ABSTRACT
Secretory immunoglobulin A (SIgA) provides the first line of defence against pathogens initiating infection via the mucosal route, e.g. the influenza virus. The aim of this study was to examine the basal level of influenza-specific antibody-secreting cell (ASC) in the local mucosa of the upper respiratory tract. Nineteen patients scheduled for tonsillectomy were enrolled for the study, and they had not experienced influenza during the previous year. Tonsils, blood, oral fluid and a nasal biopsy were sampled, and the basal levels of ASC and antibodies (Abs) were determined. We found low numbers of influenza-specific ASC in the blood and tonsils, but there were about 10-100 times higher numbers of specific ASC in the nasal mucosa tissue despite no recent influenza exposure. Thus, the basal level of influenza-specific ASC in the mucosa of the respiratory tract may be important in the protection against influenza infection.
Subject(s)
Antibodies, Viral/immunology , Antibody-Producing Cells/immunology , Influenza A virus/immunology , Influenza B virus/immunology , Influenza, Human/immunology , Nasal Mucosa/immunology , Adult , Antibodies, Viral/blood , Female , Humans , Influenza, Human/blood , Influenza, Human/epidemiology , Male , Nasal Mucosa/cytology , PrevalenceABSTRACT
From experimental surface tension data for water solutions of dodecyl-beta-maltoside, C12M, and dodecyl-penta-(ethylene oxide), C12EO5, in the range below the CMC, the corresponding head group surface pressure functions vs. packing density were derived. These functions were compared with theoretical expressions based on some different models of the mixed head group/water film. Tentatively, we concluded that the two-dimensional hard fluid approach provides a convenient starting-point in order to account for the observed surface pressures of both the maltoside and EO head groups.
ABSTRACT
Heparin can be bound to polymer surfaces by precipitation of an ionic heparin-amine complex which can be stabilized against dissolution by treatment with glutardialdehyde. The aim of this investigation was to study the degree and course of desorption of heparin from such a heparinized surface on contact with blood. This desorption must be considered when analysing the interaction between the heparinized surface and blood. Different heparinized surfaces were prepared by using 35S-labelled heparin, and the desorption of heparin on exposure in vitro to citrated plasma or heparinized blood as well as during exposure at in vivo conditions was quantified. During in vitro experiments, the glutardialdehyde stabilized surface became stable with no further desorption of heparin after an initial loss of about 3% of the initial surface-bound heparin. Under in vivo conditions, there was an initial loss of about 12%. There was no further loss from surfaces inserted into the circulation of the dog for seven days as compared to those inserted for one hour.