A role for granulomatous inflammation in the transmission of infectious disease: schistosomiasis and tuberculosis

Parasitology ◽  
1997 ◽  
Vol 115 (7) ◽  
pp. 113-125 ◽  
Author(s):  
M. J. DOENHOFF
Keyword(s):  
Lymph Node ◽  
Immune Cell ◽  
Bacterial Pathogen ◽  
Granulomatous Inflammation ◽  
Immune Serum ◽  
Lung Pathology ◽  
A Cell ◽  
Lymph Node Cells ◽  
Excretion Rates ◽  
The Relationship

The relationship between cell-mediated granulomatous inflammation and transmission of disease in schistosomiasis and tuberculosis has been explored. In 2 experiments involving Schistosoma mansoni-infected normal and T cell-deprived mice, and infected deprived mice that had been variously reconstituted with immune or normal lymphocytes or immune serum, there was a significant positive numerical correlation between mean liver granuloma diameters and faecal egg counts in individual animals. Lymphocytes from donors with recently patent infections were more active than cells from chronically infected or uninfected donors in reconstituting egg excretion rates in deprived recipients, and mesenteric lymph node (MLN) cells were more active than spleen cells. Modulation of granulomatous activity with increasing chronicity of infection in the donors, resulting in a decrease in granuloma size around freshly produced tissue-bound eggs, was paralleled by a waning of the capacity of transferred lymph node cells to reconstitute egg excretion in the recipients. Serum taken from chronically infected donor mice over the same period and transferred to infected deprived recipients became more active in enhancing egg excretion in the recipients as the cell-mediated activity declined. A recent study in Kenya has found that S. mansoni-infected patients with concurrent human immunodefficiency virus (HIV) infection excrete fewer eggs than patients exposed to the same levels of schistosome infection, but who are not HIV-infected, thus indicating that schistosome egg excretion in humans is also immune-dependent. Attention is drawn to an apparently parallel situation in human tuberculosis, another pathogen which induces a cell-mediated granulomatous immune response. Several studies have shown that patients with tuberculosis who are also HIV-seropositive tend to have fewer tubercle bacilli detectable in their saliva than those with tuberculosis, but who are HIV-negative. This discrepancy, associated with differences in lung pathology in HIV-positive patients, suggests that in tuberculosis immune cell-mediated granulomatous inflammation causes the destruction of host tissue in a manner which facilitates onward transmission of the bacterial pathogen.

Interaction of Alveolar Macrophages with Nocardia asteroides : Immunological Enhancement of Phagocytosis, Phagosome-Lysosome Fusion, and Microbicidal Activity

1980 ◽  
Vol 30 (2) ◽  
pp. 578-587
Author(s):  
Carole Davis-Scibienski ◽  
Blaine L. Beaman
Keyword(s):  
Lymph Node ◽  
Alveolar Macrophages ◽  
Cell Damage ◽  
Immune Serum ◽  
Nocardia Asteroides ◽  
Bacterial Cells ◽  
Activated Macrophages ◽  
Additional Increase ◽  
Lining Material ◽  
Lymph Node Cells

