scholarly journals Legionella pneumophila inhibits acidification of its phagosome in human monocytes.

1984 ◽  
Vol 99 (6) ◽  
pp. 1936-1943 ◽  
Author(s):  
M A Horwitz ◽  
F R Maxfield
Keyword(s):  
Legionella Pneumophila ◽  
Sheep Erythrocyte ◽  
Bacterial Pathogen ◽  
Human Monocytes ◽  
E Coli ◽  
The Mean ◽  
Intracellular Multiplication ◽  
Fluorescence Images ◽  
Activated Monocytes ◽  
Quantitative Fluorescence

We used quantitative fluorescence microscopy to measure the pH of phagosomes in human monocytes that contain virulent Legionella pneumophila, a bacterial pathogen that multiplies intracellularly in these phagocytes. The mean pH of phagosomes that contain live L. pneumophila was 6.1 in 14 experiments. In the same experiments, the mean pH of phagosomes containing dead L. pneumophila averaged 0.8 pH units lower than the mean pH of phagosomes containing live L. pneumophila, a difference that was highly significant (P less than 0.01 in all 14 experiments). In contrast, the mean pH of phagosomes initially containing live E. coli, which were then killed by monocytes, was the same as for phagosomes initially containing dead E. coli. The mean pH of L. pneumophila phagosomes in activated monocytes, which inhibit L. pneumophila intracellular multiplication, was the same as in nonactivated monocytes. To simultaneously measure the pH of different phagosomes within the same monocyte, we digitized and analyzed fluorescence images of monocytes that contained both live L. pneumophila and sheep erythrocytes. Within the same monocyte, live L. pneumophila phagosomes had a pH of approximately 6.1 and sheep erythrocyte phagosomes had a pH of approximately 5.0 or below. This study demonstrates that L. pneumophila is capable of modifying the pH of its phagocytic vacuole. This capability may be critical to the intracellular survival and multiplication of this and other intracellular pathogens.

scholarly journals Formation of a novel phagosome by the Legionnaires' disease bacterium (Legionella pneumophila) in human monocytes.

1983 ◽  
Vol 158 (4) ◽  
pp. 1319-1331 ◽  
Author(s):  
M A Horwitz
Keyword(s):  
Legionella Pneumophila ◽  
Vacuolar Membrane ◽  
Common Mechanism ◽  
Cytoplasmic Vacuole ◽  
Human Monocytes ◽  
Vacuole Formation ◽  
Cytoplasmic Organelles ◽  
Membrane Bound ◽  
Legionnaires Disease ◽  
Intracellular Multiplication

Previous studies have shown that L. pneumophila multiplies intracellularly in human monocytes and alveolar macrophages within a membrane-bound cytoplasmic vacuole studded with ribosomes. In this paper, the formation of this novel vacuole is examined. After entry into monocytes, L. pneumophila resides in a membrane-bound vacuole. During the first hour after entry, vacuoles containing L. pneumophila are found surrounded by smooth vesicles fusing with or budding off from the vacuolar membrane and by mitochondria closely apposed to the vacuolar membrane. By 4 h, vacuoles are found less frequently surrounded by these cytoplasmic organelles, but now ribosomes and rough vesicles are found gathered about the vacuole. By 8 h, the ribosome-lined vacuole has formed. Erythromycin, at concentrations that completely inhibit the intracellular multiplication of L. pneumophila, has no effect on vacuole formation. Formalin-killed L. pneumophila also reside in a membrane-bound vacuole after entry into monocytes. In contrast to the situation with live L. pneumophila, cytoplasmic organelles are not found surrounding vacuoles containing formalin-killed L. pneumophila at any time after entry. Formalin-killed bacteria are rapidly digested, and by 4 h, few remain intact. The L. pneumophila-containing vacuole has certain features in common with other intracellular organisms that inhibit phagosome-lysosome fusion; these organisms may share a common mechanism for vacuole formation and inhibition of phagosome-lysosome fusion.

scholarly journals Phagocytosis of Legionella pneumophila is mediated by human monocyte complement receptors.

