Literature DB >> 7033658

Response of the murine lymphoid system to a chronic infection with Trypanosoma congolense. I. The spleen.

W I Morrison, M Murray, D L Bovell.   

Abstract

The response within the different cellular compartments of the spleen in mice infected with Trypanosoma congolense was evaluated using histologic and cytologic methods and immunofluorescence to detect intracellular and cell surface immunoglobulin. The isolate of T. congolense used produces a chronic infection in C3H/He mice leading to death 40 to 70 days after inoculation. Previous studies had shown that this infection resulted in a marked immunodepression as judged by a range of in vitro assays of splenic cellular responses. It was found that the splenic cellular changes occurred in two phases. First, coincident with and following the first peak of parasitemia, there was a marked proliferative phase characterized by widespread hyperplasia of the white pulp with the production of large numbers of plasma cells and an expansion of the erythropoietic component of the red pulp. During this period, there was a marked decrease in the intensity of staining for surface Ig on cells of the follicular regions of the white pulp. Following the initial proliferative changes, a more protracted phase ensued during which, although the proliferative activity continued, there was a gradual disorganization of the white pulp with eventual lymphoid depletion. This was accompanied by a progressive expansion of the red pulp due to increased numbers of erythropoietic cells and to a lesser extent granulopoietic cells and macrophages. At the same time, there was a gradual decrease in the number of plasma cells found in the red pulp, although many were still present in the periarteriolar regions. The end result of these changes was an approximately 17-fold increase in total splenic cellularity of which erythropoietic cells contributed more than 50 per cent, and lymphocytes were reduced in absolute numbers to below control levels. A striking feature during both phases of the infection was the lack of discrete germinal centers.

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Year:  1981        PMID: 7033658

Source DB:  PubMed          Journal:  Lab Invest        ISSN: 0023-6837            Impact factor:   5.662


  6 in total

1.  Response of the murine hematopoietic system to chronic infection with Mycobacterium lepraemurium.

Authors:  M Resnick; E Fibach; M Lebastard; L Levy; H Bercovier
Journal:  Infect Immun       Date:  1988-12       Impact factor: 3.441

2.  T cells and macrophages in Trypanosoma brucei-related glomerulopathy.

Authors:  M L van Velthuysen; A E Mayen; N van Rooijen; G J Fleuren; E de Heer; J A Bruijn
Journal:  Infect Immun       Date:  1994-08       Impact factor: 3.441

Review 3.  Vaccination against trypanosomiasis: can it be done or is the trypanosome truly the ultimate immune destroyer and escape artist?

Authors:  Florencia La Greca; Stefan Magez
Journal:  Hum Vaccin       Date:  2011-11

4.  Influence of the Draining Lymph Nodes and Organized Lymphoid Tissue Microarchitecture on Susceptibility to Intradermal Trypanosoma brucei Infection.

Authors:  Omar A Alfituri; Barry M Bradford; Edith Paxton; Liam J Morrison; Neil A Mabbott
Journal:  Front Immunol       Date:  2020-06-03       Impact factor: 7.561

5.  Trypanosomiasis-induced B cell apoptosis results in loss of protective anti-parasite antibody responses and abolishment of vaccine-induced memory responses.

Authors:  Magdalena Radwanska; Patrick Guirnalda; Carl De Trez; Bernard Ryffel; Samuel Black; Stefan Magez
Journal:  PLoS Pathog       Date:  2008-05-30       Impact factor: 6.823

Review 6.  Histological Disorganization of Spleen Compartments and Severe Visceral Leishmaniasis.

Authors:  Micely d'El-Rei Hermida; Caroline Vilas Boas de Melo; Isadora Dos Santos Lima; Geraldo Gileno de Sá Oliveira; Washington L C Dos-Santos
Journal:  Front Cell Infect Microbiol       Date:  2018-11-13       Impact factor: 5.293

  6 in total

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