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Cellular Profiles (cellular + profile)
Selected AbstractsInflammatory infiltrate of chronic periradicular lesions: an immunohistochemical studyINTERNATIONAL ENDODONTIC JOURNAL, Issue 7 2003S. Liapatas Abstract Aim, To determine the cellular profile of human chronic periradicular lesions using immunohistochemical methods in order to study the differences in the cell infiltrate of periradicular granulomas and cysts. Methodology, The study population consisted of 45 individuals without any systemic disease. Biopsies were obtained during periradicular surgery. Paraffin-embedded sections were stained by the avidin,biotin complex method (ABC), whilst cryostat tissue sections were stained using the alkaline phosphatase antialkaline phosphatase assay (APAAP). These methods are highly valid and sensitive using a panel of specific monoclonal antibodies: CD4, CD8, CD3, CD10, HLADR, CD20, CD45RO, CD68 and CD57. The 45 specimens were characterized by the use of both techniques. Results, The 45 specimens were histologically diagnosed as: 25 periradicular granulomas, 17 periradicular cysts and 3 scar tissues. No statistically significant differences were detected in the inflammatory infiltrate between periradicular granulomas and cysts. Observation of the sections showed that the majority of inflammatory cells consisted of T and B lymphocytes and macrophages. T and B lymphocytes were equally distributed in 60% of the cases. The T4/T8 ratio ranged approximately from 1 to 3 and greater, being consistent with inflammation of periradicular tissues. The final differentiation of B lymphocytes to plasma cells was also detected, whilst natural killer (NK) cells were found in only 10 cases (22%). Moreover, antigen presenting cells and T suppressor/cytotoxic cells were found to be associated with both pre-existing and newly formed epithelium. Conclusions, Periradicular granulomas and cysts represent two different stages in the development of chronic periradicular pathosis as a normal result of the process of immune reactions that cannot be inhibited. [source] Follicular dendritic cells confirm lymphoid organization in the minor salivary glands of primary Sjögren's syndromeJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 9 2008Malin V. Jonsson Background:, Sjögren's syndrome (SS) is an autoimmune chronic inflammatory disorder affecting the salivary and lacrimal glands. The aim of this study was to explore immunophenotypic features of chronic inflammatory reactions in the minor salivary glands in patients with primary SS (pSS). Methods:, Formalin-fixed, paraffin-embedded labial minor salivary gland tissue sections from randomly selected patients with pSS (n = 60) were investigated for the expression of CD21, CD23, CD35 and IgD by immunohistochemistry. Results:, Based on the distribution and staining pattern of CD21, CD23, CD35 and IgD in lymphoid aggregates, several stages of chronic inflammatory reactions were observed. In 12/60 (20%) patients, lymphoid infiltrates with germinal centre (GC)-like features such as extensive networks of CD21-, CD23- and CD35-positive cells were observed in the minor salivary gland tissue. Smaller networks and,/or focal infiltrates with scattered CD21+, CD23+ and CD35+ cells were observed in the remaining 48/60 (80,%) cases. When dividing patients according to the presence (GC+) or the absence (GC,) of GC in the minor salivary glands, the mean focus score was significantly higher in the GC+ patients (P < 0.05). Double staining of the minor salivary glands revealed focal infiltrates with follicular dentritic cell networks and B cells resembling normal GCs in tonsillar tissue. Conclusion:, A particular cellular profile was demonstrated in a sub-group of patients with pSS and could be linked to serological aberrations. These findings warrant further prospective studies. [source] Alteration of normal cellular profiles in the scleractinian coral (Pocillopora damicornis) following laboratory exposure to fuel oilENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 12 2006Luc Rougée Abstract Petroleum contamination from oil spills is a continuing threat to our ocean's fragile ecosystems. Herein, we explored the effects of the water-soluble fraction of crude oil on a stony coral, Pocillopora damicornis (Linneaeus 1758). We developed methods for exposing corals to various concentrations of crude oil and for assessing the potential molecular responses of the corals. Corals were exposed to water-accommodated fraction solutions, and appropriate cellular biomarkers were quantified. When compared to the "healthy" control specimens, exposed corals exhibited shifts in biomarker concentrations that were indicative of a shift from homeostasis. Significant changes were seen in cytochrome P450 1-class, cytochrome P450 2-class, glutathione- S -transferase-pi, and