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Biomedical subjects

D Keast

Publications and source records attributed to D Keast.

At least 91 records · Page 5Linked to original sources
PubMed1975

Humoral immune response of mice with long-term exposure to cigarette smoke.

Mice were exposed to fresh cigarette smoke for 1,17, and 38 weeks. After each period the primary and secondary humoral immune response to intraperitoneal inoculation of sheep erythrocytes was studied. Direct and indirect plaque forming cell responses in the spleen and in a pool of cervical and mediastinal lymph nodes, as well as serum hemolytic and hemagglutinating antibodies were examined. Primary plaque forming cell and antibody response to sheep erythrocytes was first enhanced and then depressed by continual cigarette smoke exposure, while the secondary response was unaffected. Serum antibody response to polyvinylpyrrolidone, an immunogen independent of thymus-derived lymphocytes, was not impaired by 41 weeks of cigarette smoke exposure.

Animals↗
PubMed1975

Inhibition of migration of murine spleen cells by Rauscher leukemia virus-infected syngeneic cells.

The in vitro migration of spleen cells from BALB/c mice infected with Rauscher leukemia virus (RLV) was markedly inhibited 10 days after RLV inoculation. Mixtures of infected and uninfected spleen cells used in the ratio of 1:4 in an effector-cell/indicator-cell system showed that viable RLV-infected spleen cells could inhibit the migration of uninfected spleen cells in a manner indistinguishable from that mediated by sensitized spleen cell reacting to specific antigen.

Animals↗
PubMed1975

Cell-mediated immune responses to transplanted tumors in mice chronically exposed to cigarette smoke.

C57BL and BALB/c mice were exposed to fresh cigarette smoke for 7-8 minutes per day for varying periods up to 30 weeks before subcutaneous or intratracheal inoculation of viable tumor cells. The growth rates of subcutaneous tumors in the mice exposed to smoke were significantly higher than those of controls and more lung metastases were noted. Enhanced tumor growth rates in the respiratory tracts of smoke-exposed mice were evidenced by the markedly increased death rates in these animals after the intratracheal inoculation of tumor cells. Increased tumor growth rates in mice that inhaled smoke were assoicated with depressed tumor-specific cytotoxic responses in both spleens and regional lymph nodes. Short-term exposure (10 wk) of mice to cigarette smoke resulted in decreased tumor growth rates concomitant with enhanced cytotoxic responses.

Animals↗
PubMed1975

Development of two manifestations of T-lymphocyte reactivity during tumor growth: altered kinetics associated with elevated growth rates.

Tumor-specific, cell-mediated immune responses (CMI) in mice were measured during the growth of transplantable tumors with the use of lymphocyte-mediated cytotoxicity and the recently developed leukocyte adherence inhibition (LAI) microtest. When both tests were used in parallel to assess CMI, no consistent correlation was found, which suggested that each test was a measure of the activity of a functionally different T-lymphocyte subpopulation. The results of blocking factor (BF) assays with both tests agreed in 78% of the instances; the LAI microtest was much more sensitive for BF determination than lymphocyte cytotoxicity, since blocking serum concentrations as low as 0.25% could demonstrate BF activity in the microstest. In other experiments, the kinetics of development of tumor-specific CMI was followed in normal mice and those under toxic stress; the stressed animals showed depressed humoral and cell-mediated immune responses and enhanced tumor growth rates after the inoculation of tumor cells. In normal mice, a cytotoxic response always appeared in the spleens and regional lymph nodes 3-5 days before an LAI response. Enhanced tumor growth rates in the animals under toxic stress were associated with a reversal in the order in which these two manifestations of T-lymphocyte responsiveness developed; LAI responses always developed before, and often in the complete absence of, cytotoxicity.

Animals↗
PubMed1974

The growth of transplanted tumours in mice after chronic inhalation of fresh cigarette smoke.

The subcutaneous growth of the Lewis lung tumour in C57BL mice chronically exposed to fresh cigarette smoke was increased above that in age-matched control mice. When murine sarcoma virus (Harvey) induced tumour cells were introduced to the lungs of groups of BALB/c mice, only mice chronically exposed to fresh cigarette smoke died with tumour cells in the lungs. Tumour cell growth in mice during short term cigarette smoke exposure was indistinguishable from that in controls.

Animals↗
PubMed1974

Cigarette smoking, air pollution, and immunity: a model system.

BALB/c mice were exposed to fresh cigarette smoke, a mixture of SO(2) (5 ppm) and CO (50 ppm), or both for periods up to 18 weeks. After varying exposure times, animals were intratracheally inoculated with 10(8) sheep erythrocytes and sacrificed 7 days later, during which time the various exposure regimes were continued. Plaque-forming-cell responses were measured in spleens and a pool of the cervical and mediastinal lymph nodes, together with serum hemagglutinating and hemolytic responses, and compared with those of age-matched control animals. Both the organ and serum responses exhibited stimulation in the early phase of exposure, before a depression with prolonged exposure. The greatest depression was seen in animals that had been chronically exposed to both fresh cigarette smoke and the gas mixture.

Air Pollution↗