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.

牙龈卟啉单胞菌 （牙龈卟啉单胞菌）是牙周炎最重要的病原体之一，与牙周炎和全身性疾病的恶化和复发密切相关。抗菌肽LL-37，从cathelicidin抗菌肽（营）基因，具有广泛的抗菌活性，并调节免疫系统。在这项研究中，我们证明了LL-37减少了活体数量牙龈卟啉单胞菌（ATCC 33277）通过抗生素保护试验以剂量依赖的方式在HaCaT细胞中表达。LL-37促进内吞HaCaT细胞的自噬牙龈卟啉单胞菌。3-甲基腺嘌呤（3-MA）抑制自噬减弱了LL-37对细胞内数目的抑制作用牙龈卟啉单胞菌。直系同源群体（COG）和基因本体论（GO）功能分析用于分别将65个（10％）差异表达基因（DEG）分配给“细胞内运输，分泌和囊泡运输”集群和306（47.08 ％）参与包括自噬在内的代谢过程。自噬相关基因，包含三方基序的22（修剪22）和溶酶体相关膜蛋白3（灯3被鉴定为可能参与LL-37诱导的自噬。最后，利用生物信息学软件来构建和预测CAMP-TRIM22 / LAMP3-自噬的蛋白质-蛋白质相互作用（PPI）网络。研究结果表明LL-37可以减少活体数量牙龈卟啉单胞菌通过促进HaCaT细胞自噬而使其内在化。转录组测序和分析还揭示了LL-37诱导的自噬的潜在分子途径。