Interleukin-6 Promotes Anti-OspA Borreliacidal Antibody Production In Vitro

Munson, Erik; Nardelli, Dean T.; Luk, K. H. Kevin; Remington, Monica C.; Callister, Steven M.; Schell, Ronald F.

doi:10.1128/cvi.13.1.19-25.2006

Cited by 4 publications

(2 citation statements)

References 38 publications

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“…Moreover, as IL‐6 is not directly neutralized in these arthritic mice, it may be free to exert its arthritic effects and enhance anti‐OspA borreliacidal activity. We showed previously that recombinant IL‐6 enhances anti‐OspA borreliacidal antibody (Munson et al ., 2006).…”

Section: Discussionmentioning

confidence: 95%

“…Moreover, as IL-6 is not directly neutralized in these arthritic mice, it may be free to exert its arthritic effects and enhance anti-OspA borreliacidal activity. We showed previously that recombinant IL-6 enhances anti-OspA borreliacidal antibody (Munson et al, 2006). The individual roles of IL-17 and TGF-b in the induction of arthritis following Borrelia vaccination and challenge were also examined through administration of antibodies to these cytokines.…”

Section: Discussionmentioning

confidence: 99%

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Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

Nardelli

Luk

Kotloski

et al. 2008

FEMS Immunol Med Microbiol

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We showed recently that the adaptive immune events leading to the development of arthritis in Borrelia burgdorferi isolate 297-vaccinated and Borrelia bissettiichallenged mice involve IL-17. Here, we show in Borrelia-vaccinated and -challenged mice that two cytokines known to induce the production of IL-17, IL-6 and transforming growth factor (TGF)-b, are also involved in the development of arthritis. Vaccinated and challenged mice administered either anti-TGF-b or anti-IL-6 antibodies developed histopathologic changes of the hind paws similar to or greater than untreated control mice. By contrast, simultaneous blockage of these cytokines reduced the severity of arthritis in Borrelia-vaccinated and -challenged mice. Moreover, administration of anti-IL-17 antibodies to these dual-antibodytreated mice completely prevented the development of histopathologic changes of the ankle joints, significantly reduced edema of the hind paws, and prevented the production of anti-outer surface protein A borreliacidal antibodies. These findings demonstrate a role for the combined effects of IL-17, IL-6, and TGF-b in the adaptive immune events leading to the development of Borrelia-induced arthritis.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

Nardelli

Luk

Kotloski

et al. 2008

FEMS Immunol Med Microbiol

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The Important and Diverse Roles of Antibodies in the Host Response to Borrelia Infections

LaRocca¹,

Benach²

2008

Current Topics in Microbiology and Immunology

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Arthritis is inhibited in Borrelia-primed and infected interleukin-17A-deficient mice after administration of anti-gamma-interferon, anti-tumor necrosis factor alpha and anti-interleukin-6 antibodies

Kuo

Warner

Schell

2017

Pathogens and Disease

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The role that cytokines play in the induction of Lyme arthritis is gradually being delineated. We showed previously that severe arthritis developed in a T-cell-driven murine model, even in mice lacking interleukin-17A (IL-17A) and administered anti-gamma-interferon (IFN-γ) antibody. Increased levels of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6), two pro-inflammatory cytokines, were detected in cultures of popliteal lymph node cells obtained from these mice. We hypothesized that concomitantly administered anti-IL-6, anti-TNF-α and anti-IFN-γ antibodies would inhibit the development of arthritis in IL-17A-deficient mice. Our results showed that swelling of the hind paws and histopathological changes consistent with arthritis were significantly reduced in IL-17A-deficient mice that administered the three anti-cytokine antibodies. These results suggest that treatment with multiple anti-cytokine antibodies can abrogate the induction of Lyme arthritis in mice.

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Interleukin-6 Promotes Anti-OspA Borreliacidal Antibody Production In Vitro

Cited by 4 publications

References 38 publications

Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

Role of IL-17, transforming growth factor-β, and IL-6 in the development of arthritis and production of anti-outer surface protein A borreliacidal antibodies inBorrelia-vaccinated and -challenged mice

The Important and Diverse Roles of Antibodies in the Host Response to Borrelia Infections

Arthritis is inhibited in Borrelia-primed and infected interleukin-17A-deficient mice after administration of anti-gamma-interferon, anti-tumor necrosis factor alpha and anti-interleukin-6 antibodies

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