bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cutaneous and other lupus-like symptoms in carriers of X-linked chronic granulomatous disease: incidence and autoimmune serology
Authors: Cale C M , Morton L , Goldblatt D 
Published: August 2010

Summary
The objective of this study was to determine the utility of anti-nuclear antibody (ANA) testing in the investigation of cutaneous and other lupus symptoms in female carriers of X-linked chronic granulomatous disease (CGD). We undertook a prospective study of 19 carrier mothers attending our institution, with direct questioning of carriers concerning symptoms and testing for anti-nuclear and anti-phospholipid antibodies. A total of 58% reported significant photosensitive skin rashes, 42% reported mouth ulcers and 37% complained of joint pains that could not be attributed to other known causes. Anti-nuclear antibody (ANA) testing was negative in 73% of all carriers. The five positive ANAs were of low titre (maximum 1 : 320 on Hep 2 cells in two women) and only one weak positive double-stranded DNA antibody and no extractable nuclear antibodies were found. Several of the mothers, despite negative serology, benefited from referral to a specialist, and in some cases to specific treatment. A history of skin rashes, joint pain, fatigue and mouth ulcers should be sought actively in the female relatives of X-CGD patients but negative lupus serology should not preclude referral to appropriate dermatology or rheumatology services. as symptoms may respond well to appropriate treatment.
Vasoactive intestinal polypeptide enhances oral tolerance by regulating both cellular and humoral immune responses
Authors: Wang Y , Mei Y , Bao S , Xu L 
Published: August 2010

SummaryVasoactive intestinal polypeptide (VIP) is an important signal molecule of the neuroendocrine–immune network. In the immune system, VIP has been found to act as an endogenous anti-inflammatory mediator. In the current study, it was found that VIP administration regulated oral tolerance by inhibiting both cellular and humoral responses. Compared with vehicle-treated mice, mice treated with VIP during the development of ovalbumin (OVA)-induced oral tolerance exhibited the least delayed-type hypersensitivity (DTH), showed profoundly reduced proliferative capacity and produced less interferon (IFN)-γ, interleukin (IL)-6, IL-5, IL-10 and interferon-inducible protein (IP-10). IgA-secreting cells in the gut as well as OVA-specific IgG and other isotypes levels in plasma were inhibited significantly after VIP-treatment. The VPAC2 receptor may be involved in VIP-mediated oral tolerance enhancement. Taken together, these results suggest that VIP enhanced oral tolerance via regulating both cellular and humoral responses.
Ultraviolet B irradiation selectively increases the production of interleukin-8 in human cord blood-derived mast cells
Authors: Endoh I , Di Girolamo N , Hampartzoumian T , Cameron B , Geczy C L , Tedla N 
Published: August 2010

SummaryUVB irradiation modulates immune responses in the skin and is a major cause of sunburn, during which neutrophils accumulate in the skin. Because of their abundance in skin and ability to produce a variety of proinflammatory mediators, we propose that mast cells may play a key role in ultraviolet B (UVB)-induced skin inflammation. Cord blood-derived human mast cells were treated in vitro with varying doses of UVB and production of multiple cytokines was measured in culture supernatants. UVB exposure significantly increased the release of interleukin (IL)-8 and modestly increased IL-1α production, but cytokines such as IL-2, IL-4, IL-6, IL-10, IL-12, IL-13, tumour necrosis factor (TNF)-α and interferon (IFN)-γ were unaffected. Cycloheximide reduced the UVB-mediated induction of IL-8 by 30–40%, suggesting that new protein synthesis contributed to IL-8 production. In line with this, UVB treatment of mast cells significantly increased IL-8 mRNA. In contrast to its effect on IL-8 production, optimal doses of UVB did not provoke histamine or tryptase release, indicating little effect on degranulation. Our data suggest that mast cells may play a major role during UVB-induced acute inflammation by selectively inducing cytokines involved in neutrophil recruitment.
Allergic sensitization and microbial load – a comparison between Finland and Russian Karelia
Authors:   The EPIVIR study group, Seiskari T , Kondrashova A , Viskari H , Kaila M , Haapala A-M , Aittoniemi J , Virta M , Hurme M , Uibo R , Knip M , Hyöty H 
Published: August 2010