Normal and specifically activated rabbit alveolar macrophages were infected in vitro with Nocardia asteroides GUH-2. In the presence of serum from normal rabbits, no significant differences were noted between normal and activated alveolar macrophages with respect to phagocytosis, incidence of phagosomelysosome fusion, or nocardicidal activity. However, all of these macrophage functions were enhanced by various immunological components. Serum from immunized rabbits enhanced phagocytosis of nocardial cells by activated macrophages, and there was an additional increase in phagocytosis observed when alveolar lining material was present. Complement had no effect on the ability of the macrophages to phagocytize nocardial cells. The greatest percentage of organisms phagocytized was observed when specifically primed lymph node cells, alveolar lining material, and serum from immunized rabbits were present in the incubation medium. N. asteroides GUH-2 inhibited phagosome-lysosome fusion in normal macrophages in the presence of serum from normal rabbits. However, addition of serum from immunized rabbits or the addition of specifically primed lymphocytes increased the amount of phagosome-lysosome fusion, whereas complement had no effect on this fusion process. Nocardial viability was not reduced when either normal or activated macrophages were infected with bacteria in the presence of normal serum, immune serum, or alveolar lining material. However, specifically activated macrophages incubated with primed lymph node cells obtained from immunized rabbits were able to both decrease the number of viable organisms recovered and to increase the incidence and extent of bacterial cell damage. The greatest number of organisms were killed by specifically activated macrophages when the bacterial cells were incubated with primed lymph node cells suspended in immune serum and alveolar lining material. These results indicate that activated macrophages alone are not sufficient to kill ingested N. asteroides GUH-2 and that specifically primed lymphocytes are important in host resistance to nocardial infections.

scholarly journals A cell-mediated reaction against glomerular-bound immune complexes.

1979 ◽  
Vol 150 (6) ◽  
pp. 1410-1420 ◽  
Author(s):  
A K Bhan ◽  
A B Collins ◽  
E E Schneeberger ◽  
R T McCluskey
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Immune Complexes ◽  
Gamma Globulin ◽  
Mononuclear Phagocytes ◽  
A Cell ◽  
Lymph Node Cells ◽  
Soluble Immune Complexes ◽  
Histologic Changes ◽  
Glomerular Capillaries

Lewis rats were given a single i.v. injection of soluble immune complexes containing human serum albumin (HSA) and rabbit anti-HSA antibodies, prepared in antigen excess. This resulted in localization of HSA and rabbit gamma globulin (RGG) in glomerular mesangial regions without producing definite histologic changes. 24 h after the injection of immune complexes, groups of these rats received lymph node cells or T-cell preparations from syngeneic donors sensitized to RGG, HSA, or ovalbumin; another group received no cells. All of these groups and a group of normal control rats were given injections of [3H]thymidine at 18, 27, and 44 h. The animals were killed 48 h after the time of cell transfer. In histologic sections, glomerular abnormalities were found only in some of the animals that had received immune complexes and lymph node cells or T-cell populations from donors sensitized to HSA or RGG; the lesions were characterized by focal and segmental increase in cells in mesangial regions. Autoradiographs revealed significantly greater numbers of labeled cells in mesangial regions and glomerular capillaries in the groups that had received immune complexes and cells from HSA- or RGG-sensitized donors than in any of the other groups. Electronmicroscopic studies suggested that the increase in cellularity in mesangial regions resulted from an influx of mononuclear phagocytes. The findings indicate that cell-mediated reactions can be initiated by the interaction between sensitized T lymphocytes and antigens present in immune complexes within mesangial regions.

scholarly journals ANTIBODY FORMATION INITIATED IN VITRO

1963 ◽  
Vol 117 (4) ◽  
pp. 595-602 ◽  
Author(s):  
M. Fishman ◽  
F. L. Adler
Keyword(s):  
Lymph Node ◽  
Specific Antibody ◽  
Antibody Formation ◽  
Diffusion Chamber ◽  
A Cell ◽  
Lymph Node Cells ◽  
Chamber Technique

The diffusion chamber technique permitted the demonstration of specific antibody formation in x-irradiated recipients of such chambers filled with normal lymph node cells and a cell-free homogenate of macrophages which had been incubated in intro with T2 bacteriophage. The activity of the cell-free homogenate was retained in its RNA fraction isolated by means of the phenol method. No antibody formation occurred if such RNA was treated with RNAase. On sucrose gradients (5 to 20 per cent), the active RNA was found to be present in the top third layer. The question of the possible presence of antigen complexed to the RNA is discussed.

scholarly journals Incomplete inhibition of HIV infection results in more HIV infected lymph node cells by reducing cell death

