Bacterial Polysaccharides, Endotoxins, and Immunomodulation

Baker, Phillip J.; Taylor, Christopher E.; Ekwunife, Felix S.

doi:10.1007/978-1-4615-3434-1_4

Cited by 8 publications

(3 citation statements)

References 24 publications

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“…LPS exerts its fatal action not directly, but stimulates various types of cells, including monocytes/macrophages (1,2), endothelial cells (3), or granulocytes (4), to release inflammatory mediators, including IL-1, IL-6, and TNF-␣ . In addition, murine B lymphocytes were shown to respond to LPS by reacting with differential proliferation and antibody production (5)(6)(7). In recent years, it became evident that LPS is also a potent inducer of human as well as murine T lymphocyte proliferation and cytokine production (8)(9)(10)(11)(12).…”

mentioning

confidence: 99%

CD34+ Hematopoietic Stem Cells Exert Accessory Function in Lipopolysaccharide-induced T Cell Stimulation and CD80 Expression on Monocytes

Mattern

Girroleit

Flad

et al. 1999

The Journal of Experimental Medicine

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CD34+ hematopoietic stem cells, which circulate in peripheral blood with very low frequency, exert essential accessory function during lipopolysaccharide (LPS)-induced human T lymphocyte activation, resulting in interferon γ production and proliferation. In contrast, stimulation of T cells by “conventional” recall antigens is not controlled by blood stem cells. These conclusions are based on the observation that depletion of CD34+ blood stem cells results in a loss of LPS-induced T cell stimulation as well as reduced expression of CD80 antigen on monocytes. The addition of CD34-enriched blood stem cells resulted in a recovery of reactivity of T cells and monocytes to LPS. Blood stem cells could be replaced by the hematopoietic stem cell line KG-1a. These findings may be of relevance for high risk patients treated with stem cells or stem cell recruiting compounds and for patients suffering from endotoxin-mediated diseases.

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mentioning

confidence: 99%

CD34+ Hematopoietic Stem Cells Exert Accessory Function in Lipopolysaccharide-induced T Cell Stimulation and CD80 Expression on Monocytes

Mattern

Girroleit

Flad

et al. 1999

The Journal of Experimental Medicine

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“…In this study, LPS, which is an activator of B lymphocytes, macrophages and monocytes, and enhances immunoglobulin synthesis [36,37], did not induce proliferation in rat blood lymphocytes, indicating that the preparation includes mainly T cells. In contrast, with the monoclonal antibody anti-CD3, which is a potent polyclonal mitogen of T cells in vivo and in vitro [38], results were similar to those observed in proliferation assays with Con A, in which a stimulation was observed.…”

Section: Discussionmentioning

confidence: 99%

5-HT<sub>1A </sub>and β-Adrenergic Receptors Regulate Proliferation of Rat Blood Lymphocytes