Summary
Epidemiological data have indicated that some infections are associated with a low risk of allergic diseases, thus supporting the idea (hygiene hypothesis) that the microbial load is an important environmental factor conferring protection against the development of allergies. We set out to test the hygiene hypothesis in a unique epidemiological setting in two socio-economically and culturally markedly different, although genetically related, populations living in geographically adjacent areas. The study cohorts included 266 schoolchildren from the Karelian Republic in Russia and 266 schoolchildren from Finland. The levels of total IgE and allergen-specific IgE for birch, cat and egg albumen were measured. Microbial antibodies were analysed against enteroviruses (coxsackievirus B4), hepatitis A virus, Helicobacter pylori and Toxoplasma gondii. Although total IgE level was higher in Russian Karelian children compared to their Finnish peers, the prevalence of allergen-specific IgE was lower among Russian Karelian children. The prevalence of microbial antibodies was, in turn, significantly more frequent in the Karelian children, reflecting the conspicuous difference in socio-economic background factors. Microbial infections were associated with lower risk of allergic sensitization in Russian Karelian children, enterovirus showing the strongest protective effect in a multivariate model. The present findings support the idea that exposure to certain infections, particularly in childhood, may protect from the development of atopy. Enterovirus infections represent a new candidate to the list of markers of such a protective environment. However, possible causal relationship needs to be confirmed in further studies.
Complement activation and cytokine response by BioProtein, a bacterial single cell protein
Authors: Sikkeland L I B , Thorgersen E B , Haug T , Mollnes T E 
Published: August 2010

SummaryThe bacterial single cell protein (BSCP), BioProtein, is dried bacterial mass derived from fermentation of the gram negative bacteria Methylococcus capsulatus, used for animal and fish feed. Workers in this industry suffer frequently from pulmonary and systemic symptoms which may be induced by an inflammatory reaction. The aim of the present study was to examine the effect of BSCP on inflammation in vitro as evaluated by complement activation and cytokine production. Human serum was incubated with BSCP and complement activation products specific for all pathways were detected by enzyme-linked immunosorbent assay (ELISA). Human whole blood anti-coagulated with lepirudin was incubated with BSCP and a panel of 27 biological mediators was measured using multiplex technology. BSCP induced a dose-dependent complement activation as revealed by a pronounced increase in alternative and terminal pathway activation (fivefold and 20-fold, respectively) at doses from 1 µg BSCP/ml serum and a similar, but less extensive (two- to fourfold) increase in activation of the lectin and classical pathways at doses from 100 and 1000 µg BSCP/ml serum, respectively. Similarly, BSCP induced a dose-dependent production of a number of cytokines, chemokines and growth factors in human whole blood. At doses as low as 0·05–0·5 µg BSCP/ml blood a substantial increase was seen for tumour necrosis factor (TNF)-α, interleukin (IL)-1-β, IL-6, interferon (IFN)-γ, IL-8, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, MIP-1β, IL-4, IL-9, IL-17, IL-1Ra, granulocyte–colony-stimulating factor (G-CSF) and vascular endothelial growth factor (VEGF). Thus, BSCP induced a substantial activation of all three initial complement pathways as well as a pronounced cytokine response in vitro, indicating a potent inflammatory property of this agent.
Proteins specifically hyperexpressed in a coeliac disease patient with aberrant T cells
Authors: De Re V , Simula M P , Caggiari L , Orzes N , Spina M , Da ponte A , De Appollonia L , Dolcetti R , Canzonieri V , Cannizzaro R 
Published: August 2010

Summary
An aberrant T cell population is the basis for diagnosis of refractory coeliac disease and determines the risk of enteropathy-associated T cell lymphoma. This disease is serious with a poor survival. Pathogenetic mechanisms sustaining aberrant T cell proliferation remain unknown. Recently, alemtuzumab has been proposed as a promising new approach to treat these patients. Only few single cases have been tested at present; nevertheless, in all the cases a clinical improvement was observed. However, whether intraepithelial lymphocytes have been targeted effectively by alemtuzumab is still debated. This study reports, using two-dimensional difference gel electrophoresis (2D DIGE), hyperexpressed proteins associated specifically with aberrant T cells found in a patient with coeliac disease by comparison of the protein expression of this sample with that of patients with coeliac disease and polyclonal T cells or with control subjects. The data demonstrated a significantly higher expression of IgM, apolipoprotein C-III and Charcot–Leyden crystal proteins in a duodenal biopsy specimen of the patient with clonal T cells compared with that of other patients. These preliminary results allow hypothesizing different clinical effects of alemtuzumab in patients with coeliac disease and aberrant T cell proliferation, because as well as the probable effect on T cells, alemtuzumab could exert its effect by acting on inflammatory associated CD52+ IgM+ B cells and eosinophil cells, known to produce IgM and Charcot–Leyden crystal proteins, that we demonstrated to be altered in this patient. The results also emphasize the possible association of apolipoprotein with aberrant T cell proliferation.
Mucosal and peripheral immune responses to chlamydial heat shock proteins in women infected with Chlamydia trachomatis
Authors: Agrawal T , Vats V , Salhan S , Mittal A 
Published: August 2010

