scholarly journals Adherence to, Invasion by, and Cytokine Production in Response to Serotype VIII Group B Streptococci

2004 ◽  
Vol 72 (8) ◽  
pp. 4716-4722 ◽  
Author(s):  
Hiroshige Mikamo ◽  
Atul K. Johri ◽  
Lawrence C. Paoletti ◽  
Lawrence C. Madoff ◽  
Andrew B. Onderdonk
Keyword(s):  
Cytokine Production ◽  
Group B Streptococcus ◽  
A549 Cells ◽  
Interleukin 10 ◽  
Epithelial Cell Line ◽  
Group B Streptococci ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Group B

ABSTRACT The adherence to and invasion of the human epithelial cell line A549 by group B streptococcus (GBS) serotype VIII strains were compared with those of serotype III strains by a conventional method and the dynamic in vitro attachment and invasion system. Twenty GBS strains, including nine vaginal isolates and one invasive isolate each of serotypes III and VIII, were used in the conventional attachment and invasion assay. Adherence to and invasion of A549 cells by serotype VIII GBS strains were significantly greater (P < 0.0001) than those by serotype III strains for both the invasive strain and vaginal isolates. Cytokine production by A549 cells following stimulation with GBS serotypes III and VIII or their purified capsular polysaccharides (CPS) was measured. Serotype III strains stimulated significantly greater tumor necrosis factor alpha (TNF-α) (P < 0.0001) and interleukin-10 (IL-10) (P < 0.05) production than did serotype VIII strains. IL-8 production in response to serotype VIII was significantly higher (P < 0.001) than that in response to serotype III. TNF-α, IL-8, and IL-10 production was greater in A549 cells infected with GBS than in the untreated control cells. TNF-α production was significantly greater (P < 0.005) after stimulation with purified GBS serotype III CPS than after stimulation with serotype VIII CPS, a result similar to that after stimulation with whole GBS. IL-12 production by A549 cells was observed only in response to infection with GBS serotype III, resulting in the possibility of a greater TH1 response in serotype III GBS. These results suggest differences in immune responses to infection with GBS serotypes III and VIII.

scholarly journals Intracellular and Extracellular Cytokine Production by Human Mixed Mononuclear Cells in Response to Group B Streptococci

2000 ◽  
Vol 68 (1) ◽  
pp. 320-327 ◽  
Author(s):  
Daniel J. Kwak ◽  
Nancy H. Augustine ◽  
Wellington G. Borges ◽  
Joanna L. Joyner ◽  
Wayne F. Green ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Brefeldin A ◽  
Severe Infection ◽  
Human Monocyte ◽  
Group B Streptococci ◽  
Necrosis Factor Alpha ◽  
Intracellular Cytokines ◽  
Tnf Α ◽  
Ifn Γ ◽  
Group B

ABSTRACT Group B streptococci (GBS) are a major cause of severe infection in newborns, pregnant females, and other immunocompromised hosts. Infection often includes septicemia, shock, pneumonia, and respiratory failure. In previous studies, we have reported that GBS induce marked production of tumor necrosis factor alpha (TNF-α) by human mononuclear cells. The present study was designed to measure the production of TNF-α as well as additional cytokines, including interleukin 1β (IL-1β), IL-6, IL-8, IL-12, and gamma interferon (IFN-γ) but also to determine from what cells and at what time point during incubation with GBS that these cytokines are produced. Mixed mononuclear cells were incubated with heat-killed GBS, media alone, or 1 μg of Escherichia coli lipopolysaccharide (LPS). Brefeldin A was added to each sample prior to staining, which prevented the export of cytokines by the Golgi apparatus. The cells were then stained with the appropriate conjugated antibodies and analyzed by using a flow cytometer. Results indicate that intracellular cytokines appear, in almost all cases, simultaneous to or before secreted proteins are detected. In contrast to the response to LPS, where TNF-α, IL-1β, IL-6, and IL-8 appear almost simultaneously, the human monocyte response to GBS results in the production of TNF-α but delayed appearance of IL-1β, IL-6, and IL-8. The lymphocyte response to GBS was also strikingly different from that to LPS in that both secreted IFN-γ and IL-12 was detected, while LPS failed to induce production of these critical cytokines. This suggests an important role for TNF-α, IFN-γ, and IL-12 in GBS pathogenesis and/or immunity.

scholarly journals Investigating The Bioactive Properties of Cheese-Fruit Combinations Following In Vitro Digestion Using an Elderly Model.

