Research Article Apoptosis Transcriptional Profile Induced by Porphyromonas gingivalis HmuY Paulo C. Carvalho-Filho , 1,2 Lilia F. Moura-Costa, 1 Ana C. M. Pimentel, 1 Mabel P. P. Lopes, 1 Sibelle A. Freitas, 2 Patrícia M. Miranda, 1 Ryan S. Costa, 1 Camila A. V. Figueirêdo, 1 Roberto Meyer, 1 Isaac S. Gomes-Filho, 3 Teresa Olczak , 4 Márcia T. Xavier , 2 and Soraya C. Trindade 1,3 1 Department of Immunology, Federal University of Bahia, Bahia, Brazil 2 Dental School, Bahiana School of Medicine and Public Health, Brazil 3 Department of Periodontics, Feira de Santana State University, Bahia, Brazil 4 Laboratory of Medical Biology, Faculty of Biotechnology, University of Wroclaw, Wroclaw, Poland Correspondence should be addressed to Paulo C. Carvalho-Filho; pauloccf@yahoo.com Received 4 October 2018; Revised 27 December 2018; Accepted 23 January 2019; Published 18 March 2019 Guest Editor: Denisse Bravo Copyright © 2019 Paulo C. Carvalho-Filho et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This study aimed at evaluating the transcriptional profile of apoptosis-related genes after in vitro stimulation of peripheral blood mononuclear cells (PBMCs) derived from individuals with periodontitis (P) and healthy nonperiodontitis (NP) control subjects with P. gingivalis HmuY protein. PBMCs from the P and NP groups were stimulated with HmuY P. gingivalis protein, and the expression of genes related to apoptosis was assessed by custom real-time polymerase chain reaction array (Custom RT 2 PCR Array). Compared with the NP group, the P group showed low relative levels of apoptosis-related gene expression, downregulated for FAS, FAS ligand, TNFSF10 (TRAIL), BAK1, CASP9, and APAF1 after P. gingivalis HmuY protein stimulation. Furthermore, the P group exhibited low levels of relative gene expression, downregulated for CASP7 when the cells were not stimulated. Our data suggest that P. gingivalis HmuY protein might participate differently in the modulation of the intrinsic and extrinsic apoptosis pathways. 1. Introduction Periodontitis is a multifactorial disease, with significant par- ticipation of the host, environmental factors, and bacterial components. It is known that keystone pathogens, such as Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, in the subgingival biofilm elicit a host inflammatory response, which can lead to periodontal breakdown. [1]. The microbial diversity of the oral cavity is immense, and the host response during periodontitis is complex, with components of the innate and adaptive immune system that lead to chronic inflammation and bone resorption [2]. Recent metagenomic and mechanistic studies are con- sistent with a new periodontal pathogenesis model that proposes that periodontal diseases are caused by a synergis- tic and dysbiotic microbial community, not by a selected group of bacteria known as “periodontopathogens”. Bacte- ria found in low abundance in the microbiota have an effect throughout the community and are critical components for the development of dysbiosis. They are known as “key- stone” pathogens [3]. However, an increased abundance in these known pathogens is observed, related to the pres- ence as well as the severity of the disease, indicating a microbial variation in the dysbiotic process [4]. Virulence factors of P. gingivalis, the main keystone pathogen in periodontitis, can determine a great immuno- genicity to stimulate innate and adaptive immune host responses. Among them are capsule components, lipopoly- saccharide (LPS), fimbriae, and outer membrane proteins, Hindawi Mediators of Inflammation Volume 2019, Article ID 6758159, 8 pages https://doi.org/10.1155/2019/6758159