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Laurelle Jackson ◽  
Jessica Hunter ◽  
Sandile Cele ◽  
Isabella Markham Ferreira ◽  
Andrew C Young ◽  
...  
Keyword(s):  
Cell Death ◽  
Lymph Node ◽  
Hiv Transmission ◽  
Neutralizing Antibody ◽  
Force Of Infection ◽  
Infected Lymph Node ◽  
A Cell ◽  
Lymph Node Cells ◽  
Infected Cells

HIV has been reported to be cytotoxic in vitro and in lymph node infection models. Using a computational approach, we found that partial inhibition of transmissions of multiple virions per cell could lead to increased numbers of live infected cells. If the number of viral DNA copies remains above one after inhibition, then eliminating the surplus viral copies reduces cell death. Using a cell line, we observed increased numbers of live infected cells when infection was partially inhibited with the antiretroviral efavirenz or neutralizing antibody. We then used efavirenz at concentrations reported in lymph nodes to inhibit lymph node infection by partially resistant HIV mutants. We observed more live infected lymph node cells, but with fewer HIV DNA copies per cell, relative to no drug. Hence, counterintuitively, limited attenuation of HIV transmission per cell may increase live infected cell numbers in environments where the force of infection is high.

Immune expulsion of Trichuris muris from mice during a primary infection: analysis of the components involved

Parasitology ◽  
1975 ◽  
Vol 70 (3) ◽  
pp. 397-405 ◽  
Author(s):  
D. Wakelin
Keyword(s):  
Lymph Node ◽  
Mesenteric Lymph Node ◽  
Primary Infection ◽  
Immune Serum ◽  
Trichuris Muris ◽  
Mesenteric Lymph ◽  
Serum Transfer ◽  
Lymph Node Cells ◽  
Worm Expulsion ◽  
Sublethal Irradiation

Immune serum accelerated the expulsion of Trichuris muris when transferred into normal mice on days 0 and 3 after infection, but had no effect when the recipient mice had been immunosuppressed by sublethal irradiation or by cortisone treatment. Delaying serum transfer until days 7 and 8 in normal mice failed to accelerate expulsion, although immune mesenteric lymph node cells (MLNC) accelerated expulsion whether transferred early or late in infection.Expulsion from NIH mice, normally complete by 12 days, was prevented by sublethal irradiation given as late as 9 days after infection, but could be restored by subsequent transfer of immune MLNC or, to a lesser degree, non-immune MLNC. Immune MLNC were unable to restore worm expulsion in mice irradiated before infection.These results are interpreted as showing that the immune expulsion of T. muris from mice during a primary infection requires the sequential activities of antibody-mediated and lymphoid cell-mediated components.

scholarly journals Evidence for a pathogenic role of a cell-mediated immune mechanism in experimental glomerulonephritis.

1978 ◽  
Vol 148 (1) ◽  
pp. 246-260 ◽  
Author(s):  
A K Bhan ◽  
E E Schneeberger ◽  
A B Collins ◽  
R T McCluskey
Keyword(s):  
Endothelial Cells ◽  
Lymph Node ◽  
Gamma Globulin ◽  
Mononuclear Cells ◽  
Immune Mechanism ◽  
Pathogenic Role ◽  
Glomerular Lesions ◽  
A Cell ◽  
Lymph Node Cells

Lewis rats were injected intravenously with rabbit anti-rat glomerular basement membrane (GBM) antisera in doses that were sufficient to cause glomerular fixation of rabbit gamma globulin (RGG) detectable by immunofluorescence, but which failed to induce histologically detectable lesions. 24 h later, groups of rats received lymph node cells or serum from syngeneic donors that had been immunized with either RGG or ovalbumin; they were injected with [3H]thymidine three times during the next 2 days, and sacrificed 48 or 96 h after transfer. Only the rats given anti-GBM antiserum plus lymph node cells from donors sensitized to RGG showed histological glomerular lesions, in the form of segmental hypercellularly and necrosis. Autoradiographs revealed the greatest number of labeled cells in glomeruli in the same group. In analogous experiments, it was shown that T-cell-enriched populations could induce hypercellular glomerular reactions. On the basis of electronmicroscopic and autoradiographic observations, it appears that the glomerular hypercellularity resulted from both infiltration of mononuclear cells and proliferation of endothelial cells. The findings indicate that interaction of specifically sensitized lymphocytes with glomerular-bound antigen can induce a cell-mediated (delayed-type) reaction in glomeruli.

