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E M Allen

Publications and source records attributed to E M Allen.

82 records · Page 5Linked to original sources
PubMed1977

Strain variation in BCG-induced chronic pulmonary inflammation in mice. I. Basic model and possible genetic control by non-H-2 genes.

C57BL/6 mice (haplotype H-2b) responded in a dose-dependent fashion to killed BCG by marked enlargement of the spleen and lung. Neither CBA nor C3H mice (haplotype H-2k) responded to such treatment. Pulmonary inflammation in responder B6 animals was characterized by a marked chronic interstitial and alveolar granulomatous process, and was accompanied by occasional granulomata, hyperemia, and loss of architecture in the spleen. Inflammation in non-responder CBA and C3H animals was minimal in both the lung and spleen. The response does not appear to be controlled by genes within the major histocompatibility complex, but is associated with a C57 background. B10.BR mice (responder background, H-2k) were responder animals and C3H.SW mice (nonresponder background, H-2b) were nonresponders. In addition, all animals tested with a C57 background were responders even though two of these strains were not H-2b (C57BL/Ks, H-2d and C57Br/cd, H-2k). The resolution of the mechanism of genetic control of this response in mice may provide information relevant to possible genetic control of chronic pulmonary inflammation in man.

Animals↗
PubMed1975

Effect of antithymocyte globulin pretreatment on immunological reconstitution of lethally irradiated animals.

Clinical and experimental studies have shown that antithymocyte globulin pretreatment will reduce the severity of the graft-versus-host reaction after allogeneic bone marrow transplantation. To determine whether this was attributable to a persisting cytotoxic factor in the recipients' sera or a result of the "masking" of foreign antigens by the antihymocyte globulin, an experimental schema utilizing a syngeneic transfer of immunocompetent cells was devised. Lethally irradiated mice that had been pretreated with rabbit antimouse thymocyte globulin (RAMTG) were injected with syngeneic spleen or bone marrow cells and their immunological competence was measured by the response to a test antigen, sheep red blood cells. It was found that such pretreatment had an adverse effect on the immunological potential of the infused cells. Thus, the plaque-forming cell response to sheep red blood cell antigen in RAMTG-pretreated recipients injected with spleen cells was reduced when compared to the saline or normal rabbit globulin-treated controls. The immunological recovery of lethally irradiated animals protected with syngeneic bone marrow was also delayed, but not permanently impaired, when the recipients had been pretreated with RAMTG. These effects were evident although the spleen or bone marrow cells had been injected into the RAMTG-pretreated recipients at a time when their sera were devoid of any cytotoxic antibodies. It is speculated that two mechanisms may contribute to this alteration in immune function of the infused cells: (1) that RAMTG exists in the serum in amounts sufficient to attach to receptor sites on lymphocytes or their precursors but insufficient to kill the cells, interfering with the antigen recognition mechanism or migration and homing patterns, or (2) that the RAMTG treatment creates a temporary defect in the microenvironment of the spleen and other hemopoietic tissues, thereby affecting the transplantation and proliferation kinetics of the infused cells.

Animals↗
PubMedDate not supplied

The effect of iodine on lipid peroxidation and ultrastructure in the thyroids of BB/Wor rats.

There has been recent data suggesting that iodine potentiates lymphocytic thyroiditis (LT) by inciting oxidative stress. However, the mechanism by which iodine induces LT in genetically predisposed animals is unknown. This study was undertaken to examine LT-prone BB/Wor (LT-P) rat thyroids for signs of acute iodine toxicity and oxidative damage before the onset of spontaneous LT. Lipid peroxidation was assessed by the measurement of malonyldialdehyde (MDA) in thyroid homogenates after randomization to a treatment group receiving 0.05% iodide in the drinking water or tap water for 24 hours. Basal MDA levels were higher in LT-prone rat thyroids than Wistar rat thyroids, but iodine treatment did not influence intrathyroidal MDA levels. Electronmicroscopy demonstrated that prolonged treatment with excess iodine, increased the number of apical lysosomes. But there were no ultrastructural changes unique to LT-P rat thyroids. These data suggest that although LT-P rat thyroids may experience subclinical oxidative damage before the onset of histologically demonstrable LT, this activity is not affected by iodine.

Analysis of Variance↗