Immunoglobulin G response to subgingival gram-negative bacteria in human subjects

Serum and gingival crevicular fluid from normal healthy adults and patients with periodontitis were screened for immunoglobulin G antibodies to antigens from Bacteroides gingivalis 381, Bacteroides intermedius 24, Bacteroides loescheii ATCC 15930, Fusobacterium nucleatum ATCC 25586, Eikenella corrodens 1073, Actinobacillus actinomycetemcomitans ATCC 29522, and Capnocytophaga sp. strain M-12. Immunoglobulin G antibody titers to the antigens were measured by an enzyme-linked immunosorbent assay. The antibody levels to B. gingivalis in serum and gingival crevicular fluid were significantly higher in the samples from patients with periodontitis than in samples from healthy individuals. Although there were individual differences within patient groups, a positive correlation (P less than 0.01) was found between the serum immunoglobulin G levels to B. gingivalis and the development of periodontitis. The antibodies to F. nucleatum (P less than 0.05), E. corrodens (P less than 0.05), and A. actinomycetemcomitans were slightly higher in patients with periodontitis than in normal subjects. There were no remarkable differences between the two groups in titers to B. intermedius, B. loescheii, and Capnocytophaga sp.     

Plasmacytoma of Lymph Node Recurrent Lymphadenopathy Terminating in Plasma Cell Dyscrasia with Polyneuropathy and Endocrine Disturbances

A case with lymphadenopathy of the left side of the neck in a 38-year-old male is described. He had a history of several relapses of about 10 years duration. Swollen lymph nodes were histologically similar to those of the hyaline-vascular type of Castleman's disease, but contained clear-cut lymph sinus and a sheet-like proliferation of plasma cells. Lymph follicles showed proliferation and atrophic germinal centers, in which cellular hypertrophy in the wall of ramifying small blood vessels, called angiosclerosis, was frequently encountered. During its progress, the patient developed plasmacytoma of the lymph nodes with varied clinical manifestations such as polyneuropathy, disturbance of gait, unusual perspiration, hirsuitism, gynecomastia, bilateral papilledema, and albumino-cytologic dissociation in cerebrospinal fluid.     

β-Adrenergic modulation of the Na+−K+ pump in frog skeletal muscles

Adrenaline markedly increased the ouabain-sensitive 22Na+-efflux by stimulating the Na+-K+ pump in frog skeletal muscle. The facilitatory effects of adrenaline had the following properties. The effects of adrenaline on the ouabain-sensitive Na+-efflux were observed at concentrations greater than 0.1 microM and the magnitude increased with concentration up to 10 microM. At a concentration of 30 microM, adrenaline markedly augmented the ouabain-sensitive Na+-efflux, but other biogenic amines were less effective (noradrenaline and dopamine) or ineffective (histamine and serotonin). The increase of Na+-efflux induced by 1 microM adrenaline was blocked by 3 microM propranolol, but not by 3 microM phenoxybenzamine. The properties of the facilitatory action of adrenaline on the ouabain-sensitive Na+-efflux suggest that beta-adrenoceptors have an important role in modulating the Na+-K+ pump activity in the skeletal muscle membrane. The protein complex localized in excitable membranes, namely the Na+-K+ ATPase-beta-adrenoceptor complex, may be the functional unit which operates the membrane machinery driving the Na+-K+ pump.     

Expression of heme oxygenase-1 in rat ontogeny

Heme oxygenase (HO), the heme-degrading enzyme, plays an important role in heme catabolism. Among three isozymes, HO-1 is an inducible form expressed mainly in macrophages. In rat ontogeny, HO-1 immunoreactivity was detected in mononuclear cells in the yolk sac at 10 days of gestation. HO-1-expressing cells were then detected in the fetal liver and their numbers increased during the gestational period. The numbers of HO-1-positive cells and HO-1 mRNA levels in the liver peaked at 18 days of gestation. Most of the macrophages expressed both HO-1 and a macrophage scavenger receptor. Macrophages in the fetal liver showed marked hemophagocytosis. Macrophages in the lung, spleen, bone marrow, and other tissues also expressed HO-1. HO-1 immunoreactivity was also observed in syncytial cells of the chorionic villi, the endodermal layer of the yolk sac, and renal tubules of the fetus. Intestinal mucosal epithelial cells expressed HO-1 after birth. These findings imply that HO-1 is crucial for macrophages in heme catabolism from an early stage of ontogeny. HO-1 expression in non-macrophagic cells may be required for other purposes such as protection from oxidative stress and various stimuli.     

