Infection and Immunity
1098-5522
0019-9567
Mỹ
Cơ quản chủ quản: AMER SOC MICROBIOLOGY , American Society for Microbiology
Lĩnh vực:
ParasitologyInfectious DiseasesImmunologyMicrobiology
Các bài báo tiêu biểu
Relationships between <i>Staphylococcus aureus</i> Genetic Background, Virulence Factors, <i>agr</i> Groups (Alleles), and Human Disease ABSTRACT
The expression of most
Staphylococcus aureus
virulence factors is controlled by the
agr
locus, which encodes a two-component signaling pathway whose activating ligand is an
agr
-encoded autoinducing peptide (AIP). A polymorphism in the amino acid sequence of the AIP and of its corresponding receptor divides
S. aureus
strains into four major groups. Within a given group, each strain produces a peptide that can activate the
agr
response in the other member strains, whereas the AIPs belonging to different groups are usually mutually inhibitory. We investigated a possible relationship between
agr
groups and human
S. aureus
disease by studying 198
S. aureus
strains isolated from 14 asymptomatic carriers, 66 patients with suppurative infection, and 114 patients with acute toxemia. The
agr
group and the distribution of 24 toxin genes were analyzed by PCR, and the genetic background was determined by means of amplified fragment length polymorphism (AFLP) analysis. The isolates were relatively evenly distributed among the four
agr
groups, with 61 strains belonging to
agr
group I, 49 belonging to group II, 43 belonging to group III, and 45 belonging to group IV. Principal coordinate analysis performed on the AFLP distance matrix divided the 198 strains into three main phylogenetic groups, AF1 corresponding to strains of
agr
group IV, AF2 corresponding to strains of
agr
groups I and II, and AF3 corresponding to strains of
agr
group III. This indicated that the
agr
type was linked to the genetic background. A relationship between genetic background,
agr
group, and disease type was observed for several toxin-mediated diseases: for instance,
agr
group IV strains were associated with generalized exfoliative syndromes, and phylogenetic group AF1 strains with bullous impetigo. Among the suppurative infections, endocarditis strains mainly belonged to phylogenetic group AF2 and
agr
groups I and II. While these results do not show a direct role of the
agr
type in the type of human disease caused by
S. aureus
, the
agr
group may reflect an ancient evolutionary division of
S. aureus
in terms of this species’ fundamental biology.
Tập 70 Số 2 - Trang 631-641 - 2002
Translocation of Certain Indigenous Bacteria from the Gastrointestinal Tract to the Mesenteric Lymph Nodes and Other Organs in a Gnotobiotic Mouse Model
Viable bacteria were not cultured from the mesenteric lymph nodes, spleens, or livers of specific-pathogen-free (SPF) mice. Viable enteric bacteria, primarily indigenous
Escherichia coli
and lactobacilli, were present in the mesenteric lymph nodes of gnotobiotic mice inoculated intragastrically with the whole cecal microflora from SPF mice but not in the nodes of control SPF mice similarly inoculated. These indigenous
E. coli
also were cultured from the mesenteric lymph nodes of 96% of gnotobiotic mice monoassociated with
E. coli
but from none of the mesenteric lymph nodes of SPF mice inoculated with the
E. coli.
Furthermore, viable
E. coli
were detected in the mesenteric lymph nodes of these monoassociated gnotobiotes for as long as 112 days after inoculation. Indigenous
Lactobacillus acidophilus
also translocated to the mesenteric lymph nodes of gnotobiotic mice monoassociated with
L. acidophilus.
Apparently, there are mechanisms active in SPF mice inhibiting translocation of indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes, spleens, and livers, whereas these mechanisms are either absent or reduced in gnotobiotic mice. Indigenous
E. coli
maintained higher population levels in the gastrointestinal tracts of the gnotobiotes compared with their population levels in SPF mice, suggesting that high bacterial population levels might promote translocation of certain bacteria from the gastrointestinal lumen to the mesenteric lymph nodes. Gnotobiotic and SPF mice, therefore, provide experimental models for determining the nature of the mechanisms operating to confine indigenous bacteria to the gastrointestinal tract in normal, healthy animals.
