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S Ying

Publications and source records attributed to S Ying.

84 records · Page 5Linked to original sources
PubMed1991

TNF alpha mRNA expression in allergic inflammation.

Using the technique of in situ hybridization, we have attempted to identify messenger RNA for tumour necrosis factor-alpha (TNF alpha) in cells infiltrating allergen-induced late phase reaction (LPR) of the skin and the nose of atopic subjects. We have also compared the number of TNF alpha mRNA positive cells in bronchoalveolar lavage (BAL) from atopic asthmatics and normal controls. Twenty-four hours after local allergen challenge, 12/14 skin biopsies and 9/10 nasal biopsies had positive hybridization signals for TNF alpha mRNA whereas only 4/14 and 2/10 biopsies were positive in the relevant diluent controls. Compared with diluent sites significantly increased numbers of cells expressing mRNA for TNF alpha were observed in the LPR of skin (P less than 0.004) and nose (P less than 0.006). All BAL from asthmatics (n = 10) and from normal volunteers (n = 10) had cells showing positive hybridization signals for TNF alpha mRNA but these were at increased frequency in asthmatics (P less than 0.001). These results suggest that TNF alpha may be an important cytokine in atopic allergic inflammation.

Adolescent↗
PubMed1991

Interleukin-5 mRNA in mucosal bronchial biopsies from asthmatic subjects.

Using in situ hybridization, we have investigated the expression of interleukin-5 (IL-5) mRNA in bronchial biopsies from asthmatics (n = 10) and controls (n = 9). The number of IL-5-nRNA-positive cells were compared with the number of CD25+ and EG2+ cells and total eosinophil counts. Specific hybridization signals for IL-5 mRNA were demonstrated in 6 out of the 10 asthmatic subjects but in none of the controls. The 6 IL-5-mRNA-positive asthmatics tended to have more severe disease and showed a significant increase in the degree of infiltration of the bronchial mucosa by activated T lymphocytes and eosinophils.

Asthma↗
PubMed1991

Expression of mRNA for interleukin-5 in mucosal bronchial biopsies from asthma.

We have attempted to identify mRNA for IL-5 in endobronchial mucosal biopsies from asthmatics and controls, using the technique of in situ hybridization. Bronchial biopsies were obtained from 10 asthmatics and 9 nonatopic normal controls. A radio-labeled cRNA probe was prepared from an IL-5 cDNA and hybridized to permeabilized sections. These were washed extensively before processing for autoradiography. An IL-5-producing T cell clone derived from a patient with the hyper-IgE syndrome was used as a positive control. As a negative control, sections were also treated with a "sense" IL-5 probe. Specific hybridization signals for IL-5 mRNA were demonstrated within the bronchial mucosa in 6 out of the 10 asthmatic subjects. Cells exhibiting hybridization signals were located beneath the epithelial basement membrane. In contrast, there was no hybridization in the control group. No hybridization was observed with the sense probe. The six IL-5 mRNA-positive asthmatics tended to have more severe disease than the negative asthmatics, as assessed by symptoms and lung function, and showed a significant increase in the degree of infiltration of the bronchial mucosa by secreting (EG2+) eosinophils and activated (CD25+) T lymphocytes. Within the subjects who showed positive IL-5 mRNA, there was a correlation between IL-5 mRNA expression and the number of CD25+ and EG2+ cells and total eosinophil count. This study provides evidence for the cellular localization of IL-5 mRNA in the bronchial mucosa of asthmatics and supports the concept that this cytokine regulates eosinophil function in bronchial asthma.

Adult↗
PubMed1987

Structural characterization of follistatin: a novel follicle-stimulating hormone release-inhibiting polypeptide from the gonad.

Follistatin, a novel, single chain, glycosylated polypeptide bearing no homology with previously characterized inhibins but exhibiting potent and specific pituitary FSH-release inhibition has been structurally characterized by protein microsequencing, cDNA cloning, and DNA sequencing. Two populations of clones differing in their 3'-untranslated sequences were found to encode a 344 amino acid precursor protein and an identical but carboxyl terminal truncated 317 amino acid precursor, respectively. Additionally, one clone, FS18, contained two introns and probably resulted from reverse transcription of heterogeneous nuclear RNA during cDNA library construction. Follistatin is unusually cysteine-rich, containing 36 cysteines in the mature coding sequence of 315 amino acids and an extremely acidic carboxyl terminal region, FS(292-304), comprised of Glu-Asp-Thr-Glu-Glu-Glu-Glu-Glu-Asp-Glu-Asp-Gln-Asp which probably resides outside a tightly cross-linked protein sphere. The heparin-binding ability of follistatin can probably be ascribed to the basic region specified by FS(75-86), Lys-Lys-Cys-Arg-Met-Asn-Lys-Lys-Asn-Lys. Overall, follistatin is organized into three homologous domains, FS(66-135), FS(139-210), and FS(216-287) containing 70, 72, and 72 amino acids, respectively, which show a 52% homology among themselves and a 57% homology with the 56 amino acid human pancreatic secretory trypsin inhibitor protein when aligned for maximum homology.