1987 ◽  
Vol 166 (5) ◽  
pp. 1377-1389 ◽  
Author(s):  
N R Payne ◽  
M A Horwitz
Keyword(s):  
Legionella Pneumophila ◽  
Bacterial Pathogen ◽  
Human Monocyte ◽  
Complement Receptor ◽  
Complement Receptors ◽  
General Role ◽  
Fresh Serum ◽  
Intracellular Multiplication ◽  
Type 3

We have examined receptors mediating phagocytosis of the intracellular bacterial pathogen, Legionella pneumophila. Three mAbs against the type 3 complement receptor (CR3), which recognizes C3bi, inhibit adherence of L. pneumophila to monocytes by 64 +/- 8% to 74 +/- 11%. An mAb against the type 1 complement receptor (CR1), which recognizes C3b, inhibits adherence by 68 +/- 1%. mAbs against other monocyte surface antigens do not significantly influence adherence. Monocytes plated on substrates of L. pneumophila membranes modulate their CR1 and CR3 receptors but not Fc receptors; such monocytes bind 70% fewer C3b-coated erythrocytes and 53% fewer C3bi-coated erythrocytes than control monocytes. Adherence of L. pneumophila to monocytes in nonimmune sera is dependent on heat-labile serum opsonins; adherence is markedly reduced in heat-inactivated serum (84% reduction) or buffer alone (97% reduction) compared with fresh serum. mAbs against CR1 and CR3 receptors also inhibit L. pneumophila intracellular multiplication and protect monocyte monolayers from destruction by this bacterium. This study demonstrates that human monocyte complement receptors, CR1 and CR3, mediate phagocytosis of L. pneumophila. These receptors may play a general role in mediating phagocytosis of intracellular pathogens.

scholarly journals Activated human monocytes inhibit the intracellular multiplication of legionnaires' disease bacteria

1981 ◽  
Vol 154 (5) ◽  
pp. 1618-1635 ◽  
Author(s):  
MA Horwitz ◽  
SC Silverstein
Keyword(s):  
Mononuclear Cell ◽  
Cell Cultures ◽  
Present Report ◽  
Human Lymphocytes ◽  
Cell Mediated Immunity ◽  
Human Monocytes ◽  
Con A ◽  
Legionnaires Disease ◽  
Intracellular Multiplication ◽  
Activated Monocytes

We have examined the interaction between virulent egg yolk-grown L. pneumophila, Philadelphia 1 strain, and in vitro-activated human monocytes, under antibiotic-free conditions. Freshly explanted human monocytes activated by incubation with concanavalin A (Con A) and human lymphocytes inhibited the intracellular multiplication of L. pneumophila. Both Con A and lymphocytes were required for activation. Con A was consistently maximally effective at greater than or equal to 4 μg/ml. Monocytes activated by incubation with cell-free filtered supernatant from Con A-sensitized mononuclear cell cultures also inhibited the intracellular multiplication of L. pneumophil a. The most potent supernatant was obtained from mononuclear cell cultures incubated with greater than or equal to 15 μg/ml Con A for 48 h. The degree of monocyte inhibition of L. pneumophila multiplication was proportional to the length of time monocytes were preincubated with supernatant (48 {greater than} 24 {greater than} 12 h) and to the concentration of supernatant added (40 percent {greater than} 20 percent {greater than} 10 percent {greater than} 5 percent). Monocytes treated with supernatant daily were more inhibitory than monocytes treated initially only. With time in culture, monocytes progressively lost a limited degree of spontaneous inhibitory capacity and also lost their capacity to respond to supernatant with inhibition of L. pneumophila multiplication. Supernatant-activated monocytes inhibited L. pneumophila multiplication in two ways. They phagocytosed fewer bacteria, and they slowed the rate of intracellular multiplication of bacteria that were internalized. As was the case with nonactivated monocytes, antibody had no effect on the rate of intracellular multiplication in supernatant-activated monocytes. Neither supernatant-activated nor nonactivated monocytes killed L. pneumophila in the absence of antibody. Both killed a limited proportion of these bacteria in the presence of antibody and complement. We have previously reported that anti-L, pneumophila antibody and complement neither promote effective killing of L. pneumophila by human polymorphonuclear leukocytes and monocytes nor inhibit the rate of L. pneumophila multiplication in monocytes. These findings and our present report that activated monocytes do inhibit L. pneumophila multiplication indicate that cell-mediated immunity plays a major role in host defense against Legionnaires' disease.

