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L D Loose

Publications and source records attributed to L D Loose.

16 recordsLinked to original sources
PubMed1979

Environmental chemical-induced modification of cell-mediated immune responses.

It is therefore proposed that: 1) environmental chemicals can have specific mechanisms of toxicity and can influence antibody-mediated immunity while having no detectable effect on cell-mediated immunity, 2) immune dysfunction is related to exposure time to a chemical and the tissue concentration of that chemical, 3) recovery of immune function may occur even though chemical exposure continues, and 4) a single assay of immune function may not be appropriate to detect chemical induced immune dysfunction.

Animals↗
PubMed1979

A rapid, inexpensive and easily quantified assay for phagocytosis and microbicidal activity of macrophages and neutrophils.

The objective of the present study was to develop a technique to quantitate the phagocytic and intracellular microbicidal activity in different populations of phagocytes, i.e. neutrophils and macrophages. Elicited peritoneal neutrophils and macrophages as well as alveolar macrophages and adherent splenic macrophages were used as representative cell types. The method to assess intracellular killing was based upon dye uptake and concentration by a dead micro-organism; methylene blue was used as the indicator dye and the test organism was Saccharomyces cerevisiae. Phagocytosis was measured by counting, microscopically, the number of ingested yeast (Saccharomyces cerevisiae) within the neutrophils or macrophages. A number of killed yeast, i.e., those which took up the dye, were readily visualized. The temporal pattern of phagocytosis and killing was determined concurrently. Splenic macrophages demonstrated the slowest phagocytic activity whereas neutrophils and alveolar macrophages manifested a similar phagocytic activity. Peritoneal macrophages exhibited a continuous increase in activity throughout the test period. Microbicidal activity was similar for all 4 cells types. The new technique for measuring phagocytosis and killing provides a rapid, inexpensive and easily quantified assay for assessing discrete phagocytic cell functions.

Animals↗
PubMed1979

Macrophage dysfunction after burn injury.

The phagocytic and microbicidal activities of alveolar and peritoneal macrophages were evaluated 4 and 24 h after a full-thickness scald burn of 26 to 28% body surface area in anesthetized rats. The contribution of serum factors to the macrophage functions was studied concurrently. The phagocytic activity of alveolar macrophages obtained 4 or 24 postburn was reduced approximately 65% below control values when they were incubated in media containing autologous serum and approximately 45% (below controls) when they were incubated in media containing normal (control) serum. A similar, although not as marked, decrease in the phagocytic activity of peritoneal macrophages was also demonstrated. Serum obtained from rats 4 or 24 h postburn had a significant suppressive effect on the phagocytic activity of control alveolar, but not peritoneal, macrophages. The intracellular microbicidal activity of peritoneal macrophages obtained at the postburn intervals and incubated in media containing either autologous or control serum was unaltered from control values. However, alveolar macrophages obtained 24 h, but not 4 h, postburn had a significant (approximately 80%) increase, above control values, in their microbicidal activity. Serum obtained 24 h, but not 4 h, postburn stimulated control alveolar macrophage killing ability. These data indicate that thermal injury induces a defect in the phagocytic activity rather than the microbicidal activity of macrophages. This phagocytic alteration is mediated, in part, by serum.

Animals↗
PubMed1978

Environmental chemical-induced immune dysfunction.

Antibody formation, endotoxin sensitivity, and resistance to a challenge malarial infection were evaluated in mice fed a diet containing polychlorinated biphenyl (PCB) (Aroclor 1242) or hexachlorobenzene (HCB). Antibody synthesis to the antigen sheep RBC (SRBC) was significantly depressed in the PCB- and HCB-treated (167 ppm) animals as evidenced by the fact that control mice elicited an approximate twofold increase in antibody formation over the chemical-treated mice. Serum IgA concentrations in the PCB- and HCB-treated mice were consistently 40--80 mg/dl lower than control values. Gram-negative endotoxin (Salmonella typhosa) sensitivity in PCB- and HCB-treated mice was increased 5.2- and 32-fold, respectively, following the dietary administration of 167 ppm of Aroclor 1242 or HCB for 6 weeks. An endotoxin hypersusceptibility was also noted at 3 weeks after dietary administration. Decreased resistance to a malaria challenge was also demonstrated in the xenobiotic-treated mice. A 20% decrease in mean survival time of mice fed Aroclor 1242 for 3 to 6 weeks and inoculated with Plasmodium berghei (NYU-2) was observed. Infected mice which had received HCB for 3 or 6 weeks manifested reductions in mean survival time of 24 and 31%, respectively. The data indicated that environmental chemical contaminants impair host resistance and, since no concomitant histopathological alterations were observed in the treated mice, the evaluation of immune parameters may possibly be a sensitive indicator of toxicity.

Animals↗
PubMed1978

Impaired host resistance to endotoxin and malaria in polychlorinated biphenyl- and hexachlorobenzene-treated mice.