cnidarian multixenobiotic resistance protein-1 biomarkers, which are involved the cellular response to, and manipulation and excretion of, toxic compounds, including polycyclic aromatic hydrocarbons. A shift in biomarkers necessary for porphyrin production (e.g., protoporphyrinogen oxidase IX and ferrochelatase) and porphyrin destruction (e.g., heme oxygenase-1 and invertebrate neuroglobin homologue) illustrates only one of the cellular protective mechanisms. The response to oxidative stress was evaluated through measurements of copper/zinc superoxide dismutase-1 and DNA glycosylase MutY homologue-1 concentrations. Likewise, changes in heat shock protein 70 and small heat shock proteins indicated an adjustment in the cellular production of proteins. Finally, the results of this laboratory study were nearly identical to what we observed previously among corals of a different species, Porites lobata, exposed to an oil spill in the field after the grounding of the Merchant Vessel Kyowa Violet. [source] The quest for the mechanisms of lifeBIOTECHNOLOGY & BIOENGINEERING, Issue 7 2003Maria I. Klapa Abstract The genomic revolution, manifested by the sequencing of the complete genome of many organisms, along with technological advances, such as DNA microarrays and developments in high-throughput analysis of proteins, metabolites, and isotopic tracer distribution patterns, challenged the conventional ways in which questions are approached in the biological sciences: (a) rather than examining a small number of genes and/or reactions at any one time;, we can now analyze gene expression and protein activity in the context of systems of interacting genes and gene products; (b) comprehensive analysis of biological systems requires the integration of all cellular fingerprints: genome sequence, maps of gene expression, protein expression, metabolic output, and in vivo enzymatic activity; and (c) collecting, managing, and analyzing comparable data from various cellular profiles requires expertise from several fields that transcend traditional discipline boundaries. While researchers in systems biology have still to address difficult challenges in both experimental and computational arenas, they possess, for the first time, the opportunity to unravel the mechanisms of life. The enormous impact of these discoveries in diverse areas, such as metabolic engineering, strain selection, drug screening and development, bioprocess development, disease prognosis and diagnosis, gene and other medical therapies, is an obvious motivation for pursuing integrated analyses of cellular systems. © 2003 Wiley Periodicals, Inc. [source] Airway cell and cytokine changes in early asthma deterioration after inhaled corticosteroid reductionCLINICAL & EXPERIMENTAL ALLERGY, Issue 8 2007Y. H. Khor Summary Background Back-titration of inhaled corticosteroid (ICS) dose in well-controlled asthma patients is emphasized in clinical guidelines, but there are few published data on the airway cell and cytokine changes in relation to ICS reduction. In our study, 20 mild-to-moderate persistent (inspite of low-moderate dose ICS treatment) asthmatic subjects prospectively rendered largely asymptomatic by high-dose ICS were assessed again by clinical, physiological, and airway inflammatory indices after 4,8 weeks of reduced ICS treatment. We aimed at assessing the underlying pathological changes in relation to clinical deterioration. Methods Patients recorded daily symptom scores and peak expiratory flows (PEF). Spirometry and airways hyperreactivity (AHR) were measured and bronchoscopy was performed with assessment of airway biopsies (mast cells, eosinophils, neutrophils, and T lymphoctyes), bronchoalveolar lavage (BAL) IL-5 and eotaxin levels and cellular profiles at the end of high-dose ICS therapy and again after ICS dose reduction. Baseline data were compared with symptomatic steroid-free asthmatics (n=42) and non-asthmatic controls (n=28). Results After ICS reduction, subjects experienced a variable but overall significant increase in symptoms and reductions in PEF and forced expiratory volume in 1 s. There were no corresponding changes in AHR or airways eosinophilia. The most relevant pathogenic changes were increased CD4+/CD8+ T cell ratio, and decreased sICAM-1 and CD18 macrophage staining (potentially indicating ligand binding). However, there was no relationship between the spectrum of clinical deterioration and the changes in cellular profiles or BAL cytokines. Conclusions These data suggest that clinical markers remain the most sensitive measures of early deterioration in asthma during back-titration of ICS, occurring at a time when AHR and conventional indices of asthmatic airway inflammation appear unchanged. These findings have major relevance to management and to how back-titration of ICS therapy is monitored. [source] | |||||||||||||