2021 ◽  
Vol 9 (2) ◽  
pp. 465-478
Author(s):  
Aimee M. Plante ◽  
Aoife L. McCarthy ◽  
Seán Lacey ◽  
Fiona O’Halloran
Keyword(s):  
Older Adults ◽  
Healthy Aging ◽  
Functional Foods ◽  
Group B Streptococcus ◽  
In Vitro Digestion ◽  
Bioactive Properties ◽  
Tnf Α ◽  
Group B ◽  
Immunomodulatory Potential

The prevalence of disease in older adults is increasing, thus there is a need to develop functional foods for this cohort that can promote healthy aging. This study analyzed cheese combined with fruit to identify if certain cheese-fruit combinations improved the bioactive properties of the cheese. Feta, Reduced-Fat Red Cheddar (RFRC), and Goat’s cheese were combined with different fruit (goji berries, red pepper, or blackberries) and digested with a simulated gastrointestinal in vitro digestion model representative of older adults. Antioxidant potential was investigated using DPPH radical scavenging, Ferric reducing antioxidant power (FRAP) and Total phenolic content (TPC) assays. The ability of samples to inhibit digestive enzymes was determined using the α-glucosidase inhibition assay. Antimicrobial activity against Listeria monocytogenes, Group B Streptococcus and Escherichia coli was investigated by the disc diffusion method. Immunomodulatory potential of the digestates was evaluated by their ability to modulate TNF-α levels in stimulated Jurkat T cells. Results demonstrated that combining RFRC with all fruit significantly (p<0.05) increased both the antioxidant and α-glucosidase inhibitory potential of the cheese (≥90.6% DPPH inhibition, ≥980.5 FRAP µmol Fe2+/kg.fw, and ≥58.1% α-glucosidase inhibition). Reducing potential of all cheese significantly (p<0.05) increased when combined with fruit (≥977.0 FRAP µmol Fe2+/kg.fw). Group B Streptococcus was inhibited by cheese-fruit combinations containing feta and goat’s cheese. Combining fruit with feta altered the immunomodulatory potential of the cheese by significantly (p<0.05) decreasing TNF-α secretion by ≥41%, compared to the control. Novel cheese-fruit combinations that promote synergistic bioactive properties could help design functional foods for older adults that promote healthy aging.

scholarly journals Regulatory Role of Interleukin-10 in Experimental Group B Streptococcal Arthritis

2002 ◽  
Vol 70 (6) ◽  
pp. 2862-2868 ◽  
Author(s):  
Manuela Puliti ◽  
Christina von Hunolstein ◽  
Claudie Verwaerde ◽  
Francesco Bistoni ◽  
Graziella Orefici ◽  
...  
Keyword(s):  
Systemic Infection ◽  
Interleukin 10 ◽  
Dose Dependence ◽  
Necrosis Factor Alpha ◽  
Clear Cut ◽  
Type Iv ◽  
Clinical Observations ◽  
Tnf Α ◽  
Group B

ABSTRACT Intravenous inoculation of CD-1 mice with 107 CFU of type IV group B Streptococcus (GBS) results in a high incidence of diffuse septic arthritis , associated with high levels of systemic and local production of interleukin-1β (IL-1β) and IL-6. In this study, the role of the anti-inflammatory cytokine IL-10 in the evolution of GBS systemic infection and arthritis was evaluated. IL-10 production was evident in sera and joints of GBS-infected mice. Neutralization of endogenous IL-10 by administration of anti-IL-10 antibodies (1 mg/mouse) at the time of infection resulted in worsening of articular lesions and 60% mortality associated with early sustained production of IL-6, IL-1β, and tumor necrosis factor alpha (TNF-α). The effect of IL-10 supplementation was assessed by administering IL-10 (100, 200, or 400 ng/mouse) once a day for 5 days, starting 1 h after infection. Treatment with IL-10 had a beneficial effect on GBS arthritis, and there was a clear-cut dose dependence. The decrease in pathology was associated with a significant reduction in IL-6, IL-1β, and TNF-α production. Histological findings showed limited periarticular inflammation and a few-cell influx in the articular cavity of IL-10-treated mice, confirming clinical observations. In conclusion, this study provides further information concerning the role of IL-10 in regulating the immune response and inflammation and calls attention to the potential therapeutic use of IL-10 in GBS arthritis.

scholarly journals Toll-Like Receptor 2 Deficiency Is Associated with Enhanced Severity of Group B Streptococcal Disease

2009 ◽  
Vol 77 (4) ◽  
pp. 1524-1531 ◽  
Author(s):  
Manuela Puliti ◽  
Satoshi Uematsu ◽  
Shizuo Akira ◽  
Francesco Bistoni ◽  
Luciana Tissi
Keyword(s):  
Group B Streptococcus ◽  
Histopathological Analysis ◽  
Polymorphonuclear Cells ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Chemokine Production ◽  
Toll Like Receptor 2 ◽  
Group B ◽  
Tract Infections

