells challenged with
OMP29
showed reduced expressions of
and its product CXCL-8. OBA-09 cells challenged with AaΔ29Δ29P in comparison to
strain AaD7S resulted in higher expressions of genes involved in apoptosis and inflammatory response such as
α
β
, and
β and reduced expressions of
, and
. The results suggested a novel strategy of
, mediated by OMP29 and OMP29
, to evade host immune response by inhibiting CXCL-8 expression and modulating the genes involved in apoptosis and inflammatory response in GECs. Pending further confirmation, the strategy might interfere with the recruitment of neutrophils and dampen the host inflammatory response, leading to a more permissive subgingival niche for bacterial growth. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This article was submitted to Oral Infections and Microbes, a section of the journal Frontiers in Oral Health Edited by: Georgios N. Belibasakis, Karolinska Institutet (KI), Sweden Reviewed by: Anders Johansson, Umeå University, Sweden; Ashu Sharma, University at Buffalo, United States |
ISSN: | 2673-4842 2673-4842 |
DOI: | 10.3389/froh.2022.835902 |