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C Cheers

Publications and source records attributed to C Cheers.

At least 73 records · Page 4Linked to original sources
PubMed1982

Mechanism of depletion of T lymphocytes from the spleen of mice infected with Listeria monocytogenes.

Marked changes in the splenic lymphocyte populations during murine infection with Listeria monocytogenes were observed histologically and quantitated by the immunofluorescence of Thy-1+ immunoglobulin (Ig-) (T) and Ig+ (B) cells. Cells were depleted from the T-dependent areas of the spleen, and the number of T cells in suspensions prepared from spleens of mice 1 to 3 days after primary or secondary infection were less than 1/10 of normal. High numbers of alcohol-killed Listeria sp. did not cause any depletion. Depletion was not prevented by adrenalectomy. Although injected radiolabeled T cells distributed normally between spleen, liver, lymph node, and gut in infected mice, there appeared to be a barrier to their entry into depleted T-dependent areas of the spleen. Evidence for the destruction of T cells, but not of B cells, in the infected mouse spleen was obtained.

Adrenalectomy↗
PubMed1982

Recovery from T cell depletion during murine listeriosis and effect on a T-dependent antibody response.

During the infection of mice with Listeria monocytogenes, there is a profound depletion of T (Thy-1+ Ig-) lymphocytes between days 1 and 4, followed by an increase in T cells to three times normal levels by day 9. The recovery of T cell numbers required cell proliferation, being sensitive to vinblastin and cyclophosphamide. Adult thymectomy 6 months before infection had no effect on recovery. The repopulating cells were no more sensitive than normal T cells to hydrocortisone. B lymphocytes (Ig+ cells) and null (Thy-1-Ig-) cells increased from day 1 after the injection of either live or (in contrast to T cells) killed Listeria organisms. Their increase was inhibited by vinblastin and cyclophosphamide. Despite T cell depletion, no depression of the antibody response to the T-dependent antigen, sheep erythrocytes, occurred during infection or when spleen cells were adoptively transferred from infected mice to irradiated recipients.

Animals↗
PubMed1980

Resistance and susceptibility of mice to bacterial infection: histopathology of listeriosis in resistant and susceptible strains.

C57BL/10 mice have previously been shown to be 100 times more resistant to intravenously injected Listeria monocytogenes than are BALB/c mice due to the action of a single gene, Lr. Differences in the histopathology of listeriosis in the two strains were sought. Of the tissues examined, only liver, spleen, blood, and thymus showed changes. In the liver, Listeria localized in Kupffer cells within 3 h of infection. By 24 h these cells became surrounded by neutrophilic polymorphonuclear leukocytes. After high doses of Listeria, the susceptible BALB/c mice showed many foci surrounded by few polymorphs, whereas in the resistant C57BL/10 mice there were relatively few foci surrounded by many polymorphs. By 4 days in sublethally infected mice the polymorphs in the liver of both strains were being replaced by monocytes and macrophages. Liver morphology returned to normal by 8 days postinfection. In the blood of both strains there was a rise in total lymphocyte numbers at 24 h, followed by a fall in T-lymphocytes and recovery at 5 days. C57BL/10 mice showed an early monocytic response in the blood, whereas BALB/c mice showed a polymorph leukocytosis. In the spleens of both C57BL/10 and BALB/c mice there was an early neutrophil response and red pulp hyperemia. This was followed by a dramatic lymphocyte depletion in the T-dependent periarteriolar regions in both strains beginning 2 days after infection. Absolute numbers of Thy-1(+) cells in spleen cell suspensions also fell to 10% of normal, recovering 6 to 8 days postinfection. Surface immunoglobulin-positive B-lymphocytes and Thy-1(-), immunoglobulin-negative "null" cells rose in both strains at days 4 to 5, returning to normal levels on days 10 to 12. Whether the null cells represent lymphocytes or other cell types remains unresolved. Thymus atrophy was seen in the BALB/c mice but not in C57BL/10 mice.

Animals↗
PubMed1979

Macrophage activation during experimental murine brucellosis: a basis for chronic infection.

Evidence is presented that the chronicity of infection in CBA mice after injection of Brucella abortus 19 is related to a number of factors: (i) the relative resistance of B. abortus to macrophage killing, which allowed some bacteria to survive the peak of macrophage activity occurring at 14 days; (ii) the decline in macrophage activity thereafter (this decline was related in part to the presence of fewer bacteria to stimulate the bactericidal activity and also to specific, active suppressor mechanisms not identified in this study); and (iii) the insensitivity of the persistent Brucella organisms to activated macrophages. This was not due to a selection of genetically resistant bacteria, but possibly to their inaccessibility, either within "incompetent" macrophages or outside macrophages altogether.

Animals↗
PubMed1979

Ia antigens in serum during different murine infections.

There exists in the mouse a family of I-region-controlled (Ia) antigens which carry carbohydrate-defined determinants. These antigens appear in serum as glycolipids and seem to be actively secreted by antigen-activated T-cells. This paper describes the ability of selected viral, bacterial, and protozoal infections of mice to markedly alter the serum levels of these Ia antigens. All the infectious agents examined induced substantial augmentation or suppression of serum Ia concentrations or both. Lymphocytic choriomeningitis (LCM) virus first enhanced and then suppressed serum Ia levels during the course of acute infection. Enhancement occurred during the time of ongoing virus replication and splenic lymphoproliferation while suppression coincided with the peak of the cytotoxic T-cell response and virus clearance. Listeria monocytogenes infection induced a substantial reduction in Ia levels at a time just after marked depletion of T-cells in the spleen. In contrast, Brucella abortus caused a significant increase in Ia levels 7 days postinfection, which correlates with the appearance of peak numbers of bacteria in tissues. Finally, Plasmodium yoelii, a nonlethal malarial parasite which stimulates prolonged T-cell proliferation, augmented serum Ia levels, whereas P. berghei, a lethal parasite which tends to inhibit. T-cell division, suppressed Ia secretion. Possible interpretations of these different results are presented.

