Intracytoplasmic growth and virulence of Listeria monocytogenes auxotrophic mutants

Marquis, Hélène; Bouwer, H. G. A.; Hinrichs, David J.; Portnoy, Daniel A.

doi:10.1128/iai.61.9.3756-3760.1993

Cited by 138 publications

(65 citation statements)

References 32 publications

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“…While knockout of the pro-BA locus reduces salt tolerance in complex broth, it does not appear to a¡ect virulence potential when administered to mice by the intraperitoneal or peroral routes [149]. This ¢nding re£ects that of an earlier study in which Marquis et al [234], using an uncharacterised proline auxotroph, showed that proline auxotrophy fails to exhibit reduced virulence, suggesting that the host tissue contains a relatively abundant source of free proline or proline containing peptides. Furthermore, manipulation of the system resulting in proline overproduction also failed to alter the virulence potential in L. monocytogenes [150].…”

Section: Osmoprotectant Accumulationsupporting

confidence: 72%

Bacterial osmoadaptation: the role of osmolytes in bacterial stress and virulence

Sleator¹

2001

FEMS Microbiology Reviews

219

288

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Two general strategies exist for the growth and survival of prokaryotes in environments of elevated osmolarity. The 'salt in cytoplasm' approach, which requires extensive structural modifications, is restricted mainly to members of the Halobacteriaceae. All other species have convergently evolved to cope with environments of elevated osmolarity by the accumulation of a restricted range of low molecular mass molecules, termed compatible solutes owing to their compatibility with cellular processes at high internal concentrations. Herein we review the molecular mechanisms governing the accumulation of these compounds, both in Gram-positive and Gram-negative bacteria, focusing specifically on the regulation of their transport/synthesis systems and the ability of these systems to sense and respond to changes in the osmolarity of the extracellular environment. Finally, we examine the current knowledge on the role of these osmostress responsive systems in contributing to the virulence potential of a number of pathogenic bacteria. ß

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Section: Osmoprotectant Accumulationsupporting

confidence: 72%

Bacterial osmoadaptation: the role of osmolytes in bacterial stress and virulence

Sleator¹

2001

FEMS Microbiology Reviews

219

288

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“…In fact, during the vital step of microbial proliferation in vivo, if certain nutrients are unavailable or withheld within the host, then the capacity of a pathogen to synthesize or acquire these nutrients becomes crucial. Although factors utilized to acquire iron are well accepted as being important for pathogenesis (Litwin and Calderwood, 1993), the importance of acquiring or synthesizing other nutritional factors is less appreciated but supported by a variety of both old (Bacon et al, 1950;Garber et al, 1952;Furness and Rowley, 1956;Levine and Maurer, 1958;Ivanovics et al, 1968;Hatch, 1975;Baselski et al, 1978) and more recent reports (Hosieth and Stocker, 1981;Straley and Harmon, 1984;Austin et al, 1987;Nnalue and Stocker, 1987;O'Callaghan et al, 1988;Bowe et al, 1989;Leung and Finlay, 1991;Mahan et al, 1993;Marquis et al, 1993;McAdam et al, 1995;Ullman and Carter, 1995). Furthermore, the frequent identification of biosynthetic genes as virulence traits in studies that have screened libraries of random gene fusions or randomly generated transposon mutants emphasizes the importance of metabolic genes in microbial pathogenesis (Fields et al, 1986;Leung and Finlay, 1991;Mahan et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Although nucleotide and amino acid auxotrophy has been shown to attenuate many pathogens, the majority of reports are on intracellular pathogens such as salmonella, listeria, mycobacteria, yersinia, chlamydia and rickettsia (Bacon et al, 1950;Furness and Rowley, 1956; # 1996 Blackwell Science Ltd, Molecular Microbiology, 22, 217-229 Hatch, 1975;Hosieth and Stocker, 1981;Straley and Harmon, 1984;Austin et al, 1987;Nnalue and Stocker, 1987;O'Callaghan et al, 1988;Bowe et al, 1989;Leung and Finlay, 1991;Mahan et al, 1993;Marquis et al, 1993;McAdam et al, 1995;Ullman and Carter, 1995). We are unaware of any such reports involving extraintestinal isolates of E. coli.…”