Tập 23 Số 2 - Trang 403-411 - 1979
Plasmid-controlled colonization factor associated with virulence in Esherichia coli enterotoxigenic for humans An enterotoxin-producing strain of Escherichia coli isolated from a case of cholera-like diarrhea (E. coli strain H-10407) was found to possess a surface-associated colonization factor. Colonization was manifested as the ability of small inocula (10(5) bacteria) to attain large (10(9)) populations in the infant rabbit intestine with a concomitant diarrheal response. A laboratory-passed derivative of E. coli H-10407, designated H-10407-P, failed to exhibit an increase in population in the infant rabbit and also failed to induce diarrhea. Cell-free culture supernatant fluids of E. coli H-10407 and H-10407-P produced equivalent enterotoxic responses in infant and in adult rabbits. Specific anti-colonization factor antiserum was produced by adsorbing hyperimmune anti-H-10407 serum with both heat-killed and living cells E. coli H-10407-P. This specific adsorbed serum protected infant rabbits from challenge with living E. coli H-10407 although the serum did not possess bactericidal activity. The anti-colonization factor serum did not agglutinate a strain of E. coli K-12 possessing the K88 colonization factor peculiar to E. coli enterotoxigenic for swine. By electron microscopy it was demonstrated that E. coli H-10407, but not H10407-, possessed pilus-like surface structures which agglutinated with the specific adsorbed (anti-colonization factor) antiserum. E. coli H-10407 possessed three species of plasmid deoxyribonucleic acid, measuring 60 X 10(6), 42 X 10(6), and 3.7 X 10(6) daltons, respectively. E. coli H-10407-P possessed only the 42 X 10(6)- and the 3.7 X 10(6)-dalton plasmid species. Spontaneous loss of the specific H-10407 surface-associated antigen was accompanied by loss of the 60 X 10(6)-dalton species of plasmid deoxyribonucleic acid and loss of colonizing ability. Thus, it is concluded that the E. coli colonization factor described here is a virulence factor which may play an important and possibly essential role in naturally occurring E. coli enterotoxic diarrhea in man.
Tập 12 Số 3 - Trang 656-667 - 1975
In vitro model of penetration and intracellular growth of Listeria monocytogenes in the human enterocyte-like cell line Caco-2 Penetration and replication of Listeria monocytogenes within intestinal epithelial cells were studied by infecting the human enterocyte-like cell line Caco-2. Entry was due to directed phagocytosis, as suggested by the inhibiting effect of cytochalasin D on bacterial entry and by electron microscopy showing bacteria inside membrane-limiting vacuoles at the early stage of infection. Only bacteria from pathogenic species (L. monocytogenes and Listeria ivanovii) were able to induce their own phagocytosis by Caco-2 cells, as opposed to Listeria seeligeri, Listeria welshimeri, and Listeria innocua. L. monocytogenes multiplied readily within Caco-2 cells, with an apparent generation time of about 90 min. Listeriolysin O was found to be a major factor promoting intracellular growth of L. monocytogenes. After being internalized at the same rate as that of its hemolytic revertant strain, a nonhemolytic mutant from L. monocytogenes failed to replicate significantly within Caco-2 cells. Electron microscopic study demonstrated that bacteria from the nonhemolytic mutant remained inside phagosomes during cellular infection, whereas hemolytic bacteria from L. monocytogenes were released free within the cytoplasm. This indicates that disruption of vacuole membranes by listeriolysin O-producing strains of L. monocytogenes might be a key mechanism allowing bacteria to escape from phagosomes and to multiply unrestricted within cell cytoplasm.
Tập 55 Số 11 - Trang 2822-2829 - 1987
Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages ABSTRACT Lipopolysaccharide (LPS) derived from the periodontal pathogenPorphyromonas gingivalis has been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation ofP. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants. More importantly, TLR2 stimulation by thisP. gingivalis LPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages byEscherichia coli LPS. These data suggest that (i)P. gingivalis LPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively. Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.
