Virulence and cord blood mononuclear cells cytokine production induced by perinatal listeria monocytogenes strains from different phylogenetic lineages.
Some of the phylogenetic lineages of Listeria monocytogenes are more likely to cause invasive disease in humans than are strains from other phylogenetic lineages. This suggests that strains belonging to these lineages display different levels of pathogenicity. To investigate this, we carried out a plaque-forming assay with HT-29 cells to evaluate the virulence of six perinatal strains from the three lineages that compose the species. All of the strains were largely over the 3.34 cutoff (between 4.29 and 5.97 mean log) with the HT-29 model and can therefore be considered to be equally virulent. We also explored part of the immune response of cord blood mononuclear cells by measuring cytokine production. All strains induced the production of similar amounts of TNF-alpha and IL-1beta. High concentrations of IL-6 and IL-8 were produced (between 6,000 and 17,000 pg/ml), whereas little or no IFN-gamma or IL-12 was produced. Thus, there is no difference between the strains from the three genetic lineages in terms of virulence or cytokine response. Given the epidemiological distribution of the serotypes responsible for human listeriosis and the genetic structure of the L. monocytogenes species, our results suggest: (i) that all strains from lineage I (serotypes 1/2b and 4b), a genetically homogeneous subpopulation, have a similar level of pathogenicity, and (ii) that lineage II (serotypes 1/2a and 1/2c), which is genetically more heterogeneous, is composed of strains with different levels of pathogenicity. The ones responsible for invasive diseases, particularly perinatal infections, display a similar level of pathogenicity to lineage-I strains and are not virulence-attenuated strains that can only infect the most immunocompromised hosts, whereas the other lineage-II strains are probably less pathogenic for humans.
Mereghetti
Laurent
L
Bacteriology Unit, Department of Medical and Molecular Microbiology - EA 3250, Faculty of Medicine, Tours, France. laurent.mereghetti@med.univ-tours.fr
Roche
Sylvie M
SM
Lanotte
Philippe
P
Watt
Stéphane
S
van der Mee-Marquet
Nathalie
N
Velge
Philippe
P
Quentin
Roland
R
D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D005312:Fetal Blood / Q000166:cytology*; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008089:Listeria monocytogenes / Q000145:classification* / Q000235:genetics / Q000472:pathogenicity*; D008088:Listeriosis / Q000276:immunology*; D010802:Phylogeny; D011247:Pregnancy; D012329:RNA, Bacterial / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D010948:Viral Plaque Assay
D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D012329:RNA, Bacterial; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12; D007371:Interferon-gamma