Modulation of cytokine release in ex vivo stimulated blood from borreliosis patients

Diterich, Isabel; Härter, Luc; Hassler, Dieter; Wendel, Albrecht; Hartung, Thomas

doi:10.1016/s1438-4221(02)80061-3

Cited by 17 publications

(30 citation statements)

References 7 publications

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“…These data support the initial observation of similar cytokine induction by both genotypes at 16 h and expand it to include indistinguishable expression kinetics of key inflammatory mediators from as early as 2 h after pathogen contact. No difference in transcription of these cytokines upon exposure to live or heat-killed BL206 was observed, which is consistent with other studies that found no difference in the production of selected cytokines elicited by live spirochetes or by heat-killed or sonicated B. burgdorferi extracts in human (44) and canine cells (45). This suggests that the elicited host cytokine responses are most likely induced by cell membrane components rather than by secreted or cytosolic factors.…”

Section: Discussionsupporting

confidence: 92%

Pattern of Proinflammatory Cytokine Induction in RAW264.7 Mouse Macrophages Is Identical for Virulent and AttenuatedBorrelia burgdorferi

Wang

Petzke

Iyer

et al. 2008

The Journal of Immunology

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Lyme disease pathogenesis results from a complex interaction between Borrelia burgdorferi and the host immune system. The intensity and nature of the inflammatory response of host immune cells to B. burgdorferi may be a determining factor in disease progression. Gene array analysis was used to examine the expression of genes encoding cytokines, chemokines, and related factors in the joint tissue of infected C3H/HeJ mice and in a murine macrophage-like cell line in response to a disseminating or attenuated clinical isolate of B. burgdorferi. Both isolates elicited a robust proinflammatory response in RAW264.7 cells characterized by an increase in transcript levels of genes encoding CC and CXC chemokines, proinflammatory cytokines, and TNF superfamily members. Transcription of genes encoding IL-1β, IL-6, MCP-1, MIP-1α, CXCR4, and TLR2 induced in RAW264.7 cells by either live or heat-killed spirochetes did not differ significantly at any time point over a 24-h period, nor was there a difference in the protein levels of IL-10, TNF-α, IL-6, and IL-12p70 in culture supernatants. Thus, induction of host macrophage expression of proinflammatory mediators by host macrophages does not contribute to the differential pathogenicity of different B. burgdorferi strains.

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Section: Discussionsupporting

confidence: 92%

Pattern of Proinflammatory Cytokine Induction in RAW264.7 Mouse Macrophages Is Identical for Virulent and AttenuatedBorrelia burgdorferi

Wang

Petzke

Iyer

et al. 2008

The Journal of Immunology

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“…Unlike nasal lavage or induced sputum production, the volume of blood used for the assay is invariable, which allows for the determination of accurate total cell counts. Several implementations of whole blood analysis have been used to examine immune responses to various agents and conditions, including pyrogens [14][15][16], sepsis [17,18], infectious disease [17,19,20], allergens [21,22] and other environmental agents [23][24][25]. Using methods similar to this study, WOUTERS et al [26] assessed within-and between-subject variation of the WBA in normal, unexposed volunteers and found that there was relatively low within-subject variance compared with between-subject variance, particularly for IL-1b and IL-6.…”

mentioning

confidence: 99%

Biomonitoring for assessment of organic dust-induced lung inflammation

Mueller-Anneling

O'Neill²,

Thorne³

2006

Eur Respir J

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Inhalation exposure to particulate matter containing endotoxin (or lipopolysaccharide (LPS)) occurs in a variety of occupations. Nasal lavage and induced sputum have been used to evaluate lung inflammation resulting from such exposures. Whole blood assay (WBA) measures cytokine production of leukocytes after ex vivo stimulation with LPS. The present study examined the effectiveness of WBA for evaluating inflammatory responses and susceptibility.C3HeB/FEJ mice were tolerised by LPS injection or sham tolerised with saline. Animals then inhaled either swine barn dust extract containing endotoxin or saline. Bronchoalveolar lavage (BAL) fluid was assayed for leukocyte counts and pro-inflammatory cytokines (interleukin-6, tumour necrosis factor-a). Whole blood was stimulated with 10 or 100 ng?mL -1 of LPS, incubated for 5 or 18 h and assayed for cytokines. Barn dust-exposed groups revealed significantly higher total cells, neutrophils and cytokines in BAL compared with saline-exposed groups. Animals tolerised to LPS and exposed to barn dust demonstrated lower cellular and cytokine BAL responses. Similarly, WBA yielded significantly elevated cytokines with barn dust exposure and reduced responses with tolerisation.This study demonstrates the efficacy of whole blood assay as a biomarker of inhalation exposure to inflammatory agents and its use for assessing susceptibility to organic dust-induced lung inflammation.

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“…In contrast, the effects of IL-10 on IL-17 production were more pronounced after 1 week of infection. Borrelial infection in the presence or absence of IL-10 may be associated with an inverse response of various inflammatory cytokines, including not only tumor necrosis factor alpha and IFN-␥ (3,4,(28)(29)(30)(46)(47)(48)(49)(50)(51) but also IL-17. If a certain threshold of immunosuppression by IL-10 is not achieved, a significant, multifaceted inflammatory response may ensue.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10 (IL-10) Inhibits Borrelia burgdorferi-Induced IL-17 Production and Attenuates IL-17-Mediated Lyme Arthritis

et al. 2013

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Previous studies have shown that cells and cytokines associated with interleukin-17 (IL-17)-driven inflammation are involved in the arthritic response to Borrelia burgdorferi infection. Here, we report that IL-17 is a contributing factor in the development of Lyme arthritis and show that its production and histopathological effects are regulated by interleukin-10 (IL-10). Spleen cells obtained from B. burgdorferi-infected, "arthritis-resistant" wild-type C57BL/6 mice produced low levels of IL-17 following stimulation with the spirochete. In contrast, spleen cells obtained from infected, IL-10-deficient C57BL/6 mice produced a significant amount of IL-17 following stimulation with B. burgdorferi. These mice developed significant arthritis, including erosion of the bones in the ankle joints. We further show that treatment with antibody to IL-17 partially inhibited the significant hind paw swelling and histopathological changes observed in B. burgdorferi-infected, IL-10-deficient mice. Taken together, these findings provide additional evidence of a role for IL-17 in Lyme arthritis and reveal an additional regulatory target of IL-10 following borrelial infection.

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Modulation of cytokine release in ex vivo stimulated blood from borreliosis patients

Cited by 17 publications

References 7 publications

Pattern of Proinflammatory Cytokine Induction in RAW264.7 Mouse Macrophages Is Identical for Virulent and AttenuatedBorrelia burgdorferi

Pattern of Proinflammatory Cytokine Induction in RAW264.7 Mouse Macrophages Is Identical for Virulent and AttenuatedBorrelia burgdorferi

Biomonitoring for assessment of organic dust-induced lung inflammation

Interleukin-10 (IL-10) Inhibits Borrelia burgdorferi-Induced IL-17 Production and Attenuates IL-17-Mediated Lyme Arthritis

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