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Biomedical subjects

S Kohl

Publications and source records attributed to S Kohl.

At least 127 records · Page 7Linked to original sources
PubMed1981

Effect of herpes simplex virus infection on murine antibody-dependent cellular cytotoxicity and natural killer cytotoxicity.

Mice intraperitoneally inoculated with a sublethal dose of herpes simplex virus (HSV) produced immunoglobulin G antibody-dependent cellular cytotoxicity (ADCC) and radioimmunoassay (RIA) antibody as early as 3 days after infection. There was a rise in natural killer cytotoxicity (NKC) to infected and uninfected target cells 1 to 3 days postinfection mediated by nonadherent peritoneal cells (PC) in mice inoculated with HSV, but also with other substances commonly used in tissue culture media. HSV caused the highest and most consistent increase in NKC. PC-NKC, as ADCC, was inhibited by latex and silica, both macrophage inhibitors. PC-ADCC markedly declined 3 to 8 days after HSV inoculation. This was not due to a soluble or cellular suppressor factor, was not reversed by incubation or trypsin treatment of PC, was not associated with a change in PC Fc receptors, adherence, or acridine orange staining characteristics, and could not be induced by inactivated HSV. In vitro inoculation of PC with HSV similarly caused a reduction in the ability of PC to mediate ADCC to HSV-infected target cells. These data demonstrate the complex stimulatory and inhibitory interactions between virus and host defense mechanisms.

Animals↗
PubMed1981

Immune responses to labial infection of BALB/c mice with herpes simplex virus type 1.

The kinetics of appearance of five humoral antibody responses (micro-neutralization assay [NT], complement fixation [CF], enzyme-linked immunosorbent assay [ELISA], radioimmunoassay [RIA], antibody-dependent cell-mediated cytotoxicity [ADCC]), were compared during labial infection of BALB/c mice with herpes simplex virus type 1 strain Patton. The ELISA/RIA antibody responses were present in most mice by day 5 after infection, at the beginning of the herpetic lip lesions; antibody effective in ADCC showed identical early kinetics. In contrast, NT/CF antibodies were not detected in most mice until day 10, at the time of resolution of the herpetic lip lesions. The humoral immune responses persisted for at least 6 months after infection. The NT and CF responses were closely correlated in time of appearance and titers (r = 0.9), as were the ELISA and RIA responses (r = 0.99). However, there was little correlation between NT/CF and ELISA/RIA responses (r = 0.02). The kinetics of the delayed type hypersensitivity response showed similar kinetics of appearance to the ELISA/RIA/ADCC humoral responses, and peaked similarly, but waned gradually over 2 months. The importance of antibody in protection against labial herpes simplex virus type 1 infection was demonstrated by the ability of passively transferred convalescent serum (that produced a minimum NT titer of 10 in recipient mice) to protect against development of herpetic lesions and death.

Animals↗
PubMed1981

Protection of neonatal mice against herpes simplex viral infection by human antibody and leukocytes from adult, but not neonatal humans.

Neither human immune globulin nor human mononuclear leukocytes (containing lymphocytes and monocytes) from herpes simplex virus (HSV) seronegative adult donors could protect infant C57BL/6 mice from a lethal HSV infection. In contrast, a combination of 5 X 10(6) leukocytes and a subneutralizing dose of antibody protected the mice. Leukocytes (5 X 10(6) or 1 X 10(7)) from neonatal humans and antibody could not mediate this protection. This is the first correlation between defective human neonatal leukocyte antibody-dependent cellular cytotoxicity (ADCC) in vitro and defective human neonate leukocyte-antibody protection against HSV infection in vivo in mice.

Animals↗
PubMed1981

Hodgkin's disease complicated by nephrotic syndrome. New clinical observations on the response of both diseases to radiotherapy to the neck.

