Background Periodontitis, an inflammatory disease of multibacterial etiology that affects the protective and supporting tissues surrounding teeth, can influence the course of respiratory diseases, such as asthma, due to epithelial alterations arising from inflammatory and immunological processes, bronchial remodeling, or by the aspiration of pathogenic colonizers found in periodontal pockets. This study evaluated the levels of periodontal pathogens Prevotella intermedia, Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans in the subgingival biofilm of individuals with and without severe asthma. Methods A case‐control study enrolling 457 individuals (220 with asthma and 237 without asthma) was conducted at the Program for Control of Asthma in Bahia (ProAR) Clinic located in Salvador, Bahia, Brazil. A structured questionnaire was used to obtain data on sociodemographic, health status, and lifestyle habits. A clinical periodontal assessment was performed, including bleeding on probing, probing depth, and clinical attachment level. Subgingival biofilm was collected at the deepest site of each sextant, and bacterial DNA was extracted. Quantitative real‐time PCR analysis was performed to detect and relatively quantify periodontopathogens in the biofilm. Results Statistically significant positive associations were found between periodontitis and severe asthma, (odds ratio [OR]adjusted]: 4.00; 95% confidence interval [CI]: 2.26 to 7.10). High levels of P. intermedia were found in association with the presence of severe asthma (ORadjusted: 2.64; 95% CI: 1.62 to 4.39; P < 0.01). Conclusions The present results suggest that periodontitis and P. intermedia are associated with severe asthma. However, the functional consequences of this dysbiosis upon asthma susceptibility and its phenotypes remain unclear.

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Porphyromonas gingivalis (Pg) is one of the main pathogens in chronic periodontitis (CP). Studies on the immunogenicity of its virulence factors may contribute to understanding the host response to infection. The present study aimed to use in silico analysis as a tool to identify epitopes from Lys-gingipain (Kgp) and neuraminidase virulence factors of the Pg ATCC 33277 strain. Protein sequences were obtained from the NCBI Protein Database and they were scanned for amino acid patterns indicative of MHC II binding using the MHC-II Binding Predictions tool from the Immune Epitope Database (IEDB). Peptides from different regions of the proteins were chemically synthesized and tested by the indirect ELISA method to verify IgG immunoreactivity in serum of subjects with CP and without periodontitis (WP). T cell epitope prediction resulted in 16 peptide sequences from Kgp and 18 peptide sequences from neuraminidase. All tested Kgp peptides exhibited IgG immunoreactivity whereas tested neuraminidase peptides presented low IgG immunoreactivity. Thus, the IgG reactivity to Kgp protein could be reaffirmed and the low IgG reactivity to Pg neuraminidase could be suggested. The novel peptide epitopes from Pg were useful to evaluate its immunoreactivity based on the IgG-mediated host response. In silico analysis was useful for preselecting epitopes for immune response studies in CP.Electronic supplementary materialThe online version of this article (10.1186/s13568-019-0757-x) contains supplementary material, which is available to authorized users.

Caseous lymphadenitis (LC) is a chronic contagious disease caused by Corynebacterium pseudotuberculosis, which mainly affects goats and sheep. Vaccination is an effective but not yet well-established method, partly due to a lack of knowledge surrounding the most effective immunoprotective components. The present study aimed to quantify and compare the in vivo expression of genes pld (phospholipase D), cpp (CP40), nanH (neuraminidase H), sodC (superoxide dismutase C) and spaC (adhesin) using qRT-PCR, with the respective expression in vitro. Caseous material of abscesses removed from five animals was cultured, with colonies suggestive of C. pseudotuberculosis identified. RNA extraction was performed on these samples, as well as on the respective pellets derived from liquid cultures brain heart infusion. After evaluating RNA integrity, complementary DNA was synthesized, followed by the relative quantification each of the genes of interest. Mean mRNA expression of the five genes found in abscesses and in cultures differed significantly, with respective values of: nanH 811.50 ± 198.27 and 359.35 ± 75.45 (p = 0.009); cpp 856.31 ± 385.11 and 154.54 ± 94.34 (p = 0.0039); plD 922.70 ± 450.73 and 212.41 ± 153.10 (p = 0.016); sodC 1,293.53 ± 564.75 and 223.63 ± 145.58 (p = 0.016); spaC 1,157.10 ± 525.13 and 214.26 ± 125.70 (p = 0,016). Expression was observed to be 6–8 times higher in abscesses than in cultures, Indicative that is a genetic expression of the in vitro bacterium exists, yet in vivo has a greater magnitude corroborating to one of these virulence factors in the pathogenesis of LC.Electronic supplementary materialThe online version of this article (10.1186/s13568-018-0598-z) contains supplementary material, which is available to authorized users.

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 RT2 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.