Summary
Most of the studies on 60-kDa and 10-kDa chlamydial heat shock proteins (HSPs) to date have been carried out with blood lymphocytes or serum antibody responses, which do not provide a clear picture of the actual pathogenesis as they do not differentiate primary infection from recurrent infection. Thus, in the present study induction of the immune response was evaluated by studying lymphoproliferation of both cervical and peripheral lymphocytes to synthetic peptides of cHSP60, cHSP10 and major outer membrane protein (MOMP) antigen. In addition, cervical antibody prevalence to MOMP antigen, cHSP60 and cHSP10 and cytokine levels in cervical washes was also determined. Positive proliferative responses of cervical lymphocytes to cHSP10 peptide were significantly higher (P &lt; 0·05) in women with recurrent infections and that to MOMP antigen were significantly higher in primary infection. On proliferation of PBMCs with the above antigens, no significant difference was observed between primary and recurrent infection. Prevalence of cervical IgG and IgA antibodies to Chlamydia trachomatis was significantly higher (P &lt; 0·05) during primary infection than recurrent infections. In contrast, prevalence of IgG and IgA antibodies to cHSP10 and IgG antibodies to cHSP60 was higher during recurrent infections than primary infections. Interferon (IFN)-γ levels were significantly higher in cervical washes of women with recurrent infection and correlated strongly with cHSP60 antibody titres. Our data thus suggest that mucosal responses are more appropriate in understanding the pathogenesis of chlamydial infection and IFN-γ could be involved in the modulation of immune responses towards chlamydial infection directly, by causing acute inflammation, or indirectly through modulation of HSP expression.
P2X7 and NRAMP1/SLC11 A1 gene polymorphisms in Mexican mestizo patients with pulmonary tuberculosis
Authors: Niño-Moreno P , Portales-Pérez D , Hernández-Castro B , Portales-Cervantes L , Flores-Meraz V , Baranda L , Gómez-Gómez A , Acuña-Alonzo V , Granados J , González-Amaro R 
Published: August 2010

SummaryTuberculosis remains one of the most important infectious diseases worldwide. Several studies have suggested that genetic factors may affect susceptibility to tuberculosis, but the specific genes involved have not yet been fully characterized. NRAMP1/SLC11 A1 and P2X7 genes have been linked to increased risk for tuberculosis in some African and Asiatic populations. To explore the potential role of these genes in the susceptibility to pulmonary tuberculosis in a Mexican mestizo population, we evaluated the association of D543N and 3′-UTR polymorphisms in NRAMP1/SLC11 A1 and − 762 and A1513C polymorphisms in P2X7 genes with the risk for tuberculosis. Polymerase chain reaction (PCR) amplification of genomic DNA followed by restriction fragment length polymorphism analysis, and allelic-specific PCR was employed. We found no significant differences in allelic frequency in NRAMP1/SLC11 A1 gene polymorphisms in 94 patients with tuberculosis compared to 100 healthy contacts. Similarly, no significant association of the P2X7−762 gene polymorphism with tuberculosis was detected. In contrast, the P2X7 A1513C polymorphism was associated significantly with tuberculosis (P = 0·02, odds ratio = 5·28, 95% CI, 0·99–37·69), an association that had not been reported previously. However, when the function of P2X7 was assessed by an l-selectin loss assay, we did not find significant differences in patients compared to healthy contacts or between PPD+ and PPD– control individuals. This study further supports the complex role of P2X7 gene in host regulation of Mycobacterium tuberculosis infection, and demonstrates that different associations of gene polymorphisms and tuberculosis are found in distinct racial populations.
Effect of leptin on activation and cytokine synthesis in peripheral blood lymphocytes of malnourished infected children
Authors: Rodríguez L , Graniel J , Ortiz R 
Published: August 2010

