Inflammatory Response of Fibroblasts to Bb

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Inflammatory Response of Fibroblasts to Bb

Post by RitaA » Sun 8 Jul 2012 18:47

Thanks to Camp Other for blogging about the following two articles here: ... ation.html
PLoS One. 2012;7(6):e40046. Epub 2012 Jun 29.

Microarray Analyses of Inflammation Response of Human Dermal Fibroblasts to Different Strains of Borrelia burgdorferi Sensu Stricto.

Schramm F, Kern A, Barthel C, Nadaud S, Meyer N, Jaulhac B, Boulanger N.
EA 4438, Physiopathologie et Médecine Translationnelle, Facultés de Médecine et de Pharmacie, Université de Strasbourg, Strasbourg, France.

In Lyme borreliosis, the skin is the key site of bacterial inoculation by the infected tick, and of cutaneous manifestations, erythema migrans and acrodermatitis chronica atrophicans. We explored the role of fibroblasts, the resident cells of the dermis, in the development of the disease. Using microarray experiments, we compared the inflammation of fibroblasts induced by three strains of Borrelia burgdorferi sensu stricto isolated from different environments and stages of Lyme disease: N40 (tick), Pbre (erythema migrans) and 1408 (acrodermatitis chronica atrophicans). The three strains exhibited a similar profile of inflammation with strong induction of chemokines (CXCL1 and IL-8) and IL-6 cytokine mainly involved in the chemoattraction of immune cells. Molecules such as TNF-alpha and NF-κB factors, metalloproteinases (MMP-1, -3 and -12) and superoxide dismutase (SOD2), also described in inflammatory and cellular events, were up-regulated. In addition, we showed that tick salivary gland extracts induce a cytotoxic effect on fibroblasts and that OspC, essential in the transmission of Borrelia to the vertebrate host, was not responsible for the secretion of inflammatory molecules by fibroblasts. Tick saliva components could facilitate the early transmission of the disease to the site of injury creating a feeding pit. Later in the development of the disease, Borrelia would intensively multiply in the skin and further disseminate to distant organs.

[PubMed - in process]
Front Microbiol. 2012;3:104. Epub 2012 Mar 22.

Population Dynamics of Borrelia burgdorferi in Lyme Disease.

Binder SC, Telschow A, Meyer-Hermann M.
Department of Systems Immunology, Helmholtz Centre for Infection Research Braunschweig, Germany.

Many chronic inflammatory diseases are known to be caused by persistent bacterial or viral infections. A well-studied example is the tick-borne infection by the gram-negative spirochaetes of the genus Borrelia in humans and other mammals, causing severe symptoms of chronic inflammation and subsequent tissue damage (Lyme Disease), particularly in large joints and the central nervous system, but also in the heart and other tissues of untreated patients. Although killed efficiently by human phagocytic cells in vitro, Borrelia exhibits a remarkably high infectivity in mice and men. In experimentally infected mice, the first immune response almost clears the infection. However, approximately 1 week post infection, the bacterial population recovers and reaches an even larger size before entering the chronic phase. We developed a mathematical model describing the bacterial growth and the immune response against Borrelia burgdorferi in the C3H mouse strain that has been established as an experimental model for Lyme disease. The peculiar dynamics of the infection exclude two possible mechanistic explanations for the regrowth of the almost cleared bacteria. Neither the hypothesis of bacterial dissemination to different tissues nor a limitation of phagocytic capacity were compatible with experiment. The mathematical model predicts that Borrelia recovers from the strong initial immune response by the regrowth of an immune-resistant sub-population of the bacteria. The chronic phase appears as an equilibration of bacterial growth and adaptive immunity. This result has major implications for the development of the chronic phase of Borrelia infections as well as on potential protective clinical interventions.

[PubMed - in process]
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Re: Inflammatory Response of Fibroblasts to Bb

Post by X-member » Mon 9 Jul 2012 19:11

Thank you, Camp Other and RitaA!

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Re: Inflammatory Response of Fibroblasts to Bb

Post by panda » Tue 28 May 2013 9:45

Comprehensive Borrelia burgdorferi specific inflammatory immune response analysis in patients with Lyme disease
Pranay D. Khare, Ph.D.1, Meenakshi Khare, Ph.D.2, Gottfried H. Kellermann, Ph.D.1, 2
1 NeuroScience, Inc., Osceola, WI USA,
2 Pharmasan Labs, Osceola, WI
Published in Cytokine. Vol. 50 (1-2) page 99. 2010.
Lyme disease is the most prevalent vector-borne infectious disorder in humans in the United States, caused by the
spirochete Borrelia burgdorferi. The inflammatory processes induced by B. burgdorferi remains largely unknown.

The purpose of this study was to examine the inflammatory immune response to B. burgdorferi specific antigens in patients diagnosed with Lyme disease compared with asymptomatic healthy subjects.

Recombinant B. burgdorferi antigens (OspC, VlsE-1, p41, p100) were prepared and used in the study. Peripheral blood mononuclear cells (PBMCs) were purified from whole blood obtained from patients with Lyme disease (n = 40) and asymptomatic healthy subjects (n =10). Purified PBMCs were exposed to each of the specific B. burgdorferi antigens. A comprehensive multiplex cytokine analysis was performed on the supernatant of the PBMCs after the exposure of the B. burgdorferi specific antigens and compared to un-stimulated controls.

A trend for elevated levels of IL-1b, IL-6, TNF-a, IFN-y, IL-8, IL-10, G-CSF and GM-CSF was observed in patients with Lyme disease compared to healthy subjects upon spontaneous release as well as following stimulation with B. burgdorferi antigens. Compared to healthy subjects, significant elevated levels (p<0.05) of IL-6 and TNF-a were observed upon p41 stimulation, and of IL-8 upon p100 stimulation in patients with Lyme disease.

These findings indicate that the patients with Lyme disease had an active immune response with pronounced inflammation. The etiology of an active immune response in Lyme patients needs to be explored further to identify treatment regimens that go beyond antibacterial drugs. This study emphasizes the assessment of B. burgdorferi specific inflammatory biomarkers for Lyme disease in clinical practice.
Poster: ... Poster.pdf

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