Pathogenesis of lymphoid lesions in murine experimental listeriosis

Marco, Alberto; Domingo, Mariano; Prats, Mariana Moreno; Briones, V.; Pumarola, M.; Domı́nguez, Lucas

doi:10.1016/s0021-9975(08)80057-6

Cited by 24 publications

(12 citation statements)

References 27 publications

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“…The most significant histopathological changes were necrosis and inflammation in livers and spleens with splenic lymphoid depletion, which is consistent with previous reports for a murine listeriosis model (6,20,21). Mice deficient in CD18 showed markedly reduced lesions in both livers and spleens.…”

Section: Discussionsupporting

confidence: 91%

Host Resistance of CD18 Knockout Mice against Systemic Infection withListeria monocytogenes

Prince

Brayton³

et al. 2003

Infect Immun

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Mice with targeted mutations of CD18, the common ␤2 subunit of CD11/CD18 integrins, have leukocytosis, impaired transendothelial neutrophil emigration, and reduced host defense to Streptococcus pneumoniae, a gram-positive extracellular bacterium. Previous studies using blocking monoclonal antibodies suggested roles for CD18 and CD11b in hepatic neutrophil recruitment and host innate response to Listeria monocytogenes, a gram-positive intracellular bacterium. We induced systemic listeriosis in CD18 knockout (CD18-ko) and wild-type (WT) mice by tail vein injection with Listeria. By 14 days postinjection (dpi), 8 of 10 WT mice died, compared with 2 of 10 CD18-ko mice (P < 0.01). Quantitative organ culture showed that numbers of Listeria organisms in livers and spleens were similar in both groups at 20 min postinfection. By 3, 5, and 7 dpi, however, numbers of Listeria organisms were significantly lower in livers and spleens of CD18-ko mice than in WT mice. Histopathology showed that following Listeria infection, CD18-ko mice had milder inflammatory and necrotizing lesions in both spleens and livers than did WT mice. Cytokine assays indicated that baseline interleukin-1␤ and granulocyte colony-stimulating factor (G-CSF) levels were higher in CD18-ko mice than in WT mice and that CD18-ko splenocytes produced higher levels of interleukin-1␤ and G-CSF than WT splenocytes under the same amount of Listeria stimulation. These findings show that CD18 is not an absolute requirement for antilisterial innate immunity or hepatic neutrophil recruitment. We propose that the absence of CD18 in the mice results in the priming of innate immunity, as evidenced by elevated cytokine expression, and neutrophilic leukocytosis, which augments antilisterial defense.

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Section: Discussionsupporting

confidence: 91%

Host Resistance of CD18 Knockout Mice against Systemic Infection withListeria monocytogenes

Prince

Brayton³

et al. 2003

Infect Immun

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“…Also, the large bolus of Listeria introduced systemically results in its dissemination throughout the entire lymph system and blood, accumulating predominantly in spleen and liver (28), but also in the mesenteric lymph nodes and Peyer's patches (27,28). This is true for the attenuated strain as well (unpublished).…”

Section: Discussionmentioning

confidence: 90%

Systemic Immunity and Mucosal Immunity Are Induced against Human Immunodeficiency Virus Gag Protein in Mice by a New Hyperattenuated Strain ofListeria monocytogenes

Rayevskaya

Frankel

2001

J Virol

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Vaccines designed to control chronic infections by intracellular agents such as human immunodeficiency virus type 1 (HIV-1) require the induction of cell-mediated immune responses to rid the host of pathogeninfected cells. Listeria monocytogenes has characteristics that make it an attractive vaccine vector for use against such infections. Here we show that parenteral immunization with a new highly attenuated strain of this organism provided complete protection against systemic and mucosal challenges with a recombinant vaccinia virus expressing HIV-1 gag. Immunization also generated a strong, long-term memory cytotoxic-T-lymphocyte (CTL) response in spleen, mesenteric lymph nodes, and Peyer's patches directed against the gag protein. Oral immunization with this attenuated strain also produced complete, long-lasting protection against the recombinant virus but only against mucosal virus challenge. Curiously, oral immunization was associated with a transient CTL response in the three lymphoid tissues examined.

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“…Thus, in mice infected with type A F. tularensis by aerosol, the thymus involutes during the infectious process to the same extent as that reported after high dose i.p. infection with another type A strain of the pathogen [16] and during infections initiated by other pathogenic microbes such as L. monocytogenes [6], K. pneumoniae [7]), T. gondii [12] and Trypanosoma cruzi [18].…”

Section: Resultsmentioning

confidence: 99%

“…In this regard, experimental infection of mice with a number of bacteria (Listeria monocytogenes [6], Escherichia coli, Pseudomonas aeruginosa, Klebsiella pneumoniae, and Streptococcus pneumoniae [7]), viruses (murine cytomegalovirus [8], murine leukemia virus [9], HIV [10], and mouse hepatitis virus [11]), and protozoa (Toxoplasma gondii [12], and Trypanosoma cruzi) induces a severe lymphocytopaenia and marked thymus atrophy and loss of cortical lymphocytes. In addition, certain bacterial products and toxins, such as lipopolysaccharide (LPS) [13], enterotoxigenic E. coli enterotoxin [14] and mycobacterial cord factor (trehalos 6,6′-dimycolate) [15], also cause severe thymus damage.…”

Section: Introductionmentioning

confidence: 99%

Low dose aerosol infection of mice with virulent type A Francisella tularensis induces severe thymus atrophy and CD4+CD8+ thymocyte depletion

Chen

KuoLee

Austin

et al. 2005

Microbial Pathogenesis

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Francisella tularensis is a gram-negative facultative intracellular bacterium and the causative agent of tularemia. Two subspecies (type A and B strains) of the pathogen exist, the former being much more virulent than the latter for humans and other higher mammals. In this study, we examined the effect of virulent strains of F. tularensis infection on the thymus and thymocytes and the potential mechanisms involved. Low-dose aerosol exposure of C57BL/6 mice with type A, but not type B, F. tularensis caused severe reduction in thymus weight and destruction of thymocytes, particularly CD4 + CD8 + thymocytes, by day 4 after infection. The depletion of thymocytes was accompanied by a significant increase in circulating cortisone levels and could be partially prevented by adrenalectomy. Moreover, thymus atrophy and thymocyte depletion following infection were abolished in mice deficient in tumor necrosis factor receptors 1 and 2, but not in FasL-deficient mice. The severe destruction of the thymus and selective depletion of immature thymocytes during type A F. tularensis infection may represent a key pathogenic mechanism in tularemia and could hinder the development of an effective primary immune response against this highly virulent pathogen.

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Pathogenesis of lymphoid lesions in murine experimental listeriosis

Cited by 24 publications

References 27 publications

Host Resistance of CD18 Knockout Mice against Systemic Infection withListeria monocytogenes

Host Resistance of CD18 Knockout Mice against Systemic Infection withListeria monocytogenes

Systemic Immunity and Mucosal Immunity Are Induced against Human Immunodeficiency Virus Gag Protein in Mice by a New Hyperattenuated Strain ofListeria monocytogenes

Low dose aerosol infection of mice with virulent type A Francisella tularensis induces severe thymus atrophy and CD4+CD8+ thymocyte depletion

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