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PubMed1979

Inflammatory reactions in onchocerciasis: a report on current knowledge and recommendations for further study.

This report concerns the host's reactions to the presence of the parasite both in the course of the natural disease and during drug treatment. The various stages of Onchocerca volvulus are discussed in terms of the type of tissue reaction seen. The discussion then turns to basic hypotheses concerning the etiology of these reactions, emphasis being placed on the fact that while pathological changes are considerable in some locations there is a remarkable lack of reaction in others. Some of the mechanisms possibly involved in this apparent absence of host response are discussed, including anti-complement factors, poor antigenicity, acquisition of host antigen, immune tolerance, and blocking antibodies. In any study of the inflammatory response it is recommended that critical evaluations be made of histological material, haematological studies, the definition of the antigenic nature of O. volvulus, characterization of immunological reactivity of patients, and the definition of the migratory pathways of the parasite.The marked host reactions seen following chemotherapy, especially those related to the interaction of the drug diethylcarbamazine with microfilariae, are discussed at some length. The etiology of these reactions is considered and recommendations are made for the experimental elucidation of the mechanisms involved. Emphasis is placed on the necessity for detailed sequential histopathological and immunopathological studies in the definition of the tissue lesions found in onchocerciasis. Characterization of these lesions will assist greatly the approach to control of the adverse reactions seen during treatment.The use of anti-inflammatory agents in clinical trials is discussed and comments are made concerning the most suitable clinical situations for testing drugs and the types of drug that should be tested.

Anti-Inflammatory Agents↗
PubMed1979

The release of a platelet-activating factor by stimulated rabbit neutrophils.

Normal rabbit peripheral blood neutrophils released a platelet-activating factor upon stimulation by opsonized zymosan. The liberation was Ca++ dependent and the time course of release was closely associated with phagocytosis. The material extracted into chloroform and exhibited an identical mobility by thin layer chromatography to basophil-derived, IgE-stimulated, platelet-activating factor (PAFb). It was similar to PAFb in its effect on platelets in both aggregation and release but was distinguished from ADP, thrombin, arachidonic acid, and thromboxanes. This factor appears to be responsible for some previously reported neutrophil-platelet interactions.

Animals↗
PubMed1979

Candida infections.

The authors present a review of the epidemiology, pathology, diagnosis and treatment of candidiasis in the child. Their studies on the favoring factors in cutaneous forms as well as their experiences in pulmonary forms are emphasized.

Amphotericin B↗
PubMed1975

Modulation of human neutrophil polymorphonuclear leucocyte migration by human plasma alpha-globulin inhibitors and synthetic esterase inhibitors.

The exposure of isolated washed human neutrophils to purified human alpha1-antitrypsin resulted in a transient 2-fold enhancement of random migration and concomitant 70-90 per cent inhibition of chemotactic responsiveness to C5a or C3a, while treatment with alpha2-macroglobulin gave a less pronounced brief enhancement of random migration and prolonged 40-60 per cent suppression of chemotaxis. Peak effects occurred with concentrations of 1 mug/ml of alpha1-antitrypsin and 10 mug/ml of alpha2-macroglobulin. In contrast, the inhibitor of the activated first component of complement, at the highest concentration studied of 100/mug/ml, slightly enhanced chemotactic migration in response to C5a without influencing random migration. Preincubation of neutrophils with either L-1-tosylamide-2-phenylethyl-chloromethyl ketone (TPCK) or N-alpha-p-tosyl-L-lysine-chloromethyl ketone (TLCK) at concentrations of 10-8-10-4M suppressed chemotaxis with concomitant inhibition of random migration by TPCK and enhancement of random migration by TLCK. All agents worked directly and irreversibly on the cells but caused only slight stimulation of the activity of the hexose monophosphate shunt of layers of adherent neutrophils. The results suggest that interaction of the plasma alpha-globulins or synthetic esterase inhibitors with surface receptors on neutrophils can influence both the random migration and responsiveness to chemotactic factors of these cells.

Alpha-Globulins↗
PubMed1978

Separation and functional characterization of human neutrophil subpopulations.

Human neutrophils have been considered to be a functionally homogeneous population of cells. We have developed a density sedimentation technique for separation of neutrophils into two populations based on their ability to form rosettes with IgG-coated human erythrocytes (7SEA). Under the experimental conditions 80% +/- 4.3% of normal human peripheral blood neutrophilis form rosettes. Functionally rosette-forming neutrophils are more adherent to nylon wool, able to phagocytize more 14C-labeled Staphylococcus aureus, more efficient in killing S. aureus, and more responsive to endotoxin-activated human serum in a 51-cr chemotaxis assay that the non-rosette forming neutrophils. However, there is no difference among neutrophil subpopulations' ability to phagocytize latex particles. Paired samples of exudate neutrophils from cutaneous abscess fluid and peripheral neutrophils from three patients were investigated for their ability to form 7SEA rosettes. In each case exudate neutrophils contained greater than 96% rosette-forming neutrophils, whereas peripheral blood contained the normal 80% ( less than 0.01). Thus we show that peripheral blood contains at least two distinct populations of neutrophils. However, an essentially homogeneous neutrophil population is present in cutaneous exudate fluid.

Animals↗
PubMed1978

Characteristics of the chemotactic response of neoplastic cells to a factor derived from the fifth component of complement.

Chemotactic factors for malignant neoplastic cells can be generated from either the fifth component of complement or from leukotactic fractions obtained from zymosanactivated serum. Digestion of the fifth component of complement by trypsin initially produced leukotactic activity, but as digestion continues, leukotactic activity is lost and tumor cell chemotactic activity is generated. Separation of the leukotactic activity is lost and tumor cell chemotactic activity is generated. Separation of the leukotactic activity and tumor cell chemotactic activity can be accomplished by gel filtration or isoelectric focusing. Gel filtration indicates that the tumor cell chemotactic factor has a molecular weight of approximately 8000 daltons. Tumor cell chemotactic activity can be generated by trypsinizing the leukotactic fractions isolated by isoelectric focusing. The responses of cultured Walker tumor cells or of Walker ascites tumor cells are dose-dependent and truly chemotactic. Cells from a murine malignant lymphoma do not respond to the complement-derived chemotactic factor for tumor cells, indicating that not all malignant cells share this functional property.

Animals↗
PubMed1979

Induction of lysosomal enzyme secretion by alveolar macrophages in response to the purified complement fragments C5a and C5a des-arg.

Purified C5a and its "inactive" form, C5a des-arg, were shown to induce secretion of acid hydrolases from rabbit alveolar macrophages (AM) in a concentration-dependent manner. Secretion increased with time to 5 times above controls by 72 hr. Concentrations of these enzymes in the cell lysates did not decrease during the incubation, suggesting that synthesis of new enzyme was occurring. The lysosomal enzyme secretion was accompanied by increased pinocytosis and release of proteolytic enzymes from the macrophages. At no time was significant lactic dehydrogenase liberated, indicating that secretion was selective and not due to cell death. Data presented also suggest that C5a des-arg induced secretion from the macrophages of a chemotactic factor for neutrophils. It was concluded that C5a and C5a des-arg may play a role in lung injury by interactions with AM, inducing the secretion of acid hydrolases and proteolytic enzymes that can cause tissue damage, and by regulating the influx of other inflammatory cells into the interstitium and air spaces.

Anaphylatoxins↗

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