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Localization and expression profiles of gingival monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1)

Yu Lili; Firatli Yigit; Elmanfi Samira; Gürsoy Mervi; Özdemir Kabalak Meltem; Kasnak Gökhan; Pussinen Pirkko; Bikker Floris J.; Caglayan Feriha; Firatli Erhan; Gürsoy Ulvi Kahraman

Localization and expression profiles of gingival monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1)

Yu Lili
Firatli Yigit
Elmanfi Samira
Gürsoy Mervi
Özdemir Kabalak Meltem
Kasnak Gökhan
Pussinen Pirkko
Bikker Floris J.
Caglayan Feriha
Firatli Erhan
Gürsoy Ulvi Kahraman
Katso/Avaa
s00784-023-05010-5.pdf (1.188Mb)
Lataukset: 

Springer
doi:10.1007/s00784-023-05010-5
URI
https://doi.org/10.1007/s00784-023-05010-5
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Julkaisun pysyvä osoite on:
https://urn.fi/URN:NBN:fi-fe2023041436569
Tiivistelmä

Objectives: The purposes of this study were to localize monocyte chemoattractant protein-1-induced protein-1 (MCPIP-1) and its suppressor mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1) in gingival tissues and to profile their protein expression levels in relation to the clinical inflammation, Porphyromonas gingivalis colonization, and interleukin (IL)-8 levels.

Materials and methods: Study samples were collected from two independent study populations: (1) Gingival tissues were collected from eight periodontally healthy individuals and eight periodontitis patients to localize MCPIP-1 and MALT-1 immunohistochemically, and (2) forty-one gingival tissue samples with marginal, mild, or moderate to severe inflammation were collected from 20 periodontitis patients to determine MCPIP-1 and MALT-1 levels using immunoblots, P. gingivalis levels with qPCR, P. gingivalis gingipain activities with fluorogenic substrates, and IL-8 levels with multiplex technique.

Results: MCPIP-1 was detectable in the epithelium and in connective tissue, being especially prominent around the blood vessel walls in healthy periodontal tissues. MALT-1 was observed at all layers of gingival epithelium and especially around the accumulated inflammatory cells in connective tissue. No difference in gingival tissue MCPIP-1 and MALT-1 levels was observed in relation to the severity of gingival inflammation. MALT-1 levels were elevated (p = 0.023) with the increase in tissue P. gingivalis levels, and there was an association between MALT-1 and IL-8 levels (β = 0.054, p = 0.001).

Conclusions: Interactions of MALT-1 levels with gingival tissue P. gingivalis counts and IL-8 levels suggest that activation of MALT-1 can take part in P. gingivalis-regulated host immune responses.

Clinical relevance: Pharmacological targeting the crosstalk between immune response and MCPIP-1/MALT-1 may have benefits in periodontal treatment.

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