Aspergillus fumigatus diffusates suppress polymorphonuclear neutrophil phagocytic functions and respiratory burst levels in hematopoietic stem cell transplantation patients.

Invasive aspergillosis (IA) is a severe infection that commonly occurs in immunocompromised patients after hematopoietic stem cell transplantation (HSCT). The present study explores the effect of Aspergillus fumigatus diffusates (AfDs) on phagocytic function and superoxide anion (O2(-)) burst levels in polymorphonuclear neutrophils (PMNs) from post-HSCT patients. A. fumigatus conidia with or without AfD were used to stimulate the PMN from healthy donor or HSCT patient for two hours. PMN morphology was visualized by scanning electron microscopy. The levels of respiratory burst O2(-) produced by the PMNs were determined by flow cytometry. PMN phagocytic rates and phagocytic indexes were observed and calculated using periodic acid-Schiff (PAS) staining under a light-field microscope. No difference was found between the PMN phagocytic rates, phagocytic indexes, or O2(-) respiratory burst levels in health donor PMNs following treatments of A. fumigatus conidia with or without AfD. However, significant inhibition of these indices was seen in the PMNs from HSCT patients following treatment of A. fumigatus conidia plus AfD, compared to that with conidium treatment alone (P < 0.05). Therefore, AfD significantly inhibited the phagocytic function of PMNs from HSCT patients, potentially through inhibition of intracellular respiratory burst levels during phagocytosis. This suggests that the reason underlying the greater susceptibility of HSCT patients to aspergillosis might be the existence of AfD in vivo during infection. Further research on the mechanisms by which AfD affects the phagocytic function of PMNs from HSCT patients is therefore of great significance for the prevention of IA.

Association of PELI1 polymorphisms in systemic lupus erythematosus susceptibility in a Chinese population.

OBJECTIVE: Studies in animal models have indicated that Pellino 1 is involved in inflammatory and autoimmune diseases, such as systemic lupus erythematosus (SLE). The current study was designed to determine whether PELI1 confers genetic susceptibility to SLE in humans, as assessed in a Chinese Han population. METHODS: Blood samples were drawn from patients diagnosed with SLE and healthy volunteers. Three single nucleotide polymorphism (SNP) loci with a minor allele frequency of at least 0.05 were chosen to evaluate the correlation between PELI1 genotype and the incidence of SLE. RESULTS: There was a significant difference in the frequency distribution of the rs329497 allele between the SLE patients and the healthy controls (A vs. G; Bonferroni corrected p = 0.036, odds ratio = 0.75, 95% confidence interval = 0.60-0.94). No differences in the genotype and allele frequencies of other SNP loci were observed between the two groups. Furthermore, the alleles and genotypes of the three SNPs were not associated with lupus nephritis. CONCLUSION: In the Chinese Han population, PELI1 SNPs may be associated with SLE susceptibility.

[Production and identification of the monoclonal antibodies specific for MHC class I complexes bound with HPV16E7 CTL epitopic peptide.].

BACKGROUND: To produce specific monoclonal-antibodies (MAbs) for MHC class I complexes bound with HPV16E7 CTL epitopic peptide (49-57), and provide a foundation for the investigation of the present pathway of viral antigen protein after in vitro viral infection. METHODS: Highly purified HPV16E7CTL epitope (49-57) (RAHYNIVTF) was produced, and then TAP deficient RMA-S cells incubated with RAHYNIVTF were used to immunize the BALB/c mouse. The spleen cells of the mice were regularly harvested and fused with the SP2/0 cells. The growing fusion wells were screened and the abstracted Mabs were identified in terms of sensitivity, specificity and affinity. RESULTS: The screened hybriroma cells could steadily secrete the MAbs specific for MHC class I complexes bound with HPV16E7CTL epitopic peptide. The MAbs showed high reactivity with TAP-deficient RMA-S cells loaded with RAHYNIVTF and RMA-S cells which have the ability to process the endogenous MHC class I complexes, while minimally bound to class I molecules bearing other peptides, the results indicated excellent sensitivity, specificity and affinity of the MAbs. CONCLUSION: The experiments provide a method for producing MAbs for epitopic peptide bound MHC class I complexes.