The clinical course of a 14-year-old boy who developed biopsy-proven minimal change nephrotic syndrome (MCNS) prior to institution of therapy for Hodgkin's disease (HD), mixed cellularity histologic subtype, is presented. In the first week of radiotherapy to the major site of disease in the neck, BUN and creatinine levels rose to 98 mg% and 8.4 mg%, respectively. During the second week of treatment, levels gradually decreased becoming normal in the third week. Body weight gradually decreased in the second week of radiotherapy, falling rapidly in the third and fourth week when diuresis was greatest. Although urine protein concentration fell initially, the concentration remained 1 + or more for 10 weeks following radiotherapy. Following radiotherapy to the neck, staging laparotomy demonstrated a single focus of Hodgkin's disease in the spleen. Radiotherapy was given to the splenic pedicle: six courses of multiagent chemotherapy (MOPP) followed. The boy remains free of any evidence of either HD or MCNS 33 + months from the time of the diagnosis. Circulating lymphocytes showed normal responses to stimulation by phytohemaglutinin, Concanavalin A, and pokeweed mitogens. The patient's monocyte-macrophage-mediated antibody-dependent cellular cytotoxicity (ADCC) was low both prior to and following radiotherapy. Lymphocyte-mediated ADCC was normal at both of these times.

Adolescent↗
PubMed1980

Effect of antineoplastic drugs on human leukocyte-mediated cytotoxicity against herpes simplex virus infected cells.

We evaluated the effect of five antineoplastic drugs on the ability of human leukocytes to destroy herpes simplex virus (HSV) infected target cells in the presence of antibody (antibody-dependent cellular cytotoxicity) and in its absence (natural killer cytotoxicity). Leukocytes from healthy volunteers were separated into macrophages, polymorphonuclear leukocytes, and lymphocytes. Adriamycin, cyclophosphamide, prednisone, procarbazine, and vincristine, at various concentrations and incubation periods, were tested for their effects on the natural killer and antibody dependent cellular cytotoxicity of macrophages, lymphocytes, and polymorphonuclear lymphocytes in a 51Cr release microcytotoxicity assay against HSV-infected cells. All drugs at therapeutic concentrations inhibited natural killer and antibody dependent cellular cytotoxicity; an exception was cyclophosphamide, which did not inhibit the natural killer cytoxicity of lymphocytes. The antibody dependent cellular cytotoxicity of macrophages and polymorphonuclear leukocytes appeared to be more than that of lymphocytes. The results of short incubation (2 hours) of the drug with either effector cells or target cells, followed by drug removal, suggests that the drug effect occurred early and predominantly at the effector cell level. Antineoplastic drugs had an inhibitory effect on natural killer and antibody dependent cellular cytotoxicity against HSV-infected cells. This inhibitory action may partially explain the increased susceptibility of patients receiving chemotherapy to developing viral infections.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1980

Hypoglycemia as a manifestation of sepsis.

Hypoglycemia has rarely been described as a clinical sign of severe bacterial sepsis. We recently encountered nine patients in whom hypoglycemia (mean serum glucose of 22 mg/dl) was associated with overwhelming sepsis. Clinical disease in these patients included pneumonia and cellulitis; in three patients, no focus of infection was apparent. Altered mental status, metabolic acidosis, leukopenia, abnormal clotting studies and bacteremia were common features in these cases. In four patients, no cause for hypoglycemia other than sepsis was present. In five patients, another possible metabolic cause for hypoglycemia was present (alcoholism in four and chronic renal insufficiency in one) although none had been observed to be hypoglycemic on previous hospitalizations. Streptococcus pneumoniae (three cases) and Hemophilus influenzae, type b, (two cases) were the most common pathogens, and the over-all mortality was 67 per cent. The mechanism(s) for hypoglycemia with sepsis is not well defined. Depleted glycogen stores, impaired gluconeogenesis and increased peripheral glucose utilization may all be contributing factors. Incubation of bacteria in fresh blood at room temperature does not increase the normal rate of breakdown of glucose suggesting that the hypoglycemia occurs in vivo. Hypoglycemia is an important sign of overwhelming sepsis that may be more common than has previously been recognized.

Acidosis↗
PubMed1980

Clinical pharmacology of two chloramphenicol preparations in children: sodium succinate (iv) and palmitate (oral) esters.

