13 research outputs found
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Characterization of a natural agglutinin present in the hemolymph of the California sea hare, Aplysia californica.
A substance in the serum of the marine gastropod, Aplysia californica, capable of agglutinating marine bacteria and vertebrate red blood cells was subjected to physicochemical analysis in order to ascertain its possible nature. Our studies indicate that agglutinating activity is due to a heterogeneous group of high molecular weight molecules with two activity peaks exhibiting sedimentation coefficients centering ∼18.5 S and ∼31.0 S. This material has a protein component associated with the active site since it is sensitive to heat, pH extremes, and extraction with 2-mercaptoethanol, phenol, chloroform, and trichloracetic acid. Its physicochemical characteristics are different from other known invertebrate agglutinating substances and from classical vertebrate antibody. © 1971
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Characterization of a natural agglutinin present in the hemolymph of the California sea hare, Aplysia californica.
A substance in the serum of the marine gastropod, Aplysia californica, capable of agglutinating marine bacteria and vertebrate red blood cells was subjected to physicochemical analysis in order to ascertain its possible nature. Our studies indicate that agglutinating activity is due to a heterogeneous group of high molecular weight molecules with two activity peaks exhibiting sedimentation coefficients centering ∼18.5 S and ∼31.0 S. This material has a protein component associated with the active site since it is sensitive to heat, pH extremes, and extraction with 2-mercaptoethanol, phenol, chloroform, and trichloracetic acid. Its physicochemical characteristics are different from other known invertebrate agglutinating substances and from classical vertebrate antibody. © 1971
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Role of the H-2s haplotype in survival of mice after infection with Trypanosoma cruzi.
In studies of the resistance of inbred mice to infection with Trypanosoma cruzi Peru, mouse strain B10.S was the only strain which survived the infection resulting from the inoculation of 10(3) trypomastigotes. This is the only inbred mouse strain studied to survive infection. To investigate the effect of the H-2 haplotype on survival, C57BL/10 congenic mouse strains bearing H-2S recombinant haplotypes and mouse strains A.SWSn/J and SJL/J were tested for their ability to overcome the T. cruzi infection. None of the recombinant strains tested, including B10.S(7R), B10.S(8R), B10.S(9R), and B10.HTT, survived the infection, indicating that at least two or more regions of the H-2 locus must be H-2S to ensure survival. Strains A.SWSn/J and SJL/J with the H-2S haplotype did not survive, indicating that the genetic background outside the H-2 complex also influences survival. The congenic F1 hybrid (C57BL/10 X B10.S) F1 exhibited intermediate survival levels when compared with the parental strains, indicating that H-2S survival is affected by gene dosage. The F1 hybrid strain [B10.S(7R) X B10.S(8R)]F1, which possesses the complete H-2S haplotype in the trans configuration, did not survive T. cruzi infection, suggesting that H-2S-mediated survival does not operate by trans complementation
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In vitro release of lymphotoxin by spleen cells from C3H/HEJ and C57BL/6 mice infected with Trypanosoma cruzi.
Lectin (PHA-P) activated nonadherent spleen cells from uninfected inbred strains of mice known to exhibit high parasitemias when infected with Trypanosoma cruzi (A/J and C3H/HeJ), released in vitro significantly less lymphotoxin (LT) than did a mouse strain (C57BL/6) known to exhibit low parasitemia when infected with T. cruzi. The capacity of mice to release LT in vitro changed upon infection with T. cruzi. Cells from infected C57BL/6 mice released LT levels well above that from uninfected C57BL/6 animals within 4 days after initial infection, and their capacity to release LT remained high even after the parasites were not detectable in the blood. Cells from infected C3H/HeJ mice were not able to respond as rapidly as those fom C57BL/6 animals; however, they were able to release LT at the same levels as the infected C57BL/6 by day 18. The parasitemia induced by Trypanosoma cruzi in C3H/HeJ and C57BL/6 mice was compared with the in vitro ability of their spleen cells to spontaneously release LT. Spontaneous release of LT was significantly higher by spleen cells from infected C57BL/6 mice than by cells from infected C3H/HeJ mice. The kinetics of natural LT release differed from that of mitogen-(PHA-P)-stimulated LT release; LT activity peaked at 3-6 hours of incubation in the former and then declined whereas LT activity in the latter reached a plateau after 3 hours of incubation and did not decline for at least 18 hours in the presence of the inducer. Supernatants from infected C57BL/6 splenocytes, when concentrated 5x by ultrafiltration, significantly inhibited both blood stream trypomastigote motility in vitro and their infectivity (by 98%) for WI38 human embryonic lung cell cultures. Similar preparations from C3H/HeJ splenocytes only slightly inhibited bloodstream trypomastigote motility and delayed, but did not prevent, infection of WI38 cells. No agglutination of immobilized parasites was noted. Splenocyte supernatants did not affect culture epimastigote motility or growth. This is the first report of direct action by lymphokine-containing supernatants against T. cruzi bloodstream trypomastigotes
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In vitro release of lymphotoxin by spleen cells from C3H/HEJ and C57BL/6 mice infected with Trypanosoma cruzi.
Lectin (PHA-P) activated nonadherent spleen cells from uninfected inbred strains of mice known to exhibit high parasitemias when infected with Trypanosoma cruzi (A/J and C3H/HeJ), released in vitro significantly less lymphotoxin (LT) than did a mouse strain (C57BL/6) known to exhibit low parasitemia when infected with T. cruzi. The capacity of mice to release LT in vitro changed upon infection with T. cruzi. Cells from infected C57BL/6 mice released LT levels well above that from uninfected C57BL/6 animals within 4 days after initial infection, and their capacity to release LT remained high even after the parasites were not detectable in the blood. Cells from infected C3H/HeJ mice were not able to respond as rapidly as those fom C57BL/6 animals; however, they were able to release LT at the same levels as the infected C57BL/6 by day 18. The parasitemia induced by Trypanosoma cruzi in C3H/HeJ and C57BL/6 mice was compared with the in vitro ability of their spleen cells to spontaneously release LT. Spontaneous release of LT was significantly higher by spleen cells from infected C57BL/6 mice than by cells from infected C3H/HeJ mice. The kinetics of natural LT release differed from that of mitogen-(PHA-P)-stimulated LT release; LT activity peaked at 3-6 hours of incubation in the former and then declined whereas LT activity in the latter reached a plateau after 3 hours of incubation and did not decline for at least 18 hours in the presence of the inducer. Supernatants from infected C57BL/6 splenocytes, when concentrated 5x by ultrafiltration, significantly inhibited both blood stream trypomastigote motility in vitro and their infectivity (by 98%) for WI38 human embryonic lung cell cultures. Similar preparations from C3H/HeJ splenocytes only slightly inhibited bloodstream trypomastigote motility and delayed, but did not prevent, infection of WI38 cells. No agglutination of immobilized parasites was noted. Splenocyte supernatants did not affect culture epimastigote motility or growth. This is the first report of direct action by lymphokine-containing supernatants against T. cruzi bloodstream trypomastigotes