Both epidemiologic and experimental findings suggest that infection with Porphyromonas gingivalis exacerbates progression of atherosclerosis. As P. gingivalis exhibits significant strain variation, it is reasonable that different strains possess different capabilities and/or mechanisms by which they promote atherosclerosis. Using P. gingivalis strains that have been previously evaluated in the ApoE null atherosclerosis model, we assessed the ability of W83, A7436, 381, and 33277 to adhere, invade, and persist in human coronary artery endothelial (HCAE) cells. W83 and 381 displayed an equivalent ability to adhere to HCAE cells, which was significantly greater than both A7436 and 33277 (P<0.01). W83, 381, and 33277 were more invasive than A7436 (P<0.0001). However, only W83 and A7436 were able to remain viable up to 48 hours in HCAE cell cultures, whereas 381 was cleared by 48 hours and 33277 was cleared by 24 hours. These differences in persistence were in part due to strain specific differences in intracellular trafficking. Both W83 and 381 trafficked through the autophagic pathway, but not A7436 or 33277. Internalized 381 was the only strain that was dependent upon the autophagic pathway for its survival. Finally, we assessed the efficacy of these strains to activate HCAE cells as defined by production of IL-6, IL-8, IL-12p40, MCP-1, RANTES, TNF-α, and soluble adhesion molecules (sICAM-1, sVCAM-1, and sE-selectin). Only moderate inflammation was observed in cells infected with either W83 or A7436, whereas cells infected with 381 exhibited the most profound inflammation, followed by cells infected with 33277. These results demonstrate that virulence mechanisms among different P. gingivalis strains are varied and that pathogenic mechanisms identified for one strain are not necessarily applicable to other strains.
Introduction-Dissemination of oral bacteria into the bloodstream has been associated with eating, oral hygiene, and dental procedures; including tooth extraction, endodontic treatment, and periodontal surgery. Recently, studies identified Streptococcus mutans, the primary etiological agent of dental caries, as the most prevalent bacterial species found in clinical samples from patients who underwent heart valve and atheromatous plaque surgery.
The effect of organic acids as an alternative to antibiotics on the performance of broiler chickens was evaluated by meta-analysis, identifying and quantifying the main factors that influence results. A total of 51,960 broilers from 121 articles published between 1991 and 2016 were used. Interactions of additives [non-supplemented group (control), organic acids, and growth promoter antibiotics] with microbial challenge (with or without inoculation of pathogenic microorganisms) were studied on performance variables. Moreover, the effects of organic acids, used individually or in blends, were evaluated. Relative values of average daily gain (ADG) and average daily feed intake (ADFI) were obtained in relation to control: ΔADG and ΔADFI, respectively. Analysis of variance-covariance revealed lower ADG with organic acids when compared to antibiotics (P < 0.05). There was a significant interaction between the additives and the challenge on feed conversion ratio (FCR) (P < 0.01) and on viability (P < 0.05). Without challenge, organic acids improved broilers’ FCR (P < 0.01), presenting results similar to antibiotics (P > 0.05). Under challenge, the organic acids were again effective on FCR (−5.67% in relation to control, P < 0.05), but they did not match antibiotics (−13.40% in relation to control, P < 0.01). Viability was improved only under challenge conditions, and only by antibiotics (+4.39% in relation to control, P < 0.05). ADG (P < 0.05) and FCR (P < 0.01) were increased by blends of organic acids, but not by the organic acids used alone (P > 0.05). ADFI and production factor were not influenced by the treatments (P > 0.05). ΔADFI of organic-acid supplemented group showed a linear influence on ΔADG, which increases 0.64% at every 1% increase in ΔADFI. In conclusion, organic acids can be utilized as performance enhancing, but the results are lower than those found with antibiotics, particularly under microbial challenge. The blends of organic acids provide better results than the utilization of one organic acid alone.
Aggressive interactions, and their consequences, are the most important causes of poor welfare in piglets. Aggressive behaviour can be modulated by the prenatal and neonatal environment in several species. Commercially kept pregnant sows are often subjected to food restriction, which can compromise their welfare. Limited information is available on the consequences of sow hunger during pregnancy on welfare outcomes for their piglets. High fibre diets can mitigate the feeling of hunger and, consequently, it may improve welfare and productivity measures. The aim of this study was to assess the consequences of feeding pregnant gilts with high fibre diets (HFD) on agonistic behaviour, as manifested by skin lesions, and indicators of fear in their piglets at weaning. Twenty-two pregnant gilts were fed either HFD, 12.86% of crude fibre, 2.4 kg per day (N = 14), or low fibre diet (LFD), 2.53% of crude fibre, 2.0 kg per day (N = 8). During lactation, both treatments received the same diet, ad libitum. We investigated the impact of HFD on behaviour and performance measures (birth weight, average daily gain, weaning weight, see S3 File) in the offspring. Skin lesions were evaluated before and after weaning in 156 piglets (100 HFD and 56 LFD), and 142 piglets were subjected to an open field test and a novel object test (87 HFD and 55 LFD). We found no treatment effect on the performance measures. Piglets born from gilts that received HFD had fewer skin lesions before weaning (D28) than the offspring of LFD gilts, while no difference was found during days 29 and 30. In the open field and novel object tests, there was no treatment effect on the behaviour of piglets. The improved skin health at weaning in piglets of sows fed HFD suggests less agonistic interactions amongst these littermates than in piglets of sows fed LFD.
HtrA is a heat-stress protein that functions both as a chaperone and as a serine protease. HtrA has been shown in several organisms to be involved in responses to stressful environmental conditions and involvement of HtrA in virulence has been reported in pathogenic species. A Porphyromonas gingivalis htrA mutant demonstrated no significant difference to the W83 parent strain when subjected to high temperature and pH values from 3 to 11. However, the htrA mutant showed increased sensitivity to H 2 O 2 . Cell invasion assays indicated that the total interaction (adherence) with KB cells, human coronary artery endothelial cells and gingival epithelial cells (GEC) was the same for both the wild-type and the htrA mutant. However, the htrA mutant showed increased invasion in KB cells and GEC. Microarray experiments indicated that a total of 253 genes were differentially regulated in the htrA mutant, including a group of stress-related genes, which might be responsible for the observed decreased resistance to H 2 O 2 . In animal experiments, a competition assay showed that the htrA mutant did not survive as well as the wild-type. In another in vivo assay, fewer mice infected with the htrA mutant died than mice infected with W83, suggesting that the htrA gene is virulence-related. These data indicate that the htrA gene in P. gingivalis does not relate to stress conditions such as high temperature and pH, but rather to H 2 O 2 stress. The htrA gene also appears to be important for virulence and survival in in vivo animal models.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.