Influence of cationic superoxide generation enhancing protein (SGEP) on phagocytic and intracellular bactericidal activity of human polymorphonuclear cells

Cationic fraction III from the lysosomes of normal human peripheral blood polymorphonuclear cells (PMNs) was found to contain superoxide generation enhancing protein (SGEP). Herein, we report on the influence of partially purified SGEP obtained from fraction III (subfractions III-5 and III-6), on various phagocytic functions of human PMNs. SGEP markedly enhanced intracellular bactericidal activity of human peripheral PMNs. The enhancement was time and dose dependent. It also reduced adhesiveness of the PMNs. SGEP did not influence chemotaxis, phagocytosis or phagocytic index. These findings are compatible with our original observation regarding superoxide generation enhancement properties of SGEP.     

Quantitation of cutaneous inflammation induced by reactive species generated by UV-visible irradiation of Rose bengal

The present studies were undertaken to quantitate the initial inflammatory response produced by the photo-generated reactive species in rabbit skin. Rose bengal (RB), a photosensensitizer dye, was injected into the skin sites at various concentrations and exposed to UV-visible light for 30–120 min. The increase in vascular permeability and the accumulation of PMNs were investigated using¹²⁵I-labeled albumin and⁵¹Cr-labeled PMNs. RB at a concentration of 1 nmol with 120-min exposure to light enhanced vascular permeability by 3.7 times and accumulation of PMNs by 3.3 times. As low as 0.01 nmol of RB produced discernible effects.-Carofene (0.1 nmole) inhibited the inflammatory response by 75–100%, suggesting that the reactive species involved in this response was predominantly singlet oxygen. The increase in vascular permeability was inhibited by 48–70% by 25g of chlorpheniramine maleate. It is therefore suggested that histamine plays a major role in the initial vascular response. The studies demonstrate that this rabbit model is suitable for the quantitation of photoinduced inflammatory response which is not observable by gross anatomic procedures.Part of this work was presented at NATO Advanced Study Institute on Photosencitisation, July 1987, Kingston, Canada. This work was supported by research grants from Natural Sciences and Engineering Research Council, Canada and Ontario Ministry of Labour, Canada.     

Monoclonal antibodies to gonadotropin-releasing hormone (GnRH) inhibit binding of the hormone to its receptor

Monoclonal antibodies (MAbs) specific to gonadotropin-releasing hormone (GnRH) were obtained using different strategies of conjugation of the peptide to carrier protein and immunization. Of several antibodies obtained, two, namely F1D3C5 and E2D2 bound GnRH in solution phase. Though the epitopes corresponding to the two overlapped, there was a one amino acid shift in the core epitope. These two antibodies were characterized with respect to inhibition of GnRH induced responses in rat pituitary cultures and alpha-T3.1 mouse gonadotrope cell line.