Asialo-GM1 and asialo-GM2 are putative adhesion molecules for Moraxella catarrhalis

Moraxella catarrhalis is an important pathogen of respiratory and middle ear infections. We previously reported that the attachment of M. catarrhalis to pharyngeal epithelial cells is mediated by ganglioside M2 (GM2). Several sets of adhesins or receptors are involved in such attachment process. In this study, we used the same strains and similar bacterial culture conditions as those in our previous study, and demonstrated by thin layer chromatography that M. catarrhalis can also bind toasialo-GM1 (Gg4Cer) and asialo-GM2 (Gg3Cer). GalNAcβ1→4Galβ1 is a common sequence in both Gg4Cer and Gg3Cer, and in many respiratory bacteria, this sequence acts as a receptor for attachment to host cells. Treatment of human pharyngeal epithelial cells with anti-GM2 and anti-Gg4Cer antibodies significantlydecreased attachment of M. catarrhalis to these cells; however, treatment with anti-Gg3Cer antibody did not decrease M. catarrhalis attachment. Immunofluorescence microscopy revealed that human pharyngeal epithelial cells are positive for GM2 and Gg4Cer, but not for Gg3Cer. Our results indicate that Gg4Cer on human pharyngeal epithelial cells, and Gg3Cer, possibly on other cells, could serve as molecules for attachment of M. catarrhalis

Major bacteria of community-acquired respiratory tract infections in Turkey

To determine the bacterial etiology of lower respiratory tract infections (LRTIs) in Turkey, quantitative cultures of sputum were carried out. The major pathogens for LTRIs were found to be Haemophilus influenzae, followed by Streptococcus pneumoniae and Moraxella catarrhalis. Only 6.1% of the H. inlfuenzae and all strains of M. catarrhalis were β-lactamase producers. An E-test showed that 31.2% of the S. pneumoniae strains had an intermediate resistance to penicillin, and the remaining strains were susceptible; no fully resistant strains were detected

Role of lipooligosaccharide in the attachment of Moraxella catarrhalis to human pharyngeal epithelial cells

The goal of this study was to determine the role of lipooligosaccharide in the attachment of Moraxella catarrhalis to human pharyngeal epithelial cells. Strain 2951 and its Pk mutant strain 2951 galE were used in this study. This study suggests that the Pk epitope of LOS is not an adhesin for M. catarrhalis, but plays a crucial role by its surface charge in the initial stage of attachment

Variation in the attachment of Streptococcus pneumoniae to human pharyngeal epithelial cells after treatment with S-carboxymethylcysteine

S-carboxymethylcysteine (S-CMC) is a mucolytic agent that can prevent respiratory infection by decreasing the attachment of respiratory pathogens to human pharyngeal epithelial cells (HPECs). Streptococcus pneumoniae is a major cause of respiratory infections. A previous study revealed that treatment of S. pneumoniae with S-CMC caused a decrease in the attachment of this bacterium to HPECs. In the present study we found that the effect of S-CMC varied according to hosts and strains. S-CMC treatment altered the surface structure of S. pneumoniae, resulting in a decrease of attachment, without affecting the virulence of the bacteria. © 2008 Japanese Society of Chemotherapy and The Japanese Association for Infectious Diseases

Sulfatide and its synthetic analogues recognition by Moraxella catarrhalis

Moraxella catarrhalis is one of the major pathogens of respiratory and middle ear infections. Attachment of this bacterium to the surface of human pharyngeal epithelial cells is the first step in the pathogenesis of infections. This study revealed that sulfatide might act as a binding molecule for the attachment of M. catarrhalis to human pharyngeal epithelial cells. Furthermore, six different synthetic sulfatides were found to inhibit the attachment of M. catarrhalis significantly at an optimum concentration of 10 μg/ml. Synthetic sulfatides may have the potential to be used as a therapy to prevent M. catarrhalis infections

Restoration of TGF-β signalling reduces tumorigenicity in human lung cancer cells

Members of the transforming growth factor-β (TGF-β) family regulate a wide range of biological processes including cell proliferation, migration, differentiation, apoptosis, and extracellular matrix deposition. Resistance to TGF-β-mediated tumour suppressor function in human lung cancer may occur through the loss of type II receptor (TβRII) expression. In this study, we investigated the expression pattern of TβRII in human lung cancer tissues by RT–PCR and Western blot analyses. We observed downregulation of TβRII in 30 out of 46 NSCLC samples (65%) by semiquantitative RT–PCR. Western blot analyses with tumour lysates showed reduced expression of TβRII in 77% cases. We also determined the effect of TβRII expression in lung adenocarcinoma cell line (VMRC-LCD) that is not responsive to TGF-β due to lack of TβRII expression. Stable expression of TβRII in these cells restored TGF-β-mediated effects including Smad2/3 and Smad4 complex formation, TGF-β-responsive reporter gene activation, inhibition of cell proliferation and increased apoptosis. Clones expressing TβRII showed reduced colony formation in soft-agarose assay and significantly reduced tumorigenicity in athymic nude mice. Therefore, these results suggest that reestablishment of TGF-β signalling in TβRII null cells by stable expression of TβRII can reverse malignant behaviour of cells and loss of TβRII expression may be involved in lung tumour progression

Plasmodium falciparum Adhesion on Human Brain Microvascular Endothelial Cells Involves Transmigration-Like Cup Formation and Induces Opening of Intercellular Junctions

Cerebral malaria, a major cause of death during malaria infection, is characterised by the sequestration of infected red blood cells (IRBC) in brain microvessels. Most of the molecules implicated in the adhesion of IRBC on endothelial cells (EC) are already described; however, the structure of the IRBC/EC junction and the impact of this adhesion on the EC are poorly understood. We analysed this interaction using human brain microvascular EC monolayers co-cultured with IRBC. Our study demonstrates the transfer of material from the IRBC to the brain EC plasma membrane in a trogocytosis-like process, followed by a TNF-enhanced IRBC engulfing process. Upon IRBC/EC binding, parasite antigens are transferred to early endosomes in the EC, in a cytoskeleton-dependent process. This is associated with the opening of the intercellular junctions. The transfer of IRBC antigens can thus transform EC into a target for the immune response and contribute to the profound EC alterations, including peri-vascular oedema, associated with cerebral malaria

S-carboxymethylcysteine inhibits the attachment of Streptococcus pneumoniae to human pharyngeal epithelial cells, adult, article, cheek, chi square test, controlled study, DNA extraction, female, human, human cell, hypothesis, major clinical study, pathogenesis, polymerase chain reaction, preeclampsia, priority journal, statistical significance, X chromosome inactivation, Adult, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Pre-Eclampsia, Pregnancy, X Chromosome Inactivation Medline is the source for the MeSH terms of this document.

Cataloged from PDF version of article.Pre-eclampsia is a disorder that affects approximately 5% of pregnancies. We tested the hypothesis that skewed X-chromosome inactivation (XCI) could be involved in the pathogenesis of pre-eclampsia. Peripheral blood DNA was obtained from 67 pre-eclampsia patients and 130 control women. Androgen receptor (AR) was analyzed by the Hpa II/polymerase chain reaction assay to assess XCI patterns in DNA extracted from peripheral-blood cells. In addition, buccal cells were obtained from seven patients, and the analysis repeated. Extremely skewed XCI was observed in 10 of 46 informative patients (21.74%), and in 2 of 86 informative controls (2.33%, P = 0.0005; χ2 test). Our findings support a role for the X-chromosome in the pathogenesis of pre-eclampsia in a subgroup of patients. © Springer-Verlag 2006