Literature DB >> 2124401

Comparative histopathology in BALB/c mice infected with virulent and attenuated strains of Brucella abortus.

F M Enright1, L N Araya, P H Elzer, G E Rowe, A J Winter.   

Abstract

The course of infection in BALB/c mice of virulent Brucella abortus strain 2308 (S-2308) and attenuated strain 19 (S-19) varies markedly. Whereas S-19 is eliminated at an exponential rate beginning at 2 weeks post infection (p.i.), strain 2308 assumes a steady state or plateau during the first 6 weeks p.i. and thereafter is eliminated very slowly over a period exceeding 6 months. Here we compared the initiation and maintenance of inflammatory reactions in spleens and livers of mice infected with either of the two strains of B. abortus for the first 6 weeks p.i. Histological changes in the liver were similar in response to either strain and were characterized by the development of small granulomas and an influx of polymorphonuclear leukocytes (PMN) and monocytes. Tissue reactions in the spleen were similar at weeks 1 and 2 p.i. At 3 weeks p.i. and thereafter, focal granulomatous responses in S-2308-infected mice exceeded those in mice infected with S-19. Numbers of nonspecific esterase (NSE) positive mononuclear leukocytes in S-19-infected spleens had increased by 3 weeks p.i. and remained elevated. No comparable increase in NSE positive cells occurred in mice infected with S-2308, and numbers were significantly lower. At 4 weeks p.i. the influx of mature neutrophils and the intensity of extramedullary hematopoiesis were significantly greater in S-19-infected spleens. A profound depletion of periarteriolar lymphoid tissue was noted in both infections for the first 3 weeks p.i. However, repopulation of lymphoid sheaths in S-19-infected spleens became significantly greater by 4 weeks p.i. and continued to increase at significantly higher levels during the next 2 weeks. This study demonstrates quantitative differences in splenic inflammatory responses which are temporally related to the more rapid elimination of S-19. Based upon the lower susceptibility of strain 2308 to the protective effects of immune serum it is hypothesized that the different patterns of infection and inflammation displayed by the 2 strains may related to the differential capacities of antibody opsonized S-19 and S-2308 to survive in activated macrophages.

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Year:  1990        PMID: 2124401     DOI: 10.1016/0165-2427(90)90065-z

Source DB:  PubMed          Journal:  Vet Immunol Immunopathol        ISSN: 0165-2427            Impact factor:   2.046


  30 in total

1.  Lymphocyte proliferation in response to Brucella abortus 2308 or RB51 antigens in mice infected with strain 2308, RB51, or 19.

Authors:  M G Stevens; S C Olsen; G W Pugh
Journal:  Infect Immun       Date:  1994-10       Impact factor: 3.441

2.  Course of infection with the emergent pathogen Brucella microti in immunocompromised mice.

Authors:  María P Jiménez de Bagüés; Alba de Martino; Juan F Quintana; Ana Alcaraz; Julián Pardo
Journal:  Infect Immun       Date:  2011-08-08       Impact factor: 3.441

3.  Brucella abortus ΔrpoE1 confers protective immunity against wild type challenge in a mouse model of brucellosis.

Authors:  Jonathan W Willett; Julien Herrou; Daniel M Czyz; Jason X Cheng; Sean Crosson
Journal:  Vaccine       Date:  2016-08-31       Impact factor: 3.641

4.  Immune and pathologic responses in mice infected with Brucella abortus 19, RB51, or 2308.

Authors:  M G Stevens; S C Olsen; G W Pugh; M V Palmer
Journal:  Infect Immun       Date:  1994-08       Impact factor: 3.441

5.  Innate immune recognition of flagellin limits systemic persistence of Brucella.

Authors:  Jean-Jacques Letesson; Renée M Tsolis; Matthieu Terwagne; Jonathan Ferooz; Hortensia G Rolán; Yao-Hui Sun; Vidya Atluri; Mariana N Xavier; Luigi Franchi; Gabriel Núñez; Thomas Legrand; Richard A Flavell; Xavier De Bolle
Journal:  Cell Microbiol       Date:  2013-01-07       Impact factor: 3.715

6.  The Ton system, an ABC transporter, and a universally conserved GTPase are involved in iron utilization by Brucella melitensis 16M.

Authors:  Isabelle Danese; Valerie Haine; Rose-May Delrue; Anne Tibor; Pascal Lestrate; Olivier Stevaux; Pascal Mertens; Jean-Yves Paquet; Jacques Godfroid; Xavier De Bolle; Jean-Jacques Letesson
Journal:  Infect Immun       Date:  2004-10       Impact factor: 3.441

7.  Vaccination with Brucella abortus rough mutant RB51 protects BALB/c mice against virulent strains of Brucella abortus, Brucella melitensis, and Brucella ovis.

Authors:  M P Jiménez de Bagüés; P H Elzer; S M Jones; J M Blasco; F M Enright; G G Schurig; A J Winter
Journal:  Infect Immun       Date:  1994-11       Impact factor: 3.441

8.  Aerosol infection of BALB/c mice with Brucella melitensis and Brucella abortus and protective efficacy against aerosol challenge.

Authors:  M M Kahl-McDonagh; A M Arenas-Gamboa; T A Ficht
Journal:  Infect Immun       Date:  2007-07-30       Impact factor: 3.441

9.  Establishment of systemic Brucella melitensis infection through the digestive tract requires urease, the type IV secretion system, and lipopolysaccharide O antigen.

Authors:  Tatiane A Paixão; Christelle M Roux; Andreas B den Hartigh; Sumathi Sankaran-Walters; Satya Dandekar; Renato L Santos; Renée M Tsolis
Journal:  Infect Immun       Date:  2009-08-03       Impact factor: 3.441

10.  Brucella melitensis invades murine erythrocytes during infection.

Authors:  Marie-Alice Vitry; Delphine Hanot Mambres; Michaël Deghelt; Katrin Hack; Arnaud Machelart; Frédéric Lhomme; Jean-Marie Vanderwinden; Marjorie Vermeersch; Carl De Trez; David Pérez-Morga; Jean-Jacques Letesson; Eric Muraille
Journal:  Infect Immun       Date:  2014-07-07       Impact factor: 3.441

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