SummaryMalnutrition compromises immune function, resulting in reduced resistance to infection. Recent animal and human studies have suggested that leptin is capable of modulating the immune response and that its levels, which are regulated by nutritional status, fall rapidly during starvation. Leptin deficiency is associated with impaired cell-mediated immunity, an increased incidence of infectious disease and an associated increase in mortality. The purpose of this study was to examine the effect of leptin on activation and cytokine production in peripheral blood T cells from malnourished children. The data obtained in the present study demonstrate that leptin produced an increase in the percentage of CD4+ and CD8+ cells producing interleukin (IL)-2 and interferon (IFN)-γ in 24-h cultures. Moreover, leptin decreased the percentage of CD4+ and CD8+ cells producing IL-4 and IL-10, and enhanced activation of circulating T cells when co-stimulated by phorbol 12-myristate 13 acetate (PMA)–ionomycin. Leptin enhanced the expression of activation markers CD69 and CD25 in both CD4+ and CD8+ cells after 5 h of stimulation. In conclusion, the results obtained show that leptin modulates CD4+ and CD8+ cell activation towards a T helper 1 (Th1) phenotype by stimulating the synthesis of IL-2 and IFN-γ. In contrast, leptin decreases IL-4 and IL-10 production. Moreover, leptin enhanced the expression of CD69 and CD25 on CD4+ and CD8+ cells after stimulation with PMA–ionomycin.
Low molecular weight proteins of outer membrane ofSalmonella typhimuriumare immunogenic inSalmonellainduced reactive arthritis revealed by proteomics
Authors: Singh R , Shasany A K , Aggarwal A , Sinha S , Sisodia B S , Khanuja S P S , Misra R 
Published: August 2010

SummaryIn patients with reactive arthritis (ReA)/undifferentiated spondyloarthropathy (uSpA), synovial fluid mononuclear cells (SFMC) show proliferation to bacterial antigens that trigger ReA, i.e. Chlamydia, Yersinia, Campylobactor, Shigella and Salmonella species. We have shown previously that SFMC proliferate significantly to outer membrane proteins of S typhimurium in Salmonella induced ReA. In the present study we characterized the immunoreactive fractions of outer membrane protein (Omp) of S typhimurium in Salmonella induced ReA. Omp of Salmonella was isolated and fractionated by continuous elution sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) using Prep-Cell into eight Omp fractions based on molecular weight. Twenty-three patients with ReA were screened for the bacterial trigger using the SFMC proliferative response to crude lysates of Y enterocolitica, S flexneri, C jejuni and S typhimurium using thymidine uptake assay. SFMC from patients with salmonella induced ReA were tested against eight fractions. Seven of 23 patients with ReA had S typhimurium-induced ReA. Of these seven patients, five patients SFMC had a significant stimulation index (SI) against &lt; 22, 22–26, 25–35 and 28–40 kDa fractions of Omp. These fractions were analysed by SDS-PAGE and matrix-assisted laser desorption ionization time-of-flight (MALDI-TOF) mass spectrometry, which revealed 10 proteins. These proteins were 37 kDa OmpA, 33 kDa TsX, 28 kDa putative Omp, 28 kDa Vac J, 39 kDa OmpD, 18 kDa OmpX, 23 kDa OmpW, 43 kDa OmpS1 and 19 kDa peptidoglycan-associated lipoprotein. In conclusion, for the first time we have identified some low molecular weight proteins in the Omps of Salmonella which are T cells immunoreactive in patients with salmonella induced ReA/uSpA.
Differential binding characteristics of native monomeric and polymeric immunoglobulin A1 (IgA1) on human mesangial cells and the influence ofin vitrodeglycosylation of IgA1 molecules
Authors: Gao Y-H , Xu L-X , Zhang J-J , Zhang Y , Zhao M-H , Wang H-Y 
Published: August 2010