Tập 69 Số 3 - Trang 1477-1482 - 2001
Characterization of plasmids and plasmid-associated determinants of Yersinia enterocolitica pathogenesis Yersinia enterocolitica isolates harboring a particular species of plasmid deoxyribonucleic acid showed a high degree of lethality for gerbils and caused the detachment of HEp-2 tissue cell monolayers. Strains cured of their plasmid deoxyribonucleic acid showed loss of these properties. However, invasiveness of HEp-2 cells was shown not to be a plasmid-mediated property. The expression of plasmid-associated properties, including at least three major outer membrane polypeptides, occurred during growth at 37 but not at 25 degrees C and was related to the concentration of calcium in the growth medium. The plasmid species associated with these properties ranged in molecular mass from 40 x 10(6) to 48 x 10(6) daltons and comprised a family of related plasmids.
Tập 31 Số 2 - Trang 775-782 - 1981
Virulent Combinations of Adhesin and Toxin Genes in Natural Populations of <i>Staphylococcus aureus</i> ABSTRACT
Most cases of severe
Staphylococcus aureus
disease cannot be explained by the action of a single virulence determinant, and it is likely that a number of factors act in combination during the infective process. This study examined the relationship between disease in humans and a large number of putative virulence determinants, both individually and in combination.
S. aureus
isolates (
n
= 334) from healthy blood donors and from patients with invasive disease were compared for variation in the presence of 33 putative virulence determinants. After adjusting for the effect of clonality, seven determinants (
fnbA
,
cna
,
sdrE
,
sej
,
eta
,
hlg
, and
ica
) were significantly more common in invasive isolates. All seven factors contributed independently to virulence. No single factor predominated as the major predictor of virulence, their effects appearing to be cumulative. No combinations of the seven genes were either more or less likely to cause disease than others with the same number of virulence-associated genes. There was evidence of considerable horizontal transfer of genes on a background of clonality. Our findings also suggested that allelic variants of a polymorphic locus can make different contributions to the disease process, further study of which is likely to expand our understanding of staphylococcal disease pathogenesis.
Tập 70 Số 9 - Trang 4987-4996 - 2002
Two toxin-converting phages from Escherichia coli O157:H7 strain 933 encode antigenically distinct toxins with similar biologic activities Escherichia coli O157:H7 strain 933 contains two distinct toxin-converting phages (933J and 933W). The biologic activities and antigenic relationship between the toxins produced by 933J and 933W lysogens of E. coli K-12, as well as the homology of the genes that encode the two toxins, were examined in this study. The 933J and 933W toxins, like Shiga toxin produced by Shigella dysenteriae type 1, were cytotoxic for the same cell lines, caused paralysis and death in mice, and caused fluid accumulation in rabbit ileal segments. The cytotoxic activity of 933J toxin for HeLa cells was neutralized by anti-Shiga toxin, whereas the activity of 933W toxin was not neutralized by this antiserum. In contrast, an antiserum prepared against E. coli K-12(933W) neutralized 933W toxin but not 933J toxin or Shiga toxin. For E. coli 933, most of the cell-associated cytotoxin was neutralized by anti-Shiga toxin, whereas most of the extracellular cytotoxin was neutralized by anti-933W toxin. However, a mixture of these antisera indicated the presence of both toxins in cell lysates and culture supernatants. Among 50 elevated cytotoxin-producing strains of E. coli, we identified 11 strains isolated from cases of diarrhea, hemorrhagic colitis, or hemolytic uremic syndrome that produced cell-associated cytotoxins which were neutralized by the 933W antitoxin. Southern hybridization studies showed that the cloned toxin structural genes from phage 933J hybridized with DNA from phage 933W under conditions estimated to allow no more than 26% base-pair mismatch. These findings indicate that E. coli produces two genetically related but antigenically distinct cytotoxins with similar biologic activities which we propose to name Shiga-like toxins I and II. Strains of E. coli that produce elevated levels of Shiga-like toxin I or Shiga-like toxin II, or both, have been associated with the clinical syndromes of diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome.