Amino Acid Sequence↗
PubMedDate not supplied

Eosinophil development and bone marrow and tissue eosinophils in atopic asthma.

BACKGROUND: Eosinophils develop from bone marrow (BM) progenitors, and interleukin-5 (IL-5) and eotaxin may act in expansion and mobilisation of BM eosinophils in asthma. METHODS: We have examined phenotypic changes as CD34+ cells develop to the eosinophil lineage in vitro, and have evaluated BM eosinophils from asthmatic and control subjects for expression of the eotaxin receptor, CCR3. RESULTS: Acquisition of receptors for IL-5 and CCR3 was an early event in eosinophil development. There were increased CD34+ cells, and mature and immature CCR3+ eosinophils in BM from asthmatics. CONCLUSION: These data suggest that IL-5 may act early in eosinophil development, and that eotaxin has the capacity to mobilise a BM eosinophil pool in asthma.

Antigens, CD34↗
PubMedDate not supplied

Mechanisms of T cell peptide epitope-dependent late asthmatic reactions.

Short peptide sequences corresponding to T cell epitopes have been identified in the major cat allergen Fel d 1. In order to directly activate allergen-specific T cells in cat-allergic asthmatic individuals, peptides were administered by intradermal injection. Subsequently, a proportion of subjects experienced a delayed reduction of airway calibre manifested as a decrease in FEV(1). Changes in lung function occurred approximately 3 h after peptide injection, peaked at 6 h and resembled an isolated late asthmatic reaction (LAR). Using molecular tissue typing techniques, it was determined that many of the individuals experiencing isolated LAR expressed particular HLA-DR molecules. These molecules were shown in subsequent experiments to bind individual peptides within the preparation and thus to activate T cells in a major histocompatibility complex (MHC)-restricted fashion. The precise mechanisms whereby MHC-restricted activation of allergen-specific T cells gives rise to bronchoconstriction are currently under investigation.

Animals↗
PubMedDate not supplied

Phenotype of cells positive for interleukin-4 and interleukin-5 mRNA in allergic tissue reactions.

We have investigated the phenotype of cells positive for IL-4 and IL-5 mRNA in the nasal mucosa of subjects with allergic rhinitis and in bronchoalveolar lavage and bronchial biopsies from atopic asthmatic subjects. The method employed was immunochemistry followed by in situ hybridization using either 35S- or digoxigenin-labelled riboprobes. With nasal and bronchial tissue, this double ICC/ISH method revealed that more than 70% of IL-4 and IL-5 mRNA+ cells were T cells. The remaining IL-4 and IL-5 signals were co-localized to tryptase-positive mast cells and EG2+ eosinophils. Occasional IL-4 and IL-5 mRNA cells were observed in non-asthmatic control subjects, the large majority being CD3+ cells. These results indicate that CD3+ cells are the principal cellular source of IL-4 and IL-5 transcripts in atopic asthma and allergic rhinitis.

Antigens, CD↗
PubMedDate not supplied

Eosinophils and eosinophil-associated cytokines in allergic inflammation.

Eosinophils are major effector cells in allergic tissue reactions. Their capacity to synthesize and store cytokines, particularly Th2-type cytokines, which may have autocrine effects such as increased cell survival in tissues, is of particular current interest. We have shown that eosinophils infiltrating the site of human cutaneous late-phase reactions (LPR) express mRNA and protein product for IL-4 and IL-5. Stimulation of peripheral blood eosinophils in vitro with either IgG or sIgA produces time-dependent induction of IL-4 and IL-5 transcription, indicating that mature cells may undergo local cytokine synthesis. We also demonstrated that bronchial biopsies from patients with both atopic and non-atopic (intrinsic) asthma express IL-4 and IL-5 mRNA which mainly co-localized to T cells, although clear hybridization signals were also obtained with eosinophils and mast cells. On the other hand, immunoreactivity for the corresponding protein was detectable predominantly in eosinophils and mast cells; a finding believed to reflect granule storage of cytokines. We also studied the resolution of the cutaneous LPR. Apoptosis of eosinophils persisted slightly longer than neutrophils in the tissues. The eventual decline in both neutrophil and eosinophil numbers followed on from the peak of the LPR. This was associated with terminal-deoxynucteotidyl-transferase-mediated nick and labelling positive (TUNEL+) (apoptotic) cells with the subsequent removal of apoptotic neutrophils and eosinophils by tissue macrophages. Thus, IL-4 and IL-5 production by eosinophils may amplify local allergic inflammatory responses and, in the case of IL-5, may prolong local tissue survival. However, in the allergen-induced LPR, inflammation rapidly resolves, possibly through the initiation of programmed cell death and phagocytosis of apoptotic cells by macrophages.

Asthma↗