scholarly journals Incomplete inhibition of HIV infection results in more HIV infected lymph node cells by reducing cell death

2017 ◽  
Author(s):  
Laurelle Jackson ◽  
Jessica Hunter ◽  
Sandile Cele ◽  
Isabella Markham Ferreira ◽  
Andrew Young ◽  
...  
Keyword(s):  
Cell Death ◽  
Lymph Node ◽  
Hiv Transmission ◽  
Neutralizing Antibody ◽  
Force Of Infection ◽  
Infected Lymph Node ◽  
A Cell ◽  
Lymph Node Cells ◽  
Infected Cells

AbstractHIV has been reported to be cytotoxic in vitro and in lymph node infection models. Using a computational approach, we found that partial inhibition of transmission which involves multiple virions per cell could lead to increased numbers of live infected cells if the number of viral DNA copies remains above one after inhibition, as eliminating the surplus viral copies reduces cell death. Using a cell line, we observed increased numbers of live infected cells when infection was partially inhibited with the antiretroviral efavirenz or neutralizing antibody. We then used efavirenz at concentrations reported in lymph nodes to inhibit lymph node infection by partially resistant HIV mutants. We observed more live infected lymph node cells, but with fewer HIV DNA copies per cell, relative to no drug. Hence, counterintuitively, limited attenuation of HIV transmission per cell may increase live infected cell numbers in environments where the force of infection is high.

scholarly journals SPECIFICITY OF THE INFLAMMATORY RESPONSE IN VIRAL ENCEPHALITIS

1972 ◽  
Vol 136 (2) ◽  
pp. 216-226 ◽  
Author(s):  
Henry F. McFarland ◽  
Diane E. Griffin ◽  
Richard T. Johnson
Keyword(s):  
Bone Marrow ◽  
Lymph Node ◽  
Inflammatory Response ◽  
Sindbis Virus ◽  
Bone Marrow Cells ◽  
Immune Serum ◽  
Inflammatory Reactions ◽  
Virus Content ◽  
Lymph Node Cells ◽  
Marrow Cells

The viral-induced perivascular inflammatory response in Sindbis virus encephalitis of mice was shown to be immunologically specific. Mice were inoculated intracerebrally with Sindbis virus, and 24 hr later a single dose of cyclophosphamide was given which ablated the inflammatory response. 3 days after virus inoculation, cells and/or sera from specifically and nonspecifically sensitized donor mice were given, and the inflammatory reactions, virus content, and antibody response of recipients were examined 5 days later. Reconstitution of the viral inflammatory response required virus-specific sensitized lymph node cells and was enhanced when these lymph node cells were combined with bone marrow cells. Reconstitution was not achieved with Sindbis virus immune serum even when combined with nonspecifically sensitized cells. Combination of immune serum with Sindbis virus-sensitized cells did not produce an accentuation of the reaction. In distinction, reconstitution of the inflammatory reaction surrounding the stab wound was reconstituted with bone marrow cells from mice inoculated with Sindbis virus or control antigens. Reconstitution of the perivascular reaction was associated with a reduction in brain virus content. Although the transfer of Sindbis virus-sensitized lymph node cells and bone marrow cells resulted in the limited production of neutralizing antibody in the immunosuppressed recipient, the reduction in virus was significantly greater with the transfers of Sindbis virus-sensitized lymph node cells than with the passive transfer of immune serum alone.

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