ABSTRACT Group B streptococcus (GBS) has been recognized as an ever-growing cause of serious invasive infections in nonpregnant adults, in particular, in association with severe underlying diseases. The most common manifestations include primary bacteremia, urinary tract infections, pneumonia, meningitis, peritonitis, and osteoarticular infections. Toll-like receptor-2 (TLR2) mediates host responses to gram-positive bacteria. TLR2 function was investigated in murine GBS-induced sepsis and arthritis in wild-type (wt) and TLR2-deficient (TLR2−/−) mice. Mice were infected with different doses of GBS (107, 5 × 106, or 106 CFU per mouse). Mortality, appearance of arthritis, GBS growth in the organs, and local and systemic cytokine and chemokine production were examined. TLR2−/− mice showed earlier and higher mortality rates and increased incidence and severity of arthritis than wt mice at all the infecting doses employed. Histopathological analysis of the joints confirmed clinical observations. TLR2−/− mice exhibited a higher microbial load in blood, kidneys, and joints than wt animals. In vitro experiments performed with peritoneal polymorphonuclear cells and macrophages showed a significantly lower bactericidal ability of cells from TLR2−/− mice. Increased systemic and local levels of interleukin-1β (IL-1β), IL-6, tumor necrosis factor alpha, macrophage inflammatory protein-1α (MIP-1α), and MIP-2 accompanied the more severe development of sepsis and arthritis in TLR2−/− mice. In conclusion, the lack of TLR2 was associated with an impaired host resistance to GBS infection, likely due to a diminished bacterial clearing and a consequent enhanced inflammatory response.

scholarly journals Host-Pathogen Interaction and Signaling Molecule Secretion Are Modified in thedpp3Knockout Mutant of Candida lusitaniae

2013 ◽  
Vol 82 (1) ◽  
pp. 413-422 ◽  
Author(s):  
Ayman Sabra ◽  
Jean-Jacques Bessoule ◽  
Vessela Atanasova-Penichon ◽  
Thierry Noël ◽  
Karine Dementhon
Keyword(s):  
Interleukin 10 ◽  
Gene Inactivation ◽  
Physical Contact ◽  
Knockout Mutant ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Tnf Α ◽  
Candida Lusitaniae

ABSTRACTCandida lusitaniaeis an emerging opportunistic yeast and an attractive model to discover new virulence factors inCandidaspecies by reverse genetics. Our goal was to create adpp3Δ knockout mutant and to characterize the effects of this gene inactivation on yeastin vitroandin vivointeraction with the host. The secretion of two signaling molecules inCandidaspecies, phenethyl alcohol (PEA) and tyrosol, but not of farnesol was surprisingly altered in thedpp3Δ knockout mutant. NO and reactive oxygen species (ROS) production as well as tumor necrosis factor alpha (TNF-α) and interleukin 10 (IL-10) secretion were also modified in macrophages infected with this mutant. Interestingly, we found that the wild-type (WT) strain induced an increase in IL-10 secretion by zymosan-activated macrophages without the need for physical contact, whereas thedpp3Δ knockout mutant lost this ability. We further showed a striking role of PEA and tyrosol in this modulation. Last, theDPP3gene was found to be an essential contributor to virulence in mice models, leading to an increase in TNF-α secretion and brain colonization. Although reinsertion of a WTDPP3copy in thedpp3Δ knockout mutant was not sufficient to restore the WT phenotypesin vitro, it allowed a restoration of those observedin vivo. These data support the hypothesis that some of the phenotypes observed followingDPP3gene inactivation may be directly dependent onDPP3, while others may be the indirect consequence of another genetic modification that systematically arises when theDPP3gene is inactivated.

scholarly journals Immunity to the group B streptococci: interaction of serum and macrophages with types Ia, Ib, and Ic.