Sempere¹,

Urbina²,

Lima³

2004

Neuroimmunomodulation

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Lymphocytes possess serotonin 5-HT_1A and β-adrenergic receptors, which have been related to cell proliferation. In the present report, lymphocytes of rat blood were isolated by Ficoll-Hypaque gradients and differential adhesion to plastic. They were cultured in RPMI medium for 72 h in the presence of the mitogens lipopolysaccharide concanavalin A and anti-CD3 antibody. The latter two stimulated the proliferation of lymphocytes, but not the first. Serotonin (0.1–100 µM) was added alone or in the presence of suboptimal concentrations of concanavalin A (2 µg/ml) or anti-CD3 antibody (0.4 µg/ml). The 5-HT_1A receptor agonists, 8-hydroxy-2-(di-n-propylamino)tetralin and buspirone (0.1–100 µM) were also tested in the cultures. Serotonin, 8-hydroxy-2-(di-n-propylamino)tetralin and buspirone neither had any effect by themselves, nor modified the proliferation induced by the mitogens. Noradrenaline (25–1,000 µM) and the β-adrenergic receptor agonist, isoproterenol (5–100 µM), produced a reduction of the activation induced by concanavalin A or anti-CD3 antibody in a dose-dependent manner. Increasing serotonin concentrations reduced the inhibitory effect of noradrenaline (300 µM). Variable concentrations of 8-hydroxy-2-(di-n-propylamino)tetralin or buspirone also reduced the inhibition produced by isoproterenol (100 µM). The antagonist of 5-HT_1A receptors, WAY-100,478 (0.1–100 µM), inhibited concanavalin A- or anti-CD3 antibody-induced proliferation. Serotonin (0.1–100 µM) impaired the inhibitory effect of the 5-HT_1A antagonist (10 µM). The inhibitor of tryptophan hydroxylase, p-chlorophenylalanine (50–1,000 µM), decreased the stimulatory effect of concanavalin A, serotonin (0.5–100 µM) and 8-hydroxy-2-(di-n-propylamino)tetralin (1–100 µM) reverted the effect of p-chlorophenylalanine (1,000 µM). The serotonin reuptake blockers zimelidine, imipramine and clomipramine decreased concanavalin A-induced proliferation. The concentrations of serotonin and noradrenaline increased in lymphocytes cultured in the presence of concanavalin A, probably as a mechanism for modifying the final effect on proliferation. The present results indicate that 5-HT_1A receptors play a stimulatory role on rat blood lymphocytes, and they interact in a parallel and opposite manner with β-adrenergic receptors. Furthermore, endogenous serotonin is relevant in displaying its stimulatory effect.

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“…A leading medical journal recommended to 'Eat Dirt' (Weiss, 2002) based on inverse trends of infections on one side and allergic diseases on the other side (Bach, 2002) and the decrease of asthma development in children living on farms compared with rural controls (Braun-Fahrländer et al, 2002). Higher environmental loads of bacterial endotoxins in the farm environment were linked with the strong immunomodulating effects of bacterial lipopolysaccharide (Baker et al, 1992), which led recently to clinical trials testing bacterial lysates from two enteric commensals, Escherichia coli and Enterococcus faecalis, against atopic dermatitis (AD) (Lau et al, 2012). Also, animal experiments demonstrated that the intestinal microflora was an important inducer for the maturation of the immune system (Chung et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Turning the inside out: the microbiology of atopic dermatitis

Brüssow¹

2015

Environmental Microbiology

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SummaryAllergy is on the rise worldwide. The hygiene hypothesis of atopic diseases linked microbes with atopic dermatitis (AD) both as drivers and modulators of skin pathology. The earlier literature favoured an inside-outside model of AD where an immunological abnormality compounded by a gut microbiota dysbiosis is the primary event. Probiotic intervention trials with lactobacilli and bifidobacteria as well as the application of bifidogenic oligosaccharide prebiotics showed indeed promising clinical results, but no consistent gut microbiota dysbiosis could be linked with AD. An alternative hypothesis known as outsideinside model of AD considers a genetic skin barrier effect compounded by a skin microbiota dysbiosis as primary pathogenic event. Cultivation microbiology has demonstrated strong skin colonization with superantigen-encoding Staphylococcus aureus in AD patients; microbiota and molecular microbiome analyses demonstrated that S. aureus abundance fluctuates and parallels clinical symptoms. In a mouse model, δ-toxin of S. aureus induced mast cell degranulation, leading to AD-like symptoms. Mutant mice developing AD symptoms showed increased skin colonization with S. aureus; antibiotic treatment alleviated the symptoms. Clinical trials showed that various treatments reducing S. aureus skin load also reduced AD symptoms, suggesting S. aureus as a potential critical driver of AD and a target for antimicrobial interventions other than antibiotics.

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Bacterial Polysaccharides, Endotoxins, and Immunomodulation

Cited by 8 publications

References 24 publications

CD34+ Hematopoietic Stem Cells Exert Accessory Function in Lipopolysaccharide-induced T Cell Stimulation and CD80 Expression on Monocytes

CD34+ Hematopoietic Stem Cells Exert Accessory Function in Lipopolysaccharide-induced T Cell Stimulation and CD80 Expression on Monocytes

5-HT<sub>1A </sub>and β-Adrenergic Receptors Regulate Proliferation of Rat Blood Lymphocytes

Turning the inside out: the microbiology of atopic dermatitis

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