Background and Objective:Local persistent infection by Porphyromonas gingivalis leads to inflammatory systemic diseases, such as atherosclerosis. We have reported previously that avirulent P. gingivalis fimbriae-dependent invasion into endothelial cells might be involved in progression of atherosclerosis. Although interleukin-6 (IL-6) regulates progression of atherosclerosis, little is known about the relationship of P. gingivalis fimbriae-dependent invasion to IL-6 regulation in endothelial cells.Material and Methods:We examined the secretion of IL-6 and the expression of the IL-6 signal transducer gp130 in human umbilical vein endothelial cells (HUVEC) infected with the wild-type FDC381 strain of P. gingivalisand a fimbriae-deficient mutant (fimA) by enzyme-linked immunosorbent assay, quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry (fluorescence-activated cell sorting, FACS) analysis.Results:Coculture of HUVEC with P. gingivalis resulted in increase of IL-6 secretion at 24 h postinfection. Interestingly, the increase was inhibited significantly in HUVEC infected with the P. gingivalis fimA mutant. In addition, the increase of IL-6 secretion induced by P. gingivalis infection was significantly impaired by the meiosis specific kinase 1 inhibitor, PD98059, or the nuclear factor kappa B inhibitor, Bay11-7082. Furthermore, we demonstrated that gp130 expression increased with P. gingivalis infection. Importantly, gp130 expression was significantly impaired by P gingivalis fimA mutant infection compared with wild-type P. gingivalis infection, as assessed by both quantitative RT-PCR and FACS analysis.Conclusion:Our findings indicate that P. gingivalis fimbriae are important factors in the autocrine regulation of IL-6, by increasing gp130 in endothelial cells.

The immunohistochemical method and electron spin resonance (ESR) spin trapping assay were employed to detect the localization and biochemical activity of superoxide dismutases (SODs) in the rat nasal mucosa. Manganese SOD and copper-zinc SOD were immunohistochemically illustrated to be richly expressed in the epithelial cells and the subepithelial glands of nasal mucosa. The olfactory vesicles also showed positive immunostaining for manganese SOD and copper-zinc SOD. ESR spin trapping assay revealed that SOD activity in the mucosa of olfactory areas was significantly higher than in the mucosa of respiratory areas; however, the ratio of SOD activity in the mitochondrial fraction to SOD activity in the cytosolic fraction was similar, approximating 17:83 in the mucosa of both the olfactory and respiratory areas. The predominant localization of SODs in epithelial cells of nasal mucosa suggests the importance of mucosal epithelium in protecting nasal mucosa against cytotoxic superoxide (O2-) radicals. Epithelial goblet cells and the connective tissue of lamina propria, which showed no positive immunostaining for SODs, are considered to be vulnerable to oxidative insults implicated in the generation of O2- radicals. The higher SODs activity in the mucosa of olfactory areas implies that there is a different requirement of SOD in mucosa of the respiratory and olfactory areas on scavenging microenvironmental O2- radicals.

In order to investigate the protective system of human palatine tonsils against the cytotoxic superoxide radicals (O(-)(2)) generated from the oxygen-related bactericidal system, immunohistochemistry and electron spin resonance (ESR) spectrometry were used to detect the distribution and activities of superoxide dismutases (SODs) in tonsils of different related systemic diseases. Immunohistochemistry showed that SODs distribute in extrafollicular lymphatic tissue and crypt epithelium. No distribution difference could be found between tonsils of different related systemic diseases. ESR revealed no significant difference between SODs activities in tonsils of different related systemic diseases. However, the mitochondrial SOD activity was found to constitute approximately 50%-60% of the total tonsillar cellular SODs activity. The results suggest: i)tonsils possess the ability to control cytotoxic O(-)(2), ii) crypt epithelium and extrafollicular lymphatic tissue may encounter more O(-)(2) threat, iii) SODs may be important in protecting germinal centers from O(-)(2) injury, and iv) systemic diseases are less related to the local expression of tonsillar SODs.

A modified immunoglobulin peroxidase bridge sequence method was used to detect the localization of manganese superoxide dismutase (MnSOD), a superoxide radical (O2-) scavenging enzyme locating in mitochondrial matrix, in the vestibular labyrinth of pigmented rats. Strong positive MnSOD immunostaining was demonstrated in the dark cell regions of the ampullae, utricle, and common crus. The result provides for the first time direct evidence demonstrating the existence of mitochondrial O2- scavengers in the vestibular labyrinth and illustrates that the specific sites for vestibular MnSOD immunolocalization are the dark cell regions. This site specificity of MnSOD immunolocalization suggests that dark cell regions may possess high metabolic activity and may encounter constant threat from O2-. We assume MnSOD is needed in protecting some physiologic functions of the dark cell regions. Cell types showing negative MnSOD immunostaining may conceivably be relatively vulnerable to acute O2- damage.

We present a case of superficial siderosis (SS) of the central nervous system (CNS) with an unruptured intracranial aneurysm to illustrate that the commonly encountered unexplainable progressive sensorineural hearing loss (SNHL) can be an important sign for the early awareness of this rare disorder. The literature on SS is reviewed and the pathogenesis of SS is discussed.