1976 ◽  
Vol 143 (5) ◽  
pp. 1186-1198 ◽  
Author(s):  
B F Anthony
Keyword(s):  
Group B Streptococcus ◽  
Immune Serum ◽  
Normal Serum ◽  
Rabbit Serum ◽  
Group B Streptococci ◽  
Opsonic Activity ◽  
Heat Stable ◽  
Group B ◽  
Antigen Antibody

The opsonization and phagocytosis of group B streptococci of types Ia, Ib, and Ic were studied in vitro by measuring the uptake of radioactivity by coverslip cultures of rabbit alevolar macrophages during incubation with radiolabeled, nonviable bacteria which had been exposed to rabbit serum. The uptake of counts per minute was quantitative, reproducible, and reversibly inhibited by cold, indicating that it was largely a measurement of phagocytic ingestion rather than of attachment of bacteria-immunoglobulin complexes to macrophage membranes. Moreover, suspended macrophages killed approximately 90% of viable streptococci in the presence of specific antiserum. The opsonic activity of immune serum was heat stable, and phagocytosis of streptococci was insignificant after incubation with normal serum and antiserum to some heterologous group B streptococci. By absorption studies, it was possible to identify the effect of antibodies to specific bacterial antigens. Phagocytosis of streptococci containing the corresponding antigens was maximal after opsonization with homologous or heterologous sera containing antibody to IaCHO, IbCHO, or Ibc protein. Phagocytosis of all three serotypes was intermediate when opsonization could be attributed to anti-IabcCHO. The opsonization of a specific group B streptococcus is complex and may involve two or more antigen-antibody systems.

scholarly journals ROLE OF SUGARS IN SURFACE MICROBE-HOST INTERACTIONS IN GROUP B STREPTOCOCCUS INVASION

2020 ◽  
pp. 54-58
Author(s):  
MANJU O PAI ◽  
VENKATESH S ◽  
PRATIMA GUPTA ◽  
ANURADHA CHAKRABORTI
Keyword(s):  
Cell Lines ◽  
Group B Streptococcus ◽  
A549 Cells ◽  
Alternative Therapies ◽  
Host Interactions ◽  
Specific Receptors ◽  
Group B ◽  
Sizeable Reduction

Objective: Metabolic sources for food play a very important role in developing a niche for a microbe to invade and cause infection in the host. The influence of various sugars on invasion of Streptococcus agalactiae or Group B streptococcus (GBS) into HeLa and A549 cells in vitro were evaluated. Methods: The cell lines and the bacteria were pretreated separately with different sugars before invasion. These observations were also corroborated with light microscopy. Results: Our results showed that the maximum GBS invasion observed at 2h, decreased significantly (p<0.05) when the cells were pretreated with N-acetyl galactosamine (GlcNAc), D-xylose, sucrose, lactose, D-mannose, and D-glucose. In contrast, mannitol was seen to support the invasion of GBS. In addition, when a combined effect of GlcNAc and xylose was studied, 87.5%–91% inhibition to GBS invasion was observed in HeLa and A549 cell lines, respectively. A sizeable reduction in invasion was observed when the bacteria were pretreated with 10 mM of D-Glucose (79.32%), GlcNAc (69.66%), and mannose (48.28%). In conclusion, GlcNAc, D-xylose, and D-glucose proved to be excellent inhibitors to GBS invasion. Furthermore, bacterial pretreatment results might indicate that these sugar specific receptors might be present on the epithelial cells which possibly gets blocked and thus inhibits the entry of GBS. Conclusion: These findings are the first to suggest the role of these sugars as a way to alternative therapies to GBS infection by altering the host-pathogen environment during invasion.

scholarly journals Modulation of Cytokine Release in Ex Vivo-Stimulated Blood from Borreliosis Patients

2001 ◽  
Vol 69 (2) ◽  
pp. 687-694 ◽  
Author(s):  
Isabel Diterich ◽  
Luc Härter ◽  
Dieter Hassler ◽  
Albrecht Wendel ◽  
Thomas Hartung
Keyword(s):  
Ex Vivo ◽  
Interleukin 10 ◽  
Cytokine Response ◽  
Healthy Controls ◽  
Cytokine Release ◽  
Necrosis Factor Alpha ◽  
Cell Counts ◽  
Tnf Α ◽  
Ifn Γ

ABSTRACT In lipopolysaccharide-stimulated blood from 71 late-stage borreliosis patients, the ex vivo cytokine release capacity of tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ) was reduced to 28% ± 5% and to 31% ± 5% (P ≤ 0.001), respectively, compared to that of 24 healthy controls. White blood cell counts were normal in both groups. To investigate direct interactions between the pathogen and the immune cells, blood from healthy controls was exposed in vitro to live or heat-killedBorrelia or to Borrelia lysate. Compared to the pattern induced by bacterial endotoxins, a reduced release of TNF-α and IFN-γ and an enhanced secretion of interleukin-10 and granulocyte colony-stimulating factor was found. In blood from 10 borreliosis patients stimulated with Borrelia lysate, TNF-α formation was decreased to 31% ± 14% and IFN-γ formation was decreased to 8% ± 3% (P ≤ 0.001) compared to the cytokine response of blood from healthy controls (n = 24). We propose to consider anti-inflammatory changes in the blood cytokine response capacity elicited by Borrelia as a condition that might favor the persistence of the spirochete.

