Antibacterial Activity of Hypericum Erectum

In recent years, the potential of oral care in preventing aspiration pneumonia has been recognized. Consuming drinks is thought to be an easy and effective method of oral care, and the antibacterial activities of various drinks have been examined. However, the side effects associated with, for example, caffeine as an ingredient in tea (e.g. sleep disorders) need to be taken into consideration. As yet, a safe caffeine-free tea to be taken orally to prevent aspiration pneumonia has not been reported. Thus, in the present study we evaluated the antibacterial effects of hot water extracts of four teas, namely Hypericum Erectum, Crataegus cuneata, Rosa canina, and Matricaria rectita, thought to be caffeine-free. The effects of the extracts against 19 bacteria and 1 fungus were investigated by the dilution plate technique. In addition, the components of the teas were analyzed by HPLC analysis. The strongest antibacterial activity was observed for the hot water extract of H. erectum, which exhibited significant activity against oral bacteria, including Streptococcus oralis. However, the H. erectum extract did not kill microbiota, such as Escherichia coli and Lactobacillus casei. Neither hypericin nor caffeine, both of which have notable side effects, were detected in the H. erectum extract following HPLC analysis. These results suggest that H. erectum tea may be a good candidate for simple, safe oral care to prevent aspiration pneumonia in the elderly

Duodenal Tube Feeding: An Alternative Approach for Effectively Promoting Weight Gain in Children with Gastroesophageal Reflux and Congenital Heart Disease

We tested whether duodenal tube feeding effectively improves the clinical symptoms and body weight gain in children with congenital heart disease (CHD) and gastroesophageal reflux (GER). In the retrospective analysis of 17 consecutive children with CHD who were treated with duodenal tube feeding for symptomatic GER, we found that clinical symptoms of persistent emesis or respiratory wheezing after feeding disappeared with duodenal tube feeding in all patients. Duodenal tube feeding facilitated a stable nutritional supply, resulting in marked improvement of weight gain from 6 to 21 g/day (). In a patient with trisomy 21 and persistent pulmonary hypertension after the closure of a ventricular septal defect, duodenal tube feeding ameliorated pulmonary hypertension, as evidenced by the improvement of the pressure gradient of tricuspid regurgitation from 77 to 41 mm Hg. In 14 of the 17 patients, the duodenal tube was successfully removed, with the spontaneous improvement of GER (median duration of duodenal tube feeding: 7 months). In conclusion, duodenal tube feeding improves the weight gain of infants with GER who need treatment for CHD-associated heart failure. It also allows for the improvement of pulmonary hypertension

Hydrogen peroxide contributes to the epithelial cell death induced by the oral mitis group of streptococci.

Members of the mitis group of streptococci are normal inhabitants of the commensal flora of the oral cavity and upper respiratory tract of humans. Some mitis group species, such as Streptococcus oralis and Streptococcus sanguinis, are primary colonizers of the human oral cavity. Recently, we found that hydrogen peroxide (H2O2) produced by S. oralis is cytotoxic to human macrophages, suggesting that streptococcus-derived H2O2 may act as a cytotoxin. Since epithelial cells provide a physical barrier against pathogenic microbes, we investigated their susceptibility to infection by H2O2-producing streptococci in this study. Infection by S. oralis and S. sanguinis was found to stimulate cell death of Detroit 562, Calu-3 and HeLa epithelial cell lines at a multiplicity of infection greater than 100. Catalase, an enzyme that catalyzes the decomposition of H2O2, inhibited S. oralis cytotoxicity, and H2O2 alone was capable of eliciting epithelial cell death. Moreover, S. oralis mutants lacking the spxB gene encoding pyruvate oxidase, which are deficient in H2O2 production, exhibited reduced cytotoxicity toward Detroit 562 epithelial cells. In addition, enzyme-linked immunosorbent assays revealed that both S. oralis and H2O2 induced interleukin-6 production in Detroit 562 epithelial cells. These results suggest that streptococcal H2O2 is cytotoxic to epithelial cells, and promotes bacterial evasion of the host defense systems in the oral cavity and upper respiratory tracts

Streptococcal H2O2 inhibits IgE-triggered degranulation of RBL-2H3 mast cell/basophil cell line by inducing cell death.