SummaryRecent studies had demonstrated that serum and mesangial immunoglobulin A1 (IgA1) in patients with IgA nephropathy (IgAN) were polymeric and deglycosylated. The current study was to investigate the binding characteristics of monomeric and polymeric normal human IgA1 on mesangial cells and the influence of in vitro deglycosylation of IgA1 molecules. The normal human IgA1 was desialylated and degalactosylated with specific enzymes, respectively. The monomeric IgA1 (mIgA1) and polymeric IgA1 (pIgA1) were separated by Sephacryl S-300 chromatography. The binding capacities of the mIgA1 and pIgA1 to primary human mesangial cells (HMC) were evaluated by classical radioligand assay. Both the native mIgA1 and pIgA1 could bind to HMC in a dose-dependent and saturable manner. The maximal binding capacity of the native pIgA1 were significantly higher than that of the native mIgA1 (P &lt; 0·05). However, the affinity of the native mIgA1 was almost 100 times higher than that of the native pIgA1. After deglycosylation, binding of the two deglycosylated mIgA1 to HMC could not be detected. However, the maximal binding capacities of the two deglycosylated pIgA1 to HMC were increased significantly compared with that of native pIgA1. The affinity of the two deglycosylated pIgA1 was similar to that of native pIgA1 (P &gt; 0·05). The current study suggests differential binding characteristics of native monomeric and polymeric IgA1 on mesangial cells. Glycosylation of IgA1 molecules could significantly affect the binding of IgA1 on HMC.
Autoantibodies to plasminogen and tissue plasminogen activator in women with recurrent pregnancy loss
Authors: Bu C , Zhang C , Li Z , Gao L , Xie Z , Cai G 
Published: August 2010

Summary
Reduced fibrinolytic activity has been described in primary anti-phospholipid syndrome (PAPS), and may be responsible for thrombotic events. Antibodies to tissue type plasminogen activator (t-PA) or plasminogen (PLG) might contribute to the hypofibrinolytic state in autoimmune diseases, but the clinical significance of these antibodies is still unclear in recurrent pregnancy loss (RPL). The aim of this study is to evaluate the prevalence and clinical significance of anti-PLG and anti-t-PA antibodies in 87 patients with a history of RPL: 54 women with well-defined PAPS (mean age 32·5 years; range 26–38) and 33 women with unexplained RPL (mean age 30 years; range 24–39). IgG anti-PLG antibodies were found in 20 and four patients from the group with RPL/PAPS and unexplained RPL, respectively; IgG anti-t-PA antibodies were found in 11 and two patients from the above two groups, respectively. IgG anti-PLG antibodies were associated with the high risk of RPL (OR 7·2, P = 0·004), especially with RPL/PAPS (OR 11·2, P &lt; 0·001) evaluated by Fisher's exact test, while IgG anti-t-PA were associated with RPL/PAPS (OR 10·0, P = 0·01) but not with RPL (OR 6·8, P = 0·06). A significant inhibition of exogenous fibrinolysis was observed by IgG fractions from patients with anti-PLG or anti-t-PA antibodies on microplates and on the human umbilical vein endothelial cells, compared with those from healthy controls. The prevalence of IgG anti-PLG antibodies was high in RPL patients, especially in RPL/PAPS, while the prevalence of IgG anti-t-PA antibodies was high in RPL/PAPS but not in RPL, and some of them might inhibit fibrinolysis in patients.
Low mannose-binding lectin complement activation function is associated with predisposition to Legionnaires' disease
Authors: Eisen D P , Stubbs J , Spilsbury D , Carnie J , Leydon J , Howden B P 
Published: August 2010

SummaryInnate immune system deficiency may predispose to severe infections such as Legionnaires' disease. We have investigated the role of mannose-binding lectin (MBL) deficiency in the Melbourne Aquarium Legionnaires' disease outbreak. Serum samples from patients and controls that were exposed but shown to be uninfected from the Melbourne Aquarium Legionnaires' disease outbreak were tested for MBL function (C4 deposition) and level (mannan-binding). MBL function was lower in Legionnaires' disease cases than in age- and sex-matched uninfected, exposed controls. The frequency of MBL deficiency with C4 deposition &lt; 0·2 U/µl was significantly higher in Legionnaires' disease cases than in controls. This also applied to Legionnaires' disease cases requiring hospital care. There was no difference in MBL mannan-binding levels between Legionnaires' disease patients and controls. There was no significant interval change in MBL function or level after a mean of 46 days. MBL complement activation functional deficiency appears to predispose to Legionnaires' disease.