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Biomedical subjects

K A Knauer

Publications and source records attributed to K A Knauer.

5 recordsLinked to original sources
PubMed1984

Platelet augmentation of IgE-dependent histamine release from human basophils and mast cells.

A factor(s) from human platelets enhances IgE-mediated histamine release from human basophils and mast cells. This effect is directly related to the platelet number; at physiological platelet/leukocyte ratios (40:1), the enhancement was 66 +/- 11%. Platelet stimulation by thrombin more than doubled the enhancement, to 172 +/- 10% at 40:1. Mast cell release was also enhanced by platelets although the magnitude was more limited (86 +/- 13% at 40:1 with thrombin). Direct basophil/platelet contact was unnecessary in that platelet supernatants were fully active; a direct platelet factor/basophil interaction is suggested, however, by the fact that basophils purified 100-fold with respect to other leukocytes were enhanced by the platelet factors. The appearance of platelet-enhancing activity is associated with the release of an alpha-granule marker (PF4) rather than with products of arachidonic acid metabolism (thromboxane B2). The platelet factor(s) responsible for these effects are not dialyzable, are heat stable and do not appear to be identical to PF4 or platelet-derived growth factor (PDGF). Since anti-IgE-stimulated basophils cause PF4 release and this correlates with the release of enhancing factor, we suggest that a pro-inflammatory feed forward relationship exists. Together with our previous data showing that platelets are activated in vivo during antigen challenge of allergic asthmatic subjects, these results suggest that platelets may be important in modulating IgE-mediated allergic reactions in man.

Basophils↗
PubMed1984

Deuterium-oxide-induced histamine release from basophils of allergic subjects. I. Responsiveness to deuterium oxide requires an activation step.

Basophils from many atopic persons, and especially asthmatic patients, have been shown to release histamine in response to 44% deuterium oxide (D2O), whereas basophils from nonatopic persons do not release histamine. The present experiments analyzed the mechanisms by which D2O mediated release. It was found that although D2O induced release from washed leukocytes, it failed to induce release from whole blood or from leukocytes that had sedimented but had not been washed. The kinetics of release after washing were rapid and were equivalent regardless of the temperature at which cells were sedimented (O degrees or 37 degrees C). Washed cells became desensitized to the action of D2O within 30 to 60 min at 37 degrees C, whereas unwashed leukocytes did not become desensitized. Serum or plasma inhibited D2O-induced release, although high concentrations (1/5) were less inhibitory than lower ones (1/10 to 1/100). Basophils from D2O responders also released histamine in response to a "platelet enhancing factor" (PEF), whereas those from D2O nonresponders did not. As with D2O-mediated release, PEF-mediated release occurred only with washed leukocytes, desensitized within 30 to 60 min at 37 degrees C, and was inhibited by serum. These results suggest that D2O induces histamine release by augmenting the effects of an endogenous activation mechanism, and that PEF acts on the same (D2O-responsive) donors to augment this activation mechanism. Cell activation, as well as desensitization of this activation mechanism, occurs rapidly when basophils are washed free of plasma inhibitors and placed at 37 degrees C.

Asthma↗
PubMed1976

Pathobiologic features of human candidiasis. A common deep mycosis of the brain, heart and kidney in the altered host.

In a review of 2,616 consecutive autopsies done at the University of Kentucky Medical Center over a 12-year period, 46 patients with complete postmortem examinations had tissue-verified candidiasis in two distinct patterns, with Candida albicans being most frequently cultured. Superficial candidiasis involving only lining surfaces was observed in 21 patients (46%). Usually, it complicated other lethal problems such as malignancy and bacterial sepsis. Nineteen of these patients (95%) had received antibiotics. No vessel invasion or deep organ involvement was evident in this group. The other pattern of candidiasis was a deep or systemic variety recognized in the remaining 25 patients (54%). It was characterized by deep parenchymal organ lesions usually involving the brain (52%), heart (48%), and kidney (80%), but any tissue seemed susceptible. Vessel invasion was seen in 8 patients (32%); intravenous lines were used in 13 (52%); and major operations were done in 16 (64%). All these patients were hospitalized for either benign or malignant conditions and were treated for bacterial sepsis with antibiotics for seven days or more. This investigation indicates that candidiasis occurs when the host's environment is altered primarily by antibiotic therapy. Candida then can colonize lining surfaces and from there could invade adjacent vessels and disseminate throughout the body.

Adolescent↗