Animals↗
PubMed1978

Resistance and susceptibility of mice to bacterial infection: genetics of listeriosis.

A survey of various strains of mice showed distinct differences in resistance or susceptibility to Listeria monocytogenes. C57B1, related sublines, NZB, and SJL were resistant to Listeria, whereas BALB/c, CBA, A, DBA/1, C3H, LP.RIII, 129, and WB were susceptible. The gene(s) responsible for resistance and susceptibility to Listeria were studied in detail. C57BL6/6, B10.D2, and B10.A mice were 100 times more resistant than were BALB/c, CBA, and A. Resistance of the (C57B1/6 X BALB/C)F1 was intermediate between the two parents, suggesting partial penetration of a dominant gene. Backcross studies in which the (C57B1/6 X BALB/c)F1 were crossed with the susceptible BALB/c parent suggested that a single gene or group of linked genes were the major determinant of resistance, although the possibility that other genes exerted a modifying influence was not excluded. By using the backcross and various congenic and recombinant mice, linkage of the genes involved to the H-1, H-2, H-3, H-4, H-7, or H-8 loci, to the immunoglobulin allotype, to the Thy-1 gene, to the Hc gene specifying C5, or to coat color genes (B, c) was excluded. There was no difference in the response of males and females. In all studies, the powerful overriding influence of the C57B1 genome was evident.

Animals↗
PubMed1978

Resistance and susceptibility of mice to bacterial infection: course of listeriosis in resistant or susceptible mice.

Resistance and susceptibility to Listeria monocytogenes in mice was found to be related to (i) the innate ability of the nonimmune macrophages to kill or inhibit the growth of the organism during the first 24 to 48 h after infection, and (ii) the time of onset of acquired cell-mediated resistance. Resistant C57Bl/6 mice were 10 times more efficient than susceptible BALB/c mice at suppressing the early growth of Listeria in the liver. Furthermore, the onset of acquired immunity occurred 24 to 48 h earlier in C57Bl/6 than in BALB/c mice. Acquired immunity was measured by (i) fall in bacterial numbers in spleen and livers of infected mice (ii) adoptive transfer of immunity to normal mice by using spleen cells from infected mice, (iii) delayed-type hypersensitivity skin testing, and (iv) uptake of tritiated thymidine by lymphocytes in the spleen.

Animals↗
PubMed1978

Polyadenylic acid-polyuridylic acid (poly A : U) and experimental murine brucellosis. I. Effect of single and double-stranded polynucleotides on Brucella abortus in vivo and in vitro.

The double stranded polynucleotide, poly A : U, when administered intraperitoneally at the same time as intravenous infection with Brucella abortus, suppressed the growth of that organism in the spleen and liver of mice. Single stranded poly A or poly U were not effective. On the other hand both the single and double stranded forms enhanced the growth of Br. abortus in broth culture. Poly A : U did not enhance the blood clearance of intravenously administered Br. abortus. Indeed its suppressive effect was not apparent until 2 days after administration. When mice given Br. abortus and poly A : U were given a second infection 2 days later, with either Br. abortus or Listeria monocytogens, the second infection was exacerbated, indicating a biphasic effect of poly A : U and antigen.

Animals↗
PubMed1975

Activated macrophages in congenitally athymic "nude mice" and in lethally irradiate mice.

Resistance to the facultative intracellular bacteria, Brucella abortus and Listeria monocytogenes, is principally the result of acquisition of enhanced antibacterial activity by host macrophages, probably in response to lymphokines released by T lymphocytes. However, the present paper describes a surprisingly high resistance on the part of both congenitally athymic "nude" mice and of lethally irradiated mice compared with normal controls. This enhanced bactericidal activity was evident 24 hr after infection, and could also be demonstrated in macrophages from nude mice cultured in vitro. It was concluded that the macrophages of these animals had been activated before infection.

Animals↗
PubMed1974

Cell-to-cell interaction in the immune response. X. T-cell-dependent suppression in tolerant mice.

Specific immunological tolerance was induced in CBA mice by a single injection of deaggregated fowl immunoglobulin G (FgammaG). The unresponsive state was stable on adoptive transfer and irreversible by pretreatment of tolerant cells with trypsin. Tolerant spleen cells could suppress the response of normal syngeneic recipients. They also suppressed the adoptive primary response of spleen cells to FgammaG in irradiated hosts. The inhibitory effect was on the indirect (7S) plaque-forming cell (PFC) response. Incubation of the tolerant cell population with anti-theta serum and complement reversed the suppressor effect. Furthermore, the addition of purified T cells from normal donors restored the capacity of the anti-theta serum-treated tolerant cells to transfer an adoptive response to FgammaG. The existence of FgammaG-reactive B cells was supported by the demonstration of normal numbers of antigen-binding cells in the spleen and thoracic duct lymph from tolerant animals. Moreover, the formation of caps by these cells implied that they could bind antigen normally. These experiments provided direct evidence for the existence of suppressor T cells in the tolerant population. Further evidence was derived from examination of the effect of antigen "suicide". Tolerant spleen cells were treated with radioactive FgammaG under conditions known to abrogate T-cell helper function. When these cells were transferred together with normal spleen cells into irradiated hosts, suppression of the primary adoptive response to FgammaG was no longer observed. Inhibition of an adoptive secondary response to FgammaG was obtained by transferring tolerant spleen cells with primed B cells provided high doses of tolerant cells were used. By contrast low doses exerted a helper rather than a suppressor effect in this system.

Animals↗