acid-phosphatase and Actinobacillus-Infections

This study aimed to investigate whether chronic antigen-induced arthritis (AIA) influences infection-induced periodontitis (PD) in mice and whether PD modifies the clinical course of AIA. The contribution of anti-TNF-α therapy was also evaluated.. The PD was induced in C57BL/6 mice by oral infection with Aggregatibacter actinomycetemcomitans. AIA was induced after infection. Anti-TNF-α and chlorhexidine therapies were used to investigate the role of TNF-α and oral infection on PD and AIA interaction. Maxillae, knee joints, lymph nodes and serum samples were used for histomorphometric, immunoenzymatic and/or real time-PCR analyses.. Antigen-induced arthritis exacerbated alveolar bone loss triggered by PD infection. In contrast, PD did not influence AIA in the evaluated time-points. PD exacerbation was associated with enhanced production of IFN-γ in maxillae and expression of the Th1 transcription factor tBET in submandibular lymph nodes. Increased serum levels of IL-6 and C-reactive protein were also detected. Anti-TNF-α and antiseptic therapies prevented the development and exacerbation of infectious-PD. Anti-TNF-α therapy also resulted in reduced expression of IFN-γ, TNF-α and IL-17 in maxillae.. Altogether, the current results indicate that the exacerbation of infection-induced PD by arthritis is associated with an alteration in lymphocyte polarization pattern and increased systemic immunoreactivity. This process was ameliorated by anti-TNF-α and antiseptic therapies.

Topics: Acid Phosphatase; Actinobacillus Infections; Aggregatibacter actinomycetemcomitans; Alveolar Bone Loss; Animals; Anti-Infective Agents, Local; Arthritis, Experimental; C-Reactive Protein; Chlorhexidine; Collagen Type I; Immunoglobulin G; Interferon-gamma; Interleukin-17; Interleukin-6; Isoenzymes; Lymph Nodes; Male; Maxilla; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Osteoclasts; Periodontitis; T-Box Domain Proteins; Tartrate-Resistant Acid Phosphatase; Tumor Necrosis Factor-alpha

The polymorphic mononuclear cells, arranged in whorling or palisading pattern, were usually found in the lung of Actinobacillus pleuropneumoniae-infected pigs. In order to understand the origin and characteristics of these cells, specific-pathogen free pigs were intratracheally inoculated with Actinobacillus pleuropneumoniae at a concentration of 5 x 10(6) CFU, then, sacrificed at 6, 12, 24 and 48 hours later. The cells in the alveolar spaces were observed with light and electron microscope, and cytochemically analyzed for acid phosphatase, alkaline phosphatase, alpha-naphthyl acetate esterase, and Sudan black B stains respectively. The results revealed that a lot of neutrophils were observed in the alveolar spaces at the early stage after inoculation. Twenty four hours later, polymorphic mononuclear cells abundantly appeared. Enzyme cytochemical findings indicated that some of the polymorphic mononuclear cells were macrophages, in which, acid phosphatase and alpha-naphthyl acetate esterase were detected, and others were type II pneumocytes which were positively stained with alkaline phosphatase and Sudan black B. Ultrastructural observation found that many lysosomes appeared in the macrophages' cytoplasm, and type II pneumocyte contained many lamellar bodies. Conclusively, it could be suggested that the polymorphic mononuclear cells were derived from macrophages and type II pneumocytes by cytochemical and electron microscopic examinations.

Topics: Acid Phosphatase; Actinobacillus Infections; Actinobacillus pleuropneumoniae; Alkaline Phosphatase; Animals; Azo Compounds; Coloring Agents; Leukocytes, Mononuclear; Macrophages; Male; Naphthalenes; Naphthol AS D Esterase; Swine; Swine Diseases