Home About us Contact
|
Home About us Contact | ||
|
|
||
P Component (p + component)
Kinds of P Component Selected AbstractsA female-specific pentraxin, CrOctin, bridges pattern recognition receptors to bacterial phosphoethanolamineEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2007Yue Li Abstract Pathogen recognition and binding are crucial functions of innate immunity. It has been observed that the short pentraxin superfamily including C-reactive protein (CRP) and serum amyloid,P component are pathogen pattern recognition receptors (PRR) in the plasma. We isolated and characterized a novel and distinctive pentraxin from the plasma of horseshoe crab, Carcinoscorpius rotundicauda, henceforth named CrOctin, which binds to bacteria via phosphoethanolamine (PE), a chemical component present on lipid,A and core polysaccharide moieties of bacterial lipopolysaccharide (LPS). Infection enhances the formation of the PRR interactome constituting CrOctin, CRP and galactose-binding protein. In particular, infection increases the affinity of CRP to CrOctin by 1000-fold. Furthermore, we observed that by binding to PE, CrOctin acts as a linker that bridges the PRR interactome to the inner core of LPS. On the other hand, under normal physiological conditions, binding of CrOctin to PE appears to obscure other PRR from interacting directly with PE. Interestingly, the cluster of "CrOctin-interactive PRR" is sex specific. We report, for the first time, the change in PRR protein profiles with a distinctive gender difference during Pseudomonas infection. [source] Biochemical and functional characterization of the interaction between pentraxin 3 and C1qEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 2 2003Abstract Pentraxin 3 (PTX3) is a recently characterized member of the pentraxin family of acute-phase proteins produced during inflammation. Classical short pentraxins, C-reactive protein, and serum amyloid P component can bind to C1q and thereby activate the classical complement pathway. Since PTX3 can also bind C1q, the present study was designed to define the interaction between PTX3 and C1q and to examine the functional consequences of this interaction. A dose-dependent binding of both C1q and the C1 complex to PTX3 was observed. Experiments with recombinant globular head domains of human C1q A, B, and C chains indicated that C1q interacts with PTX3 via its globular head region. Binding of C1q to immobilized PTX3 induced activation of the classical complement pathway as assessed by C4 deposition. Furthermore, PTX3 enhanced C1q binding and complement activation on apoptotic cells. However, in the fluid-phase, pre-incubation of PTX3 with C1q resulted in inhibition of complement activation by blocking the interaction of C1q with immunoglobulins. These results indicate that PTX3 can both inhibit and activate the classical complement pathway by binding C1q, depending on the way it is presented. PTX3 may therefore be involved in the regulation of the innate immune response. [source] Vascular amyloid of unknown origin and senile transthyretin amyloid in the lung and gastrointestinal tract of old age: Histological and immunohistochemical studiesPATHOLOGY INTERNATIONAL, Issue 5 2001Hironobu Matsutani The histological and immunohistochemical characteristics and the incidence of amyloid deposits in the tissues of the lung and gastrointestinal tract were investigated in 64 autopsied individuals who were 80 years and older (age range: 80,92 years; mean: 83.3 years). Immunohistochemical examination was performed with antibodies against amyloid A, transthyretin, immunoglobulin , and , light chain amyloid fibril proteins, ,2 -microglobulin, , protein, apolipoprotein AI, apolipoprotein AII, atrial natriuretic peptide, apolipoprotein E, and amyloid P component. Transthyretin amyloid fibril protein (ATTR) deposits were observed in five cases (7.8%). Gastrointestinal amyloid deposits of unknown origin were observed in the veins of the gastrointestinal tract in 26 cases (40.6%). This amyloid was regarded as portal amyloid with respect to distribution pattern. Pulmonary vascular amyloid deposits of unknown origin were observed in 12 cases (18.8%). These amyloid deposits were found mainly in medium-sized veins in the lungs and did not react with any antibodies against amyloid fibril proteins except apolipoprotein E and amyloid P component. Eleven of the 26 cases (42.3%) showing portal amyloid also showed pulmonary vascular amyloid of unknown origin. The pulmonary vascular amyloid deposits were similar to the portal amyloid deposits with respect to their morphological features and their relation to elastic fibers in the vessels. Further morphological investigation and biochemical analysis of the pulmonary vascular amyloid and portal amyloid will resolve questions of their origins and relation. [source] A 2-DE