Tập 53 Số 1 - Trang 135-140 - 1986
Pyelonephritogenic Escherichia coli and killing of cultured human renal proximal tubular epithelial cells: role of hemolysin in some strains Acute pyelonephritis, a complication of Escherichia coli bacteriuria, must represent a bacterial invasion through the kidney epithelium. To study this process, we overlaid bacterial suspensions onto monolayers of cultured human kidney proximal tubular epithelial cells and measured cytotoxicity by release of lactate dehydrogenase (LDH). Thirty-four isolates cultured from patients with acute pyelonephritis were screened for the ability to cause pyelonephritis in CBA mice by transurethral challenge. The eight most virulent strains (greater than or equal to 70% of mice challenged developed greater than or equal to 10(3) CFU/g of kidney after 48 h) were selected for study. Each strain displayed mannose-resistant hemagglutination of human O erythrocytes; three strains were phenotypically and genotypically hemolytic. Pyelonephritogenic strains were significantly more cytotoxic (30.1 +/- 9.5% LDH release after 18 h) than eight fecal control strains (13.5 +/- 11.5% LDH release; P = 0.0068). We selected the most cytotoxic strain, CFT073, for further study. Sterile filtrate from this hemolytic strain was significantly more cytotoxic than was the filtrate of the fecal control strain, FN414. Transposon mutagenesis of CFT073 with TnphoA abolished hemolytic activity and cytotoxicity by both whole cells and sterile filtrate. Southern blot analysis revealed that the Tnphoa insertion mapped to the E. coli chromosomal hly determinant within a 12-kilobase SalI restriction fragment. Transformation of a nonhemolytic strain, CPZ005 with plasmid pSF4000, which carries a cloned hemolysin determinant, resulted in highly elevated cytotoxicity. Light micrographs of proximal tubular epithelial cell cultures demonstrated cell damage by pyelonephritogenic strains that was not induced by a fecal strain or the hemolysin-deficient mutant. Results indicate that pyelonephritogenic E. coli strains are more frequently cytotoxic for a putative target, that is, human renal tubular epithelium, than are fecal isolates. Hemolysin, in some strains, is apparently responsible for this cytotoxicity.
Tập 58 Số 5 - Trang 1281-1289 - 1990
Hemagglutination of Human Group A Erythrocytes by Enterotoxigenic <i>Escherichia coli</i> Isolated from Adults with Diarrhea: Correlation with Colonization Factor
Enterotoxigenic
Escherichia coli
(ETEC) of several different serotypes isolated from adults with diarrhea and known to possess the colonization factor antigen (CFA) were found to cause mannose-resistant hemagglutination (HA) of human group A erythrocytes. CFA-negative
E. coli
isolated during the same study did not possess the mannose-resistant hemagglutinin, although some non-ETEC, CFA-negative isolates did exhibit mannose-sensitive HA activity. The mannoseresistant hemagglutinin of ETEC was found to possess many characteristics previously associated with CFA, which is a surface-associated fimbriate heatlabile antigen, and the functionally and morphologically similar K88 and K99 antigens of animal-specific ETEC. Mannose-resistant HA and CFA titers were maximal when ETEC cells were grown on an agar medium (CFA agar) composed primarily of 1% Casamino Acids and 0.15% yeast extract, pH 7.4. Neither CFA nor HA were produced at a growth temperature of 18°C; HA was completely inhibited by pretreatment of CFA-positive cells with the anti-CFA serum. The mannose-resistant hemagglutinin was lost spontaneously and simultaneously with CFA when clinical ETEC isolates were passaged on artificial medium in the laboratory, indicating plasmid control of both entities. The mannose-resistant hemagglutinin of ETEC was shown to be thermolabile, i.e., sensitive to heating at 65°C, as was the CFA. Also, there was correlation between possession of CFA, as detected serologically and by demonstration of biological activity (adherence in the infant rabbit small intestine), presence of CFA-type fimbriae, and the ability of various
E. coli
isolates to cause mannose-resistant HA of human group A erythrocytes. These results indicate that the mannose-resistant HA of ETEC is another manifestation of CFA.
Tập 18 Số 2 - Trang 330-337 - 1977