Astaxanthin limits exercise-induced skeletal and cardiac muscle damage in mice

Dietary antioxidants may attenuate oxidative damage from strenuous exercise in various tissues. Beneficial effects of the antioxidant astaxanthin have been demonstrated in vitro, but not yet in vivo. We investigated the effect of dietary supplementation with astaxanthin on oxidative damage induced by strenuous exercise in mouse gastrocnemius and heart. C57BL/6 mice (7 weeks old) were divided into groups: rested control, intense exercise, and exercise with astaxanthin supplementation. After 3 weeks of exercise acclimation, both exercise groups ran on a treadmill at 28 m/min until exhaustion. Exercise-increased 4-hydroxy-2-nonenal-modified protein and 8-hydroxy-2'-deoxyguanosine in gastrocnemius and heart were blunted in the astaxanthin group. Increases in plasma creatine kinase activity, and in myeloperoxidase activity in gastrocnemius and heart, also were lessened by astaxanthin. Astaxanthin showed accumulation in gastrocnemius and heart from the 3 week supplementation. Astaxanthin can attenuate exercise-induced damage in mouse skeletal muscle and heart, including an associated neutrophil infiltration that induces further damage.     

Immune Abnormalities Induced by Human Endogenous Retroviral Peptides: With Reference to the Pathogenesis of Systemic Lupus Erythematosus

P15E is a specific sequence among the envelope gene (env)-encoded transmembrane proteins of exogenous and endogenous retroviruses. A synthetic peptide (CKS-17) that shows homology to this p15E region in several species of retrovirus is known to induce immune abnormalities. In this study, we examined the effect of a synthetic peptide derived from a region of human endogenous retrovirus (HERV) clone 4-1 ( 4-1) similar to sequences of CKS-17 on the induction of systemic lupus erythematosus (SLE)-related immune abnormalities. Our results indicated that this peptide could induce T-cell activation and anergy in normal peripheral blood mononuclear cells, and the peptide could also promote the production of interleukins IL-6 and IL-16. These phenomena are representative immune abnormalities observed in SLE patients. Thus, our findings support the possibility that HERV acts as a pathogen in human SLE.     

The induction of intestinal metaplasia in rats by pyloroplasty or pyloroplasty plus vagotomy

The influence of increased gastric pH on induction of intestinal metaplasia in the stomach of male JCL/SD rats was examined following surgical procedures of pyloroplasty or pyloroplasty and vagotomy. Twelve months after pyloroplasty plus vagotomy serum gastric concentrations were significantly higher (group II) than in rats receiving only pyloroplasty (group I) or in sham operated animals (group III). Additionally, trehalase activity was also higher in group II than in groups I and III. The incidence of intestinal metaplasia was significantly higher in groups I and II compared with the sham operated control animals (group III). This study indicates that intestinal metaplasia could be induced by surgical procedures such as pyloroplasty with or without vagotomy. Furthermore, elevation of the pH on gastric mucosa by such procedures may play a significant role in the subsequent development of metaplasia in the stomach.     

Candidate interneurons mediating peripherally evoked disynaptic inhibition of masseter motoneurons of both sides

Location and axonal projection of interneurons presumed to mediate disynaptic inhibition evoked from the trigeminal sensory nerve in the ipsi- and contralateral masseter motoneurons were studied in pentobarbital anesthetized cats. Neurons monosynaptically excited from the periphery and antidromically activated from the contralateral trigeminal motor nucleus at low current intensity, hence probably terminating there, were found in the supratrigeminal region. Intracellular staining of such cells revealed collaterals terminating in the ipsilateral masseter motor nucleus. It is suggested that both the crossed and uncrossed disynaptic inhibition of masseter motoneurons are at least in part relayed by the same neurons in the supratrigeminal region.