T cell proliferative responses to molecular fractions of periodontopathic bacteria

Abstract

SUMMARYSoluble antigenic preparations of Veillonella parvula and Bacteroides gingivalis were separated by SDS-PAGE and used after electroblotting and solubilization for in vitro lymphocyte stimulation in 13 patients with severe periodontitis and 12 controls. The cellular responses of controls and patients to V. parvula antigens were represented by four main proliferation-inducing fractions with 74-66, 52-46, 22-19 and 12 kD mol, wt. These fractions induced slightly enhanced DNA synthesis in lymphocytes from eight patients who failed to respond to whole antigenic extract. Lymphocyte samples from Veillonella whole extract unresponsive patients were also examined for in vitro proliferation by B. gingivalis fractions. Almost all stimulatory activities could be classified into five regions of 84-74, 35-31, 28-25, 17-15 and 12 kD,

Decreased Interleukin‐2 Responses to Fusobacterium nucleatum and Porphyromonas gingivalis in Generalized Aggressive Periodontitis

“…The literature 4–14 contains numerous contradictions with respect to T‐cell responses of patients with periodontitis. These contradictions may be due to differences in selected patient groups and the use of a great variety of experimental models and methods.…”

“…However, the results of subsequent studies have been contradictory. Some investigators 5–10 confirmed an association between AgP and a compromised proliferative activity of mononuclear cells (MNCs), whereas other investigators 11–14 found no such connection.…”

Oral Bacterial and Fungal Microbiome Impacts Colorectal Carcinogenesis

“…In germ-free mice and rats, it was demonstrated that periodontal disease and caries, similarly to other human inflammatory diseases, cannot be experimentally induced in the absence of microbiota ( Heijl et al, 1980 ; Tlaskalova-Hogenova et al, 2004 ). Experimental animal models (e.g., the gavage model of periodontal disease) and in vitro studies revealed that certain components of oral microbiota, mainly P. gingivalis , play a crucial role in the innate host defense of periodontium and that dysregulation of the immune response in the presence of oral microbiota leads to inflammation and alveolar bone loss ( Ivanyi et al, 1991 ; Darveau et al, 2012 ; Papadopoulos et al, 2013 ). The mechanisms by which microbiota triggers the pathological changes are not yet fully understood, however, new approaches promise to shed light on the role of oral microbiota ( Kinane et al, 2017 ; Pitts et al, 2017 ).…”