MALDI-TOF study to identify disease regulated serum proteins in lung cancer of c-myc transgenic micePROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 4 2009Bijon Chatterji Abstract We previously reported targeted overexpression of c-myc to alveolar epithelium to cause lung cancer. We now extended our studies to the serum proteome of tumor bearing mice. Proteins were extracted with a thiourea-containing lysis buffer and separated by 2-DE at pH,4,7 and 3,10 followed by MALDI-TOF/TOF analysis. Forty-six proteins were identified in tumor bearing mice of which n,=,9 were statistically significant. This included disease regulated expression of orosomucoid-8, ,-2-macroglobulin, apolipoprotein-A1, apolipoprotein-C3, glutathione peroxidase-3, plasma retinol-binding protein, and transthyretin, while expression of apolipoprotein-E was decreased at late stages of disease. Moreover, serum amyloid P component was uniquely expressed at late stages of cancer. It is of considerable importance that most disease regulated proteins carried the E-Box sequence (CACGTG) in the promoter of the coding gene, therefore providing evidence for their regulation by c-myc. Notably, expression of ,-2-macroglobulin, transthyretin, ,-1-antitrypsin, and properdin was in common in different lung tumor models, but regulation of orosomucoid-8, apolipoprotein-A1, apolipoprotein-C3, apolipoprotein-E, glutathione peroxidase-3, plasma retinol-binding protein, and serum amyloid P component was unique when the serum proteomes of c-myc and c-raf tumor bearing mice were compared. Therefore, candidate biomarkers to differentiate between atypical adenomatous hyperplasias (AAH) and bronchiolo-alveolar carcinomas (BAC)/papillary adenocarcinomas (PLAC) can be proposed. [source] Lack of effect of a single injection of human C-reactive protein on murine lupus or nephrotoxic nephritisARTHRITIS & RHEUMATISM, Issue 1 2010Francesco Carlucci Objective It has been reported that a single dose of human C-reactive protein (CRP) can prevent and reverse the renal damage in murine models of spontaneous lupus, as well as the rapid-onset immune complex disease induced in the accelerated nephrotoxic nephritis (ANTN) model. This study was undertaken to attempt to replicate these observations using a highly purified and fully characterized human CRP preparation. Methods (NZB × NZW)F1 (NZB/NZW) mice were treated with a single 200-,g subcutaneous injection of CRP or control reagents either before disease onset at 4 months of age or when high-grade proteinuria was present at 7 months of age. Mice were monitored at least monthly for proteinuria and autoantibody levels. ANTN was induced by preimmunizing C57BL/6 mice with sheep IgG, followed 5 days later by injection of sheep anti-mouse glomerular basement membrane antibody and CRP or control reagents. Renal disease was assessed by regular urinalysis and histologic evaluation. Results CRP treatment of NZB/NZW mice, either early or late in the disease, had no effect on proteinuria, autoantibody titers, or survival. CRP administration did not reduce renal injury or alter disease in the ANTN model. Human serum amyloid P component, a pentraxin protein that is very closely related to CRP, similarly had no effect. Conclusion Our completely negative observations do not confirm that human CRP has reproducible antiinflammatory or immunomodulatory effects in these murine models, nor do they support the suggestion that CRP might be useful for therapy of lupus or immune complex,mediated nephritis. [source] Pentraxins: Multifunctional proteins at the interface of innate immunity and inflammationBIOFACTORS, Issue 2 2009Livija Deban Abstract Pentraxins are a family of multimeric pattern recognition proteins highly conserved in evolution. On the basis of the primary structure of the protomer, pentraxins are divided into two groups: short pentraxins and long pentraxins. C reactive protein, the first pattern recognition receptor identified, and serum amyloid P component are classic short pentraxins produced in the liver in response to IL-6. Long pentraxins, including the prototype PTX3, are expressed in a variety of tissues. PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. Through interaction with several ligands, including selected pathogens and apoptotic cells, pentraxins play a role in complement activation, pathogen recognition and apoptotic cell clearance. In addition, PTX3 is involved in the deposition of extracellular matrix and female fertility. Unlike the classic short pentraxins CRP and SAP, PTX3 primary sequence and regulation are highly conserved in man and mouse. Thus, gene targeting identified PTX3 (and presumably other members of the family) as multifunctional soluble pattern recognition receptors acting as a nonredundant component of the humoral arm of innate immunity and involved in tuning inflammation, matrix deposition, and female fertility. