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LL-37-Induced Autophagy Contributed to the Elimination of Live Porphyromonas gingivalis Internalized in Keratinocytes.
Yang, Xue; Niu, Li; Pan, Yaping; Feng, Xianghui; Liu, Jie; Guo, Yan; Pan, Chunling; Geng, Fengxue; Tang, Xiaolin.
Afiliación
  • Yang X; Department of Periodontology, School and Hospital of Stomatology, China Medical University, Shenyang, China.
  • Niu L; Liaoning Provincial Key Laboratory of Oral Diseases, School of Stomatology, China Medical University, Shenyang, China.
  • Pan Y; Department of Periodontology, School and Hospital of Stomatology, China Medical University, Shenyang, China.
  • Feng X; Liaoning Provincial Key Laboratory of Oral Diseases, School of Stomatology, China Medical University, Shenyang, China.
  • Liu J; Department of Periodontology, School and Hospital of Stomatology, China Medical University, Shenyang, China.
  • Guo Y; Liaoning Provincial Key Laboratory of Oral Diseases, School of Stomatology, China Medical University, Shenyang, China.
  • Pan C; Department of Periodontology, Peking University School and Hospital of Stomatology, Beijing, China.
  • Geng F; Center of Science Experiment, China Medical University, Shenyang, China.
  • Tang X; Liaoning Provincial Key Laboratory of Oral Diseases, School of Stomatology, China Medical University, Shenyang, China.
Front Cell Infect Microbiol ; 10: 561761, 2020.
Article en En | MEDLINE | ID: mdl-33178622
Porphyromonas gingivalis (P. gingivalis), one of the most important pathogens of periodontitis, is closely associated with the aggravation and recurrence of periodontitis and systemic diseases. Antibacterial peptide LL-37, transcribed from the cathelicidin antimicrobial peptide (CAMP) gene, exhibits a broad spectrum of antibacterial activity and regulates the immune system. In this study, we demonstrated that LL-37 reduced the number of live P. gingivalis (ATCC 33277) in HaCaT cells in a dose-dependent manner via an antibiotic-protection assay. LL-37 promoted autophagy of HaCaT cells internalized with P. gingivalis. Inhibition of autophagy with 3-methyladenine (3-MA) weakened the inhibitory effect of LL-37 on the number of intracellular P. gingivalis. A cluster of orthologous groups (COGs) and a gene ontology (GO) functional analysis were used to individually assign 65 (10%) differentially expressed genes (DEGs) to an "Intracellular trafficking, secretion, and vesicular transport" cluster and 306 (47.08%) DEGs to metabolic processes including autophagy. Autophagy-related genes, a tripartite motif-containing 22 (TRIM22), and lysosomal-associated membrane protein 3 (LAMP3) were identified as potentially involved in LL-37-induced autophagy. Finally, bioinformatics software was utilized to construct and predict the protein-protein interaction (PPI) network of CAMP-TRIM22/LAMP3-Autophagy. The findings indicated that LL-37 can reduce the quantity of live P. gingivalis internalized in HaCaT cells by promoting autophagy in these cells. The transcriptome sequencing and analysis also revealed the potential molecular pathway of LL-37-induced autophagy.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Periodontitis / Porphyromonas gingivalis Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Front Cell Infect Microbiol Año: 2020 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Periodontitis / Porphyromonas gingivalis Tipo de estudio: Prognostic_studies Límite: Humans Idioma: En Revista: Front Cell Infect Microbiol Año: 2020 Tipo del documento: Article País de afiliación: China Pais de publicación: Suiza