The in vivo effect of polychlorinated biphenyl (PCB) and hexachlorobenzene (HCB) on murine endotoxin sensitivity and resistance to malaria (Plasmodium berghei NYU-2) infection was studied. The dietary administration of 167 ppm (167 microgram/g) of PCB 1242 or HCB for 3 weeks resulted in an enhanced sensitivity to gram-negative endotoxin (Salmonella typhosa), which was further increased in animals maintained on the diets for 6 weeks. By 6 weeks, a 5.2- or 32-fold increase in endotoxin sensitivity was seen in mice fed PCB or HCB, respectively. A 20% decrease in mean survival time of mice fed PCB 1242 for 3 or 6 weeks and inoculated with malaria was demonstrated. Infected mice that received HCB for 3 or 6 weeks manifested a reduction in mean survival time of 24 or 31%, respectively. Histopathological examination revealed a normal thymus, spleen, mesenteric lymph nodes, and lungs. Centrilobular and pericentral hepatocyte hypertrophy, common to organochlorine exposure, was observed. Electron capture gas chromatographic analysis for PCB 1242 or HCB in the tissues examined histologically revealed a significant deposit of the xenobiotics. HCB concentration was approximately 16 to 25 times greater than that of PCB. The data indicate that environmental chemicals impair host resistance and that the alteration may be related to the presence of the chemicals in the lymphoreticular organs.

Animals↗
PubMed1978

Influence of cadmium on the phagocytic and microbicidal activity of murine peritoneal macrophages, pulmonary alveolar macrophages, and polymorphonuclear neutrophils.

A significant depression in the phagocytic capacity of elicited peritoneal macrophages, pulmonary alveolar macrophages, and elicited peritoneal polymorphonucleated neutrophils was manifested when the cells were incubated in medium containing cadmium chloride. With the exception of the neutrophils, a similar influence was observed when the cells were exposed to cadmium acetate. The impaired phagocytic capacity was related to the concentration of the cadmium in the medium. Peritoneal macrophages and neutrophils did not demonstrate any alteration in their microbicidal activity (percentage of ingested yeast which were killed) in the presence of the cadmium salts. However, a significant suppression in the intracellular microbicidal activity of alveolar macrophages was observed when the cells were incubated in medium containing either cadmium chloride or cadmium acetate. This unique response to Cd2+ may be related to general metabolic characteristics of these cells living at an elevated O2 tension.

Animals↗
PubMed1976

A temporal relationship between reticuloendothelial system phagocytic alterations and antibody responses in mice infected with Plasmodium berghei (NYU-2 strain).

Malaria-induced immunosuppression has been demonstrated in humans and experimental animals. The suppressed immune response has been suggested to be primarily humoral and not cellular in nature, since classical lymphocytic cell-mediated responses have been reported to be normal. Since previous results have demonstrated that an impairment in macrophage antigen processing may be a contributing factor in malaria-induced immunosuppression, the present studies were conducted to determine if the macrophage/reticuloendothelial system (RES) alteration occurs parallel to the course of the malarial infection and if the impairment in antibody formation is temporally related to the RES alteration. The present study has demonstrated that a profound impairment in splenic direct plaque forming cell (PFC) formation occurs in malaria-infected Balb/c mice which had been immunized with sheep erythrocytes (SRBC) either 2 or 4 days after inoculation with Plasmodium berghei, NYU-2 strain. Serum hemagglutinin titers were significantly depressed in mice which received the SRBC 4 days post-inoculation; however, no alterations in antibody titers were observed in mice immunized with SRBC 2 days post-inoculation. Coincident with the depression of serum antibody titers at the day 4 immunization period was a profound increase in the vascular clearance of 51Cr-SRBC with an enhanced hepatic uptake of the 51Cr-SRBC and a decreased splenic localization of the labelled erythrocytes. It is suggested that a direct vascular exposure of the splenic lymphoid-macrophage elements to the parasite may be responsible for the initial early alterations in the PFC response while the impairment in serum antibody titers and splenic phagocytic activity may be a result of the pathological alterations occurring later in the infection, e.g., tissue anoxia, anemia, and hemolysis.

Animals↗
PubMed1975

Comparative uptake of sulfobromophthalein by isolated Kupffer and parenchymal cells.

The relative role of specific liver cells in the uptake of sulfobromophthalein (BSP) was ascertained by utilizing enzymatically isolated rat hepatic Kupffer and parenchymal cells. Kupffer cells demonstrated the ability neither to remove BSP from the incubation medium nor to form a BSP-glutathione conjugate. In contrast, parenchymal cells removed BSP from the medium and formed a BSP-glutathione conjugate. The rate and maximum uptake of BSP by the parenchymal cells were inversely related to the concentration of serum or albumin in the incubation medium. In an effort to evaluate the influence of ethanol on BSP uptake, parenchymal cells were incubated in the presence of varying concentrations of ethanol. No alteration in BSP uptake was induced by the prior addition of ethanol to the incubation medium. The uptake and conjugation of BSP are exclusive functional expressions of the hepatic parenchymal cell population.

Animals↗