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] Suggestive linkage of familial primary cutaneous amyloidosis to a locus on chromosome 1q23BRITISH JOURNAL OF DERMATOLOGY, Issue 1 2005M-W. Lin Summary Background, There is a high incidence of primary cutaneous amyloidosis (PCA) in South America, South-east Asia and Taiwan. To date, the aetiology of PCA remains unknown, but it is believed to be multifactorial. Although most cases are sporadic, some patients have a family history. Familial aggregation and different susceptibility to PCA among ethnic groups suggest that genetic factors may play an important role in its pathogenesis. However, no genetic loci for familial PCA (FPCA) have been identified so far. Objectives, In order to identify the susceptibility gene of FPCA, we took a candidate gene approach and performed linkage analysis on chromosome 1q21.3,24.2, including the 1q23.2 region where the gene encoding serum amyloid P component (APCS) is located. Patients and methods, Nine FPCA families including 29 individuals affected with PCA were recruited for this linkage study. Initially, 11 highly polymorphic microsatellite markers spanning the region from 1q21.3 to 1q24.2 were genotyped and revealed a suggestive linkage region. This region was further fine-mapped with seven additional markers. We also re-sequenced the 2·5-kb genomic region of the APCS gene in 29 affected and 42 control individuals. Two-point and multipoint linkage analyses were performed using the LINKAGE program. Nonparametric linkage (NPL) analysis and reconstruction of haplotypes were performed with the GENEHUNTER program. Results, Both two-point and multipoint linkage analysis for all 11 markers generated negative or small positive total lod scores for all nine families. However, when we considered only three families, a maximum two-point total lod score of 2·09 was obtained for the marker D1S2844 at , = 0·01. A plateau of multipoint total lod score between D1S2768 and D1S2878 with a maximum of 2·48 at the marker D1S2844 was observed. A maximum NPL score of 3·11 (P = 0·008) was also obtained for the marker D1S2878. However, re-sequencing of the APCS gene identified no functional mutation. Conclusions, Both parametric and nonparametric linkage evidence suggested that a possible susceptibility locus for a subset of FPCA might exist on chromosome 1q23. This is the first report demonstrating suggestive evidence of linkage of FPCA to a locus in this candidate region. No functional sequence variations of the APCS gene were found to be associated with this disease among the study families. Our data imply the existence of at least one additional locus responsible for FPCA in these families, confirming genetic heterogeneity of this skin disorder. [source] Upper mantle stratification by P and S receiver functionsGEOPHYSICAL JOURNAL INTERNATIONAL, Issue 3 2000Véronique Farra Summary Seismic stratification of the upper mantle is investigated by applying two complementary techniques to the records of the Graefenberg array in southern Germany. The anisotropic P receiver function technique (Kosarev et al. 1984; Vinnik & Montagner 1996) is modified by using summary seismic events instead of individual events and different weighting functions instead of the same function for the harmonic angular analysis of the SV and T components of the Pds phases. The summary events provide better separation of the second azimuthal harmonic than the individual events. The parameters of the second harmonics of SV and T thus evaluated should be similar if they reflect the effects of azimuthal anisotropy. This can be used as a criterion to identify the anisotropy. To detect the Sdp phases and their azimuthal variations caused by azimuthal anisotropy we have developed a stacking technique, which can be termed the S receiver function technique It includes axis rotation to separate interfering P and S arrivals, determination of the principal (M) component of the S -wave motion, deconvolution of the P components of many recordings by their respective M components and stacking of the deconvolved P components with weights depending on the level of noise and the angle between the M direction and the backazimuth of the event. Both techniques yield consistent results for the Graefenberg array. As indicated by the P receiver functions, the upper layer of the mantle between the Moho and 80 km depth is anisotropic with dVs/Vs around 0.03 and the fast direction close to 20° clockwise from north. The fast direction of anisotropy below this layer is around 110°, The boundary between the upper and the lower anisotropic layers is manifested by the detectable Pds and Sdp converted phases. Shear wave splitting in SKS is strongly dominated by azimuthal anisotropy in the lower layer (asthenosphere). [source] | ||||||||||