The clinical pharmacology of chloramphenicol was evaluated in 14 children with serious bacterial infections. The children received chloramphenicol sodium succinate intravenously for five to six days at which time orally administered chloramphenicol palmitate was substituted for an additional five to six days of therapy. The mean peak serum chloramphenicol concentration when given iv (28.2 +/- 5.1 micrograms/ml) occurred within one hour after the termination of the 60-minute iv infusion and when given orally (19.3 +/- 2.6 micrograms/ml) occurred two to three hours after ingestion. Differences in serum levels of chloramphenicol after iv compared to oral administration of the same dose could be demonstrated at various time points studied during the dose-response curves; however, the areas under the chloramphenicol curve were not significantly different after iv (140 +/- 116 micrograms/ml/hour) versus oral (95 +/- 26 micrograms/ml/hour) administration. In seven patients who had concomitant serum and CSF chloramphenicol levels determined, a CSF to serum ratio of 23 to 85% occurred. The CSF levels (5.5 to 13 micrograms/ml) were not directly proportional to serum levels. All patients recovered from their infection and no side effects from chloramphenicol were encountered. Administration of chloramphenicol orally in the palmitate form produces serum concentrations and areas under the disappearance curve similar to those achieved after iv administration of the same dose, indicating that the oral route is an effective method of achieving therapeutic concentrations of chloramphenicol in serum.

Administration, Oral↗
PubMed1980

Polymorphonuclear leukocytes of human colostrum. I. Oxidative metabolism and kinetics of killing of radiolabeled Staphylococcus aureus.

Polymorphonuclear leukocytes (PMNLs) were isolated from the colostrum of 57 women. Colostral cells were identified by fluorescent microscopy after supravital staining with acridine orange. Numerous intracellular fat globules within colostral PMNLs were shown by Oil Red O stain and electron microscopy. Oxidative metabolic activity during phagocytosis of opsonized zymosan particles was significantly greater in blood PMNLs compared with colostral PMNLs. The total uptake and killing of [methyl-3H]thymidine-labeled Staphylococcus aureus by blood PMNLs were significantly greater than by colostral PMNLs. Similar defects were produced in blood PMNLs incubated with the lipid fraction of colostrum, but not in those incubated with the aqueous fraction. Surface Fc receptors of colostral PMNLs and blood PMNLs incubated with colostral lipid were significantly reduced in number compared with those of control PMNLs or PMNLs preincubated with the aqueous fraction of colostrum. The metabolic and phagocytic defects of PMNLs from human colostrum appear to be related to colostral substances that alter PMNL surface structure and subsequent function.

Cell Count↗
PubMed1980

Human colostral cytotoxicity. II. Relative defects in colostral leukocyte cytotoxicity and inhibition of peripheral blood leukocyte cytotoxicity by colostrum.

Colostral cells have been previously shown to mediate antibody-dependent cellular cytotoxicity (ADCC) to herpes to simplex virus-infected cells. A comparison of colostral cells to matched peripheral blood mononuclear cells has revealed significantly lower ADCC activity, higher antibody requirements, and slower kinetics of colostral cell ADCC against infected cells. Colostral cells failed to mediate natural killer cytotoxicity. Lymphocytes, monocyte macrophages, and polymorphonuclear leukocytes isolated from peripheral blood and incubated with colostrum from virus-immune or nonimmune women markedly inhibited ADCC. Inhibitory activity was found in lipid and aqueous fractions and was due to an effect on leukocytes, not target cells. A partial explanation was inhibition of expression of leukocyte Fc receptors, a prerequisite for ADCC, by acellular colostrum. These results raise questions concerning the potential antiviral activity of colostral cells in vitro.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1980

Epidemiology of preterm delivery.

1. Defining prematurity as applying to LBW infants of less than 37 weeks' gestation and classifying those LBW infants of greater than 37 weeks as having IUGR provides an improved means of analyzing different risk factors. 2. In accordance with the method of D'Angelo and Sokol, risk factors have been assigned to the various disease entities and social factors (8). 3. There is a suspicion in some disease entities, such as chronic hypertension, that prematurity is of equal frequency to IUGR, and in others, such as renal disease, that IUGR may not be increased at all, at least in term or near-term gestation. A reevaluation of the relationship of some disease entities to IUGR and prematurity is needed, probably in the sophisticated manner of Hoffman et al (15).

Adolescent↗
PubMed1980

Mechanisms of host defense in well nourished patients with chronic alcoholism.

Tests of immune function were performed on five recently abstinent, well nourished,and disease-free patients with chronic alcoholism. No significant defects in adherence, metabolic, or bactericidal activity of polymorphonuclear leukocytes were found when compared to sex-matched controls. Antibody-dependent and natural killer cellular cytotoxicity of monocyte-macrophages and lymphocytes also were normal. These data support the concept that immunity might be intact in the group of patients with chronic alcoholism who are recently sober, well nourished, and free of underlying disease.

Alcoholism↗