scholarly journals Atypical Bacterial Pathogens and Small-Vessel Leukocytoclastic Vasculitis of the Skin in Children: Systematic Literature Review

Pathogens ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 31
Author(s):  
Céline Betti ◽  
Pietro Camozzi ◽  
Viola Gennaro ◽  
Mario G. Bianchetti ◽  
Martin Scoglio ◽  
...  
Keyword(s):  
Mycoplasma Pneumoniae ◽  
Legionella Pneumophila ◽  
Leukocytoclastic Vasculitis ◽  
Systemic Vasculitis ◽  
Bacterial Pathogen ◽  
Small Vessel ◽  
Small Vessel Vasculitis ◽  
Systemic Involvement ◽  
Symptomatic Disease ◽  
Atypical Pathogen

Leukocytoclastic small-vessel vasculitis of the skin (with or without systemic involvement) is often preceded by infections such as common cold, tonsillopharyngitis, or otitis media. Our purpose was to document pediatric (≤18 years) cases preceded by a symptomatic disease caused by an atypical bacterial pathogen. We performed a literature search following the Preferred Reporting of Systematic Reviews and Meta-Analyses guidelines. We retained 19 reports including 22 cases (13 females and 9 males, 1.0 to 17, median 6.3 years of age) associated with a Mycoplasma pneumoniae infection. We did not find any case linked to Chlamydophila pneumoniae, Chlamydophila psittaci, Coxiella burnetii, Francisella tularensis, or Legionella pneumophila. Patients with a systemic vasculitis (N = 14) and with a skin-limited (N = 8) vasculitis did not significantly differ with respect to gender and age. The time to recovery was ≤12 weeks in all patients with this information. In conclusion, a cutaneous small-vessel vasculitis with or without systemic involvement may occur in childhood after an infection caused by the atypical bacterial pathogen Mycoplasma pneumoniae. The clinical picture and the course of cases preceded by recognized triggers and by this atypical pathogen are indistinguishable.

scholarly journals THE DNA OF CAENORHABDITIS ELEGANS

Genetics ◽  
1974 ◽  
Vol 77 (1) ◽  
pp. 95-104
Author(s):  
J E Sulston ◽  
S Brenner
Keyword(s):  
Caenorhabditis Elegans ◽  
Chemical Analysis ◽  
Dna Sequences ◽  
Base Composition ◽  
Nematode Caenorhabditis Elegans ◽  
5S Rna ◽  
Base Pairs ◽  
Small Component ◽  
E Coli ◽  
The Mean

ABSTRACT Chemical analysis and a study of renaturation kinetics show that the nematode, Caenorhabditis elegans, has a haploid DNA content of 8 x IO7 base pairs (20 times the genome of E. coli). Eighty-three percent of the DNA sequences are unique. The mean base composition is 36% GC; a small component, containing the rRNA cistrons, has a base composition of 51% GC. The haploid genome contains about 300 genes for 4s RNA, 110 for 5s RNA, and 55 for (18 + 28)S RNA.

Memristive approach for estimation of bacterial pathogen E. coli concentration using ZnS quantum dots

2021 ◽  
Vol 43 ◽  
pp. 3891-3895
Author(s):  
Himadri Duwarah ◽  
Neelotpal Sharma ◽  
Jutika Devi ◽  
Kandarpa Kumar Saikia ◽  
Pranayee Datta
Keyword(s):  
Quantum Dots ◽  
Bacterial Pathogen ◽  
E Coli
Sign in / Sign up

Export Citation Format

Share Document