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M G Pappas

Publications and source records attributed to M G Pappas.

26 records · Page 2Linked to original sources
PubMed1983

Susceptibility of inbred mice to Leishmania tropica infection: correlation of susceptibility with in vitro defective macrophage microbicidal activities.

Eleven mouse strains were inoculated in footpads with amastigotes of Leishmania tropica and observed for 12 weeks. Liver and spleen impression smears from infected mice were examined for the presence of intracellular parasites. Four strains (BALB/cJ, C57L/J, NZW/N, and P/J) failed to heal the subcutaneous lesion and showed evidence of systemic infection; the remaining seven strains (A/J, C3H/HeJ, C3H/HeN, C3HeB/FeJ, C57BL/6J, C57BL/10J, and C57BL/10ScN) were each resistant to infection and resolved their lesions by Week 10. Macrophages from the four susceptible strains could not be activated to kill L. tropica amastigotes by treatment with soluble lymphocyte products in vitro. In contrast, macrophages from all seven resistant strains responded to lymphokine treatment and eliminated 80-90% of intracellular parasites. These results suggest that in vitro macrophage microbicidal activities predict the course of systemic leishmanial disease.

Animals↗
PubMed1983

Antileishmanial activities of macrophages from C3H/HeN and C3H/HeJ mice treated with Mycobacterium bovis strain BCG.

C3H/HeN and C3H/HeJ mice were infected ip with viable BCG, a macrophage-activating agent, and their peritoneal exudate macrophages exposed to Leishmania tropica amastigotes. Macrophages from BCG-infected C3H/HeN mice had both leishmanicidal activities described for lymphokine activation of C3H/HeN macrophages in vitro: increased resistance to L. tropica infection, followed by intracellular killing of the parasite. Macrophages from BCG-infected C3H/HeN mice were also activated to kill tumor cells in vitro. In contrast, macrophages from BCG-treated C3H/HeJ mice were not resistant to L. tropica infection, did not kill intracellular amastigotes over 72 hr in culture, and were not cytotoxic to tumor cells.

Adrenal Gland Neoplasms↗
PubMed1983

Evaluation of promastigote and amastigote antigens in the indirect fluorescent antibody test for American cutaneous leishmaniasis.

Leishmania braziliensis panamensis promastigotes, temperature-induced in vitro-cultivated amastigotes, Vero cell-derived amastigotes, and rodent lesion-derived amastigotes were evaluated as antigens in the indirect immunofluorescent antibody (IFA) test for American cutaneous leishmaniasis. Test sensitivity was determined using sera from 34 U.S. soldiers with leishmaniasis diagnosed by demonstrating parasites in their skin lesions. Sera were collected from 3 to 24 months after exposure to Leishmania. Positive IFA reactions among patient sera were 82% with promastigotes or lesion amastigotes, 79% with in vitro amastigotes, and 76% with Vero cell amastigotes (P = N.S.). Positive titers ranged from 1:8 to 1:128 using all antigens. Test specificity was determined with 30 sera from healthy individuals. False positive reactions ranged from 0-5% depending on the antigen and all titers were less than or equal to 1:8. Test cross-reactivity was assessed with 47 sera from patients with other diseases. Depending on the antigen, cross-reactions occurred with sera from patients with Chagas' disease, lupus erythematosus, malaria, toxoplasmosis and amebiasis. None of the antigens cross-reacted with sera from patients with viral hepatitis, coccidioidomycosis, syphilis, schistosomiasis, and trichinosis. In replicate experiments, 99-100% of the sera varied no more than +/- 1 titer dilution. As sensitivity, specificity, cross-reactivity, and reproducibility of the four antigens were statistically similar, promastigotes, which can be easily and economically cultured in large numbers in vitro are recommended for use in the IFA test for American cutaneous leishmaniasis.

Adult↗
PubMed1983

Infection and replication of Leishmania tropica in mouse peritoneal macrophages elicited by sterile inflammatory agents and BCG.

C3HeB/FeJ peritoneal exudate macrophages elicited with a variety of sterile inflammatory agents or with Mycobacterium bovis strain BCG were exposed to Leishmania tropica amastigotes in vitro. The percentages of L. tropica-infected macrophages were similar in resident and inflammatory macrophage populations over 72 hours in culture. Inflammatory macrophages supported intracellular replication of L. tropica in excess of that by resident macrophages. These macrophages also failed to demonstrate cytotoxicity to tumor cells in vitro, a defined nonspecific effector function of activated macrophages. However, macrophages from BCG-treated mice were significantly more resistant to initial infection with L. tropica, killed intracellular amastigotes by 72 hours in culture and were cytotoxic to tumor cells, indicating full immunologic activation. The inability of inflammatory macrophages to kill L. tropica parasites suggests that inflammation may actually contribute to the pathogenesis of leishmaniasis.

Animals↗
PubMed1981

Complement-mediated defect in clearance and sequestration of sensitized, autologous erythrocytes in rodent malaria.

We investigated the ability of malaria-infected and normal mice to clear particulate immune complexes consisting of autologous erythrocytes sensitized with either IgG or complement. Normal mice rapidly clear autologous erythrocytes optimally sensitized with IgG and the liver plays a major role in their sequestration. Clearance of optimally sensitized erythrocytes is complement-dependent because cobra venom factor-treated, normal mice failed to clear these cells rapidly, unless they had been pre-treated with fresh mouse serum. In the initial phase of Plasmodium berghei infection, clearance of the optimally sensitized erythrocytes was markedly increased over that observed in normal mice. 2 wk after infection, however, clearance was minimal. This defect was most likely the consequence of the hypocomplementemia observed at this stage of infection since sensitized erythrocytes were removed rapidly from the blood if they had been coated with C3 in vitro before injection into malarial mice.The functional activity of the complement receptors of phagocytic cells was assayed in malarial mice by the injection of autologous erythrocytes coated with C3 and C4 in the absence of antibody. The complement-coated erythrocytes were rapidly removed from the blood, accumulated in the liver, and then gradually returned to the circulation. Similar patterns were observed in normal animals, but the degree of clearance was considerably higher in the malarial mice late in infection. It appears, therefore, that complement receptors remain functional throughout the infection. Erythrocytes suboptimally sensitized with IgG were cleared minimally by normal mice. This clearance was not complement-dependent and was mediated mainly by the spleen. During malaria, clearance of these particles was initially enhanced but later it was abolished.The association of hypocomplementemia with a major splenic defect in clearance late in malaria infection may explain the accumulation of immune complexes in pathological sites observed in this disease.

Animals↗