Gene profiling involved in immature CD4+ T lymphocyte responsible for systemic lupus erythematosus.

We attempted to characterize the genes expression of CD4+ T lymphocytes for the pathogenesis of systemic lupus erythematosus (SLE). Genomewide gene expression profiles of CD4+ T cells, which were isolated from the disease severe activity (T4-1s) and nonactivity (T4-2s) with an SLE patient by using long serial analysis of gene expression (LongSAGE). We picked out 289 genes matching to Unigene cluster with different expression more than four copies between T4-1s and T4-2s libraries and analyzed their roles from the collectedly published articles of PubMed by genes functional clustering. The genes functions were related to a diverse cellular process including: (1) most of these genes were associated with CD4+ T cells functions, particularly related to cellular developments; (2) Ras pathway genes as RANBP10, GMIP, RASGRP2 and ARL5 might be responsible for the abnormal development of CD4+ T cells of SLE; (3) HIG2, TCF7, KHSRP, WWP1, SMAD3, TLK2, AES, CCNI and PIM2 belong to Wnt/beta-catenin way, they could play roles in modulating proliferation and differentiation of T lymphocytes; (4) uncertain viral infections may initiate autoimmunity because high levels expression genes were detected in T4-1s such as TRIM22, IER2, ABCE1, DUT, G1P2, G1P3, HNRPUL1, EVER2, IFNAR1, TNFSF14, TMP21 and PVRL2; and (5) apoptosis relating genes as EIF3S8, SH3BGRL3, GPX4, TOSO, PFDN5, BIN1, XIAPAF1, TEGT and CUGBP2 may contribute to over uploading of selfantigens in SLE cells. Abnormalities findings of multiple genes expression involving with a variety of CD4+ T cells process might be meaningful to understanding the pathogenesis of SLE, and immature CD4+ T cells may be responsible for SLE.

A comparative study of third-order nonlinear optical properties of silver phenylacetylide and related compounds via ultrafast optical Kerr effect measurements.

A comparative study of the third-order nonlinear optical properties, via the newly developed heterodyned optical Kerr effect (OHD-OKE) measurements, of silver phenylacetylide and related compounds is reported. [AgC[triple bond]CC(6)H(5)](n) (1) was found to exhibit efficient third-order nonlinear optical susceptibility chi((3)) of 2.4 x 10(-14) esu, and second hyperpolarizability gamma of 9.07 x 10(-32) esu. These results are compared with those of two related silver phenylacetylide compounds, namely, a double salt, (silver phenylacetylide).(silver tert-butylthiolate) [AgC[triple bond]CC(6)H(5).AgS(t-C(4)H(9))](n) complex (2), and a cluster, triphenylphosphine silver phenylacetylide tetramer, [(C(6)H(5))(3)PAgC[triple bond]CC(6)H(5)](4) (3), as well as that of the related organic polymer polyphenylacetylene (4). These four compounds represent different types of phenylacetylide derivatives: 1 is an organometallic polymer, 2 a polymeric double salt, 3 a discrete metal cluster, and 4 an organic polymer. It was found that the third-order optical nonlinear response was enhanced by the incorporation of silver d electrons into the delocalized conjugated organic pi system, and its magnitude is highly dependent upon the extent of the pi delocalization. Specifically, the relative magnitudes of chi((3)) and gamma follow the order silver phenylacetylide polymer (1) > (silver phenylacetylide).(silver tert-butylthiolate) double salt (2) > polyphenylacetylene polymer (4) > tetrameric (triphenylphosphine silver phenylacetylide)(4) cluster (3). The observed trend may be attributed to the decreasing length of pi conjugation. It is interesting to note that the incorporation of Ag(I) into the polymeric framework of polyphenylacetylene enhances the chi((3)) by 25-fold for the same degree of polymerization (n = 7). The signs of chi((3)) and gamma, which are related to the response mechanisms, were found to be solvent dependent.