Section: Discussionmentioning

confidence: 99%

**Identification of two previously unrecognized genes (guaA and argC) important for uropathogenesis**

Russo

Jodush

Brown

et al. 1996

Molecular Microbiology

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Our knowledge of the traits possessed by extraintestinal isolates of Escherichia coli, necessary for growth and survival in urine, is limited. To identify such determinants, transposon (TnphoA'1,4) mutant libraries of a clinical isolate (CP9) were generated and screened for derivatives exhibiting decreased growth in urine in vitro, and for mutants with active lacZ fusions that were induced in urine relative to laboratory medium. Using this approach we identified two genes, guaA (CPA24) and argC (CPI-1), which were previously unrecognized as being important for growth in human urine. Unexpectedly, not only does CPA24 (guaA) not grow in human urine in vitro, but it is sensitive to its effects, undergoing a 2-3 log loss of viability over 6 h. By contrast, CPA24 neither grows nor is killed in M9 minimal medium and artificial urine. Therefore, we postulate that lack of guanine or its derivatives in urine, and the inability of CPA24 to synthesize these compounds de novo, prevents CPA24 from synthesizing other guanine (or derivatives)-dependent products that are critical for growth and survival in urine. Although it seems logical that decreased growth in urine in vitro should correlate with diminished urovirulence, this concept was tested by challenging mice with CPA24 in vivo in a mouse model of urinary tract infection (UTI). Indeed, CPA24 was found to be significantly less virulent compared with its wild-type parent CP9. CPI-1(argC) was identified because of the significant induction of its argC::lacZ fusion in urine. Subsequent testing in urine demonstrated that its growth was significantly diminished in all urine samples tested (four females, three males). Polyamine synthesis is dependent upon, in part, the arginine biosynthetic pathway. Therefore, we tested whether the induction of argC in urine and/or the decreased growth of CPI-1 was a result of low levels of polyamines or arginine in urine. The results suggest that low levels of arginine, but not polyamines, in human urine are responsible. When tested in vivo in the mouse model of UTI, CPI-1 was also found to be significantly less virulent than CP9. In summary, we have established that guaA and argC are the first genes, which we are aware of, that have been shown to contribute to the growth of E. coli in urine in vitro and both have diminished urovirulence in vivo. These results support the concept that urine can be used in vitro as a screening tool to identify urovirulence traits.

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“…The course of Listeria infection has been well studied in the mouse. This pathogen can survive inside macrophages by escaping into the cytoplasm from the phagosomes [16][17][18][19]. Either CD4 + or CD8 + T cells help prevent listeriosis [20][21][22][23][24], and gd T cells also play an important role in survival from listeriosis [25][26][27][28][29][30].…”

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

A defective Th1 response of the spleen in the initial phase may explain why splenectomy helps prevent aListeriainfection

Kuranaga

Kinoshita

Kawabata

et al. 2005

Clinical and Experimental Immunology

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SummaryListeria monocytogenes ( Listeria ) are known to grow and proliferate in the liver while a splenectomy induces host resistance against a Listeria infection despite the fact that a splenectomy inhibits the Th1 response. Therefore, the mechanism by which a splenectomy helps to prevent the growth of Listeria still remains to be elucidated. After an i.v. challenge of Listeria (1 ¥ ¥ ¥ ¥ 10 6 CFU) in C57BL/6 mice, Listeria rapidly increased in the spleen but not in the liver until 48 h. However, after this initial phase, Listeria remarkably grew in the liver. In contrast, when the mice received a splenectomy beforehand, no remarkable growth of Listeria in the liver was observed after Listeria challenge despite the fact that serum IFN-g g g g and IL-12 levels at 24 h after Listeria challenge were significantly lower than those in the sham mice. However, the liver leucocytes from mice by 6 h after infection produced a substantial amount of IFN-g g g g while spleen MNC did not, whereas spleen leucocytes at 24 h after Listeria challenge did. Consistently, the IFN-g g g g and IL-12 levels in the tissue homogenates of the spleen were significantly lower than in those of the liver until 6 h after infection. This defective spleen Th1 response in the early phase of Listeria infection was corrected by an IL-18 i.p. injection just after the Listeria challenge. Our findings suggest that Listeria exploit the defective Th1 environment of the spleen in the initial phase and afterwards overcome the host defense mechanism of the liver.

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Intracytoplasmic growth and virulence of Listeria monocytogenes auxotrophic mutants

Cited by 138 publications

References 32 publications

Bacterial osmoadaptation: the role of osmolytes in bacterial stress and virulence

Bacterial osmoadaptation: the role of osmolytes in bacterial stress and virulence

**Identification of two previously unrecognized genes (guaA and argC) important for uropathogenesis**

A defective Th1 response of the spleen in the initial phase may explain why splenectomy helps prevent aListeriainfection

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