scholarly journals Mycobacterium tuberculosis 19-Kilodalton Lipoprotein Inhibits Mycobacterium smegmatis-Induced Cytokine Production by Human Macrophages In Vitro

2001 ◽  
Vol 69 (3) ◽  
pp. 1433-1439 ◽  
Author(s):  
Frank A. Post ◽  
Claudia Manca ◽  
Olivier Neyrolles ◽  
Bernhard Ryffel ◽  
Douglas B. Young ◽  
...  
Keyword(s):  
T Cell Activation ◽  
Cell Activation ◽  
Cytokine Production ◽  
Human Monocyte ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Vaccination of mice with Mycobacterium vaccae orM. smegmatis induces some protection against M. tuberculosis challenge. The 19-kDa lipoprotein of M. tuberculosis, expressed in M. vaccae or M. smegmatis (M. smeg19kDa), abrogates this protective immunity. To investigate the mechanism of this suppression of immunity, human monocyte-derived macrophages (MDM) were infected with M. smeg19kDa. Infection resulted in reduced production of tumor necrosis factor alpha (TNF-α) (P < 0.01), interleukin-12 (IL-12) (P < 0.05), IL-6 (P < 0.05), and IL-10 (P < 0.05), compared to infection with M. smegmatis vector (M. smegV). Infection with M. smeg19kDa and with M. smegV had no differential effect on expression of costimulatory molecules on MDM, nor did it affect the proliferation of presensitized T cells cocultured with infected MDM. When MDM were infected withM. smegmatis expressing mutated forms of the 19-kDa lipoprotein, including non-O-glycosylated (M. smeg19NOG), nonsecreted (M. smeg19NS), and nonacylated (M. smeg19NA) variants, the reduced production of TNF-α or IL-12 was not observed. When the purified 19-kDa lipoprotein was added directly to cultures of infected monocytes, there was little effect on either induction of cytokine production or its inhibition. Thus, the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-α and IL-12 production, possibly leading to reduced induction of T-cell activation.

scholarly journals Genotypic and Phenotypic Studies of Murine Intestinal Lactobacilli: Species Differences in Mice with and without Colitis

2004 ◽  
Vol 70 (1) ◽  
pp. 558-568 ◽  
Author(s):  
J. A. Peña ◽  
S. Y. Li ◽  
P. H. Wilson ◽  
S. A. Thibodeau ◽  
A. J. Szary ◽  
...  
Keyword(s):  
Interleukin 10 ◽  
23S Rrna ◽  
Gastrointestinal Microbiota ◽  
Necrosis Factor Alpha ◽  
Carbohydrate Utilization ◽  
Vitro Assay ◽  
Intergenic Spacer Region ◽  
Tnf Α ◽  
Deficient Mice

ABSTRACT Lactobacilli represent components of the commensal mammalian gastrointestinal microbiota and are useful as probiotics, functional foods, and dairy products. This study includes systematic polyphasic analyses of murine intestinal Lactobacillus isolates and correlation of taxonomic findings with data from cytokine production assays. Lactobacilli were recovered from mice with microbiota-dependent colitis (interleukin-10 [IL-10]-deficient C57BL/6 mice) and from mice without colitis (Swiss Webster and inducible nitric oxide synthetase-deficient C57BL/6 mice). Polyphasic analyses were performed to elucidate taxonomic relationships among 88 reference and murine gastrointestinal lactobacilli. Genotypic tests included single-locus analyses (16S ribosomal DNA sequencing and 16S-23S rRNA intergenic spacer region PCR) and genomic DNA profiling (repetitive DNA element-based PCR), and phenotypic analyses encompassed more than 50 tests for carbohydrate utilization, enzyme production, and antimicrobial resistance. From 20 mice without colitis, six Lactobacillus species were recovered; the majority of the mice were colonized with L. reuteri or L. murinus (72% of isolates). In contrast, only, L. johnsonii was isolated from 14 IL-10-deficient mice. Using an in vitro assay, we screened murine isolates for their ability to inhibit tumor necrosis factor alpha (TNF-α) secretion by lipopolysaccharide-activated macrophages. Interestingly, a subpopulation of lactobacilli recovered from mice without colitis displayed TNF-α inhibitory properties, whereas none of the L. johnsonii isolates from IL-10-deficient mice exhibited this effect. We propose that differences among intestinal Lactobacillus populations in mammals, combined with host genetic susceptibilities, may account partly for variations in host mucosal responses.

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