IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection

<p>Abstract</p> <p>Background</p> <p>Intercellular adhesion molecule-1 (ICAM-1) is a critical target-docking molecule on epithelial cells for 90% of human rhinovirus (HRV) serotypes. Two forms of ICAM-1 exist, membranous (mICAM-1) and soluble (sICAM-1), both expressed by bronchial epithelial cells. Interferon-gamma (IFN-γ), a crucial Th-1 immuno-regulatory mediator, can modulate mICAM-1 expression; however its simultaneous effects on mICAM-1: sICAM-1 levels and their consequent outcome on cell infectivity have not been previously explored.</p> <p>Methods</p> <p>Primary normal human bronchial epithelial cells were pre-stimulated with IFN-γ (1 ng/ml for 24 h) and subsequently inoculated with HRV-14 or HRV-1b (TCID₅₀10 ^2.5). Epithelial surface ICAM-1 expression and soluble ICAM-1 release were measured at the protein and gene level by immunofluorescence and ELISA respectively; mRNA levels were semi-quantified using RT-PCR. Molecular mechanisms regulating ICAM-1 isoform expression and effects on epithelial cell infectivity were explored.</p> <p>Results</p> <p>In IFN-γ-biased cells infected with HRV-14, but not HRV-1b, mICAM-1 expression is down-regulated, with simultaneous induction of sICAM-1 release. This differential effect on HRV-14 receptor isoforms appears to be related to a combination of decreased IFN-γ-induced JAK-STAT signalling and proteolytic receptor cleavage of the membranous form in IFN-γ-biased HRV-14 infected cells. The observed changes in relative mICAM-1: sICAM-1 expression levels are associated with reduced HRV-14 viral titres.</p> <p>Conclusion</p> <p>These findings support the hypothesis that in epithelial cells conditioned to IFN-γ and subsequently exposed to HRV-14 infection, differential modulation in the ratio of ICAM-1 receptors prevails in favour of an anti-viral milieu, appearing to limit further target cell viral attachment and propagation.</p

Simultaneous identification of GSTP1 Ile105→Val105 and Ala114→Val114 substitutions using an amplification refractory mutation systempolymerase chain reactionassay: studies in patients with asthma

BACKGROUND: The glutathione S-transferase (GST) enzyme GSTP1 utilizes byproducts of oxidative stress. We previously showed that alleles of GSTP1 that encode the Ile105→Val105 substitution are associated with the asthma phenotypes of atopy and bronchial hyperresponsiveness (BHR). However, a further polymorphic site (Ala114→Val114) has been identified that results in the following alleles: GSTP1(*)A (wild-type Ile105→Ala114), GSTP1(*)B (Val105→Ala114), GSTP1(*)C (Val105→Val114) and GSTP1(*)D (Ile105→Val114). METHODS: Because full identification of GSTP1 alleles may identify stronger links with asthma phenotypes, we describe an amplification refractory mutation system (ARMS) assay that allows identification of all genotypes. We explored whether the GSTP1 substitutions influence susceptibility to asthma, atopy and BHR. RESULTS: Among 191 atopic nonasthmatic, atopic asthmatic and nonatopic nonasthmatic individuals, none had the BD, CD, or DD genotypes. GSTP1 BC was significantly associated with reduced risk for atopy (P = 0.031). Compared with AA, trend test analysis identified a significant decrease in the frequency of GSTP1 BC with increasing severity of BHR (P = 0.031). Similarly, the frequency of GSTP1 AA increased with increasing BHR. CONCLUSION: These data suggest that GSTP1(*)B and possibly GSTP1(*)C are protective against asthma and related phenotypes

PENGEMBANGAN LEMBAR KERJA SISWA (LKS) BIOLOGI BERBASIS PROBEX (PREDICT-OBSERVE-EXPLAIN) MATERI ARCHAEBACTERIA DAN EUBACTERIA UNTUK SISWA KELAS X SMA/MA

The research aims to develope probex-based worksheet on archaebacteria and eubacteria material for Senior High School student grade X and to determine its quality. This research wass categorized as R & D research by using ADDIE model. The assessment instruments used in this research were questionnaire. Worksheet was assessed and validated by experts, peers, teachers, and students. The assessment score was generated by converting qualitative data into quantitative scores. The assessment from experts, peers, teachers, and students each categorized "very good" with ideal percentages 89.39%; 90.08%; 86.17%; and 90.75% respectively. Therefore, the product can be used as learning material

IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection-5

Ted cells, **p < 0.05, IFN-γ treated uninfected cells compared with IFN-γ treated infected cells, Fig. 6B, *p < 0.05, actinomycin D treated cells compared with equivalent untreated cells).<p><b>Copyright information:</b></p><p>Taken from "IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection"</p><p>http://www.journal-inflammation.com/content/5/1/8</p><p>Journal of Inflammation (London, England) 2008;5():8-8.</p><p>Published online 5 Jun 2008</p><p>PMCID:PMC2427029.</p><p></p

IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection-3

Lls treated with AG490 prior to stimulation with IFN-γ compared to cells stimulated with IFN-γ alone).<p><b>Copyright information:</b></p><p>Taken from "IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection"</p><p>http://www.journal-inflammation.com/content/5/1/8</p><p>Journal of Inflammation (London, England) 2008;5():8-8.</p><p>Published online 5 Jun 2008</p><p>PMCID:PMC2427029.</p><p></p

IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection-2

A) levels at 15 and 30 min of infection. Vinculin was analysed using Western blotting as a control for sample loading. Western blots from three separate experiments were analysed densitometrically (Fig. 3B) normalised against vinculin and expressed as a ratio to total STAT-1. Data are mean ± S.E. (*p < 0.05 compared to IFN-γ treated uninfected cells at equivalent time points and **p < 0.04 IFN-γ treated uninfected cells compared to control untreated and uninfected cells).<p><b>Copyright information:</b></p><p>Taken from "IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection"</p><p>http://www.journal-inflammation.com/content/5/1/8</p><p>Journal of Inflammation (London, England) 2008;5():8-8.</p><p>Published online 5 Jun 2008</p><p>PMCID:PMC2427029.</p><p></p

IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection-1

Ted cells, **p < 0.05, IFN-γ treated uninfected cells compared with IFN-γ treated infected cells, Fig. 2B, *p < 0.05, actinomycin D treated cells compared with equivalent untreated cells).<p><b>Copyright information:</b></p><p>Taken from "IFN-gamma regulation of ICAM-1 receptors in bronchial epithelial cells: soluble ICAM–1 release inhibits human rhinovirus infection"</p><p>http://www.journal-inflammation.com/content/5/1/8</p><p>Journal of Inflammation (London, England) 2008;5():8-8.</p><p>Published online 5 Jun 2008</p><p>PMCID:PMC2427029.</p><p></p