Literature DB >> 2788581

Histological changes in the spleen and liver of C57BL/6 and A/J mice during Plasmodium chabaudi AS infection.

M M Stevenson1, G Kraal.   

Abstract

The level of resistance to infection in inbred mice with the murine malaria species Plasmodium chabaudi AS is genetically determined. Resistant C57BL/6, which are able to eliminate the parasite by 4 weeks, develop marked splenomegaly and survive the infection. Susceptible A/J mice, which succumb to infection (mean survival time = 10 days), develop only minimal splenomegaly. In order to determine if gross differences in the organization, number, and type of spleen cells are related to the outcome of infection with P. chabaudi AS, the development of splenomegaly was examined by enzyme and immunohistochemical methods during the first week after infection. Cryostat sections of spleens removed from normal animals of both strains and at 4 and 7 days after intraperitoneal infection with 10(6) parasitized erythrocytes were stained for enzyme (acid phosphatase and nonspecific esterase) and immunohistochemistry with conventional monoclonal antibodies against T cells, B cells, and macrophages as well as with novel rat anti-mouse monoclonal antibodies which define discrete subpopulations of macrophages in the mouse spleen. The livers of normal and infected animals of each strain were also examined. The results of this study demonstrate (1) differences between normal, uninfected B6 and A/J mice in the organization and number of one subpopulation of macrophages in the spleen, the marginal metallophilic macrophages, and (2) marked histological changes in the spleen and liver during the course of infection in both resistant C57BL/6 and susceptible A/J mice. These changes include depletion of cells from the marginal zone of the spleen which, in the case of the marginal metallophilic macrophages, appears to be more severe in susceptible A/J mice.

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Year:  1989        PMID: 2788581     DOI: 10.1016/0014-4800(89)90009-9

Source DB:  PubMed          Journal:  Exp Mol Pathol        ISSN: 0014-4800            Impact factor:   3.362


  16 in total

1.  Deficiency in tumor necrosis factor alpha activity does not impair early protective Th1 responses against blood-stage malaria.

Authors:  H Sam; Z Su; M M Stevenson
Journal:  Infect Immun       Date:  1999-05       Impact factor: 3.441

2.  Murine malaria infection induces fetal loss associated with accumulation of Plasmodium chabaudi AS-infected erythrocytes in the placenta.

Authors:  Jayakumar Poovassery; Julie M Moore
Journal:  Infect Immun       Date:  2006-05       Impact factor: 3.441

3.  Massive destruction of malaria-parasitized red blood cells despite spleen closure.

Authors:  Jürgen Krücken; Liv I Mehnert; Mohamed A Dkhil; Manal El-Khadragy; W Peter M Benten; Horst Mossmann; Frank Wunderlich
Journal:  Infect Immun       Date:  2005-10       Impact factor: 3.441

4.  Early IL-12 p70, but not p40, production by splenic macrophages correlates with host resistance to blood-stage Plasmodium chabaudi AS malaria.

Authors:  H Sam; M M Stevenson
Journal:  Clin Exp Immunol       Date:  1999-08       Impact factor: 4.330

5.  Fatal Plasmodium falciparum malaria causes specific patterns of splenic architectural disorganization.

Authors:  Britta C Urban; Tran T Hien; Nicholas P Day; Nguyen H Phu; Rachel Roberts; Emsri Pongponratn; Margret Jones; Nguyen T H Mai; Delia Bethell; Gareth D H Turner; David Ferguson; Nicholas J White; David J Roberts
Journal:  Infect Immun       Date:  2005-04       Impact factor: 3.441

6.  Trafficking of Plasmodium chabaudi adami-infected erythrocytes within the mouse spleen.

Authors:  A Yadava; S Kumar; J A Dvorak; G Milon; L H Miller
Journal:  Proc Natl Acad Sci U S A       Date:  1996-05-14       Impact factor: 11.205

7.  Alterations of splenic architecture in malaria are induced independently of Toll-like receptors 2, 4, and 9 or MyD88 and may affect antibody affinity.

Authors:  Emma T Cadman; Asmahan Y Abdallah; Cécile Voisine; Anne-Marit Sponaas; Patrick Corran; Tracey Lamb; Douglas Brown; Francis Ndungu; Jean Langhorne
Journal:  Infect Immun       Date:  2008-06-16       Impact factor: 3.441

8.  Splenic red pulp macrophages produce type I interferons as early sentinels of malaria infection but are dispensable for control.

Authors:  Charles C Kim; Christopher S Nelson; Emily B Wilson; Baidong Hou; Anthony L DeFranco; Joseph L DeRisi
Journal:  PLoS One       Date:  2012-10-29       Impact factor: 3.240

Review 9.  Plasmodium falciparum malaria and invasive bacterial co-infection in young African children: the dysfunctional spleen hypothesis.

Authors:  Gloria P Gómez-Pérez; Robin van Bruggen; Martin P Grobusch; Carlota Dobaño
Journal:  Malar J       Date:  2014-08-26       Impact factor: 2.979

10.  Lack of avidity maturation of merozoite antigen-specific antibodies with increasing exposure to Plasmodium falciparum amongst children and adults exposed to endemic malaria in Kenya.

Authors:  Frances Ibison; Ally Olotu; Daniel M Muema; Jedida Mwacharo; Eric Ohuma; Domtila Kimani; Kevin Marsh; Philip Bejon; Francis M Ndungu
Journal:  PLoS One       Date:  2012-12-26       Impact factor: 3.240

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