Mast cells and basophils are central players in allergic reactions triggered by immunoglobulin E (IgE). They have intracellular granules containing allergic mediators (e.g., histamine, serotonin, inflammatory cytokines, proteases and β-hexosaminidase), and stimulation by IgE-allergen complex leads to the release of such allergic mediators from the granules, that is, degranulation. Mast cells are residents of mucosal surfaces, including those of nasal and oral cavities, and play an important role in the innate defense system. Members of the mitis group streptococci such as Streptococcus oralis, are primary colonizers of the human oral cavity. They produce hydrogen peroxide (H2O2) as a by-product of sugar metabolism. In this study, we investigated the effects of streptococcal infection on RBL-2H3 mast cell/basophil cell line. Infection by oral streptococci did not induce degranulation of the cells. Stimulation of the RBL-2H3 cells with anti-dinitrophenol (DNP) IgE and DNP-conjugated human serum albumin triggers degranulation with the release of β-hexosaminidase. We found that S. oralis and other mitis group streptococci inhibited the IgE-triggered degranulation of RBL-2H3 cells. Since mitis group streptococci produce H2O2, we examined the effect of S. oralis mutant strain deficient in producing H2O2, and found that they lost the ability to suppress the degranulation. Moreover, H2O2 alone inhibited the IgE-induced degranulation. Subsequent analysis suggested that the inhibition of degranulation was related to the cytotoxicity of streptococcal H2O2. Activated RBL-2H3 cells produce interleukin-4 (IL-4); however, IL-4 production was not induced by streptococcal H2O2. Furthermore, an in vivo study using the murine pollen-induced allergic rhinitis model suggested that the streptococcal H2O2 reduces nasal allergic reaction. These findings reveal that H2O2 produced by oral mitis group streptococci inhibits IgE-stimulated degranulation by inducing cell death. Consequently, streptococcal H2O2 can be considered to modulate the allergic reaction in mucosal surfaces

Toll-like receptor-dependent production of IL-12p40 causes chronic enterocolitis in myeloid cell-specific Stat3-deficient mice

Stat3 plays an essential role in IL-10 signaling pathways. A myeloid cell-specific deletion of Stat3 resulted in inflammatory cytokine production and development of chronic enterocolitis with enhanced Th1 responses in mice. In this study, we analyzed the mechanism by which a Stat3 deficiency in myeloid cells led to the induction of chronic enterocolitis in vivo. Even in the absence of Stat1, which is essential for IFN-γ signaling pathways, Stat3 mutant mice developed chronic enterocolitis. TNF-α/Stat3 double-mutant mice developed severe chronic enterocolitis with enhanced Th1 cell development. IL-12p40/Stat3 double-mutant mice, however, showed normal Th1 responses and no inflammatory change in the colon. RAG2/Stat3 double-mutant mice did not develop enterocolitis, either. These findings indicate that overproduction of IL-12p40, which induces potent Th1 responses, is essential for the development of chronic enterocolitis in Stat3 mutant mice. Furthermore, enterocolitis was significantly improved and IFN-γ production by T cells was reduced in TLR4/Stat3 double-mutant mice, indicating that TLR4-mediated recognition of microbial components triggers aberrant IL-12p40 production by myeloid cells, leading to the development of enterocolitis. Thus, this study clearly established a sequential innate and acquired immune mechanism for the development of Th1-dependent enterocolitis

IL-6 and β-defensin 2 production by <i>S. oralis</i> strains.

<p>Detroit 562 epithelial cells (2×10⁵ cells) in 24 well culture plates were infected with viable <i>S. oralis</i> WT, <i>spxB</i> KO, or <i>spxB</i> Rev strains for 2 h, and then washed and cultured in fresh medium for 18 h. <i>E. coli</i> LPS (1 µg/ml) was used as a positive control. The release of IL-6 (A) and β-defensin 2 (B) was determined by ELISA. Data are shown as the mean ± SD of triplicate samples. *<i>p</i><0.05 as compared with untreated control (None). For the <i>spxB</i> KO infected cells, **<i>p<</i>0.05 as compared with the cells infected with WT at the same MOI.</p