Interleukin-1 enhances the development of type II collagen-induced arthritis only in susceptible and not in resistant mice

Hom, Joanne T.; Cole, Harlan W.; Estridge, Thomas; Gliszczynski, Virginia L.

doi:10.1016/0090-1229(92)90022-g

Cited by 34 publications

(17 citation statements)

References 42 publications

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“…This cytokine is not only a proinflammatory substance (Stimpson et al, 1988;Hom et al, 1992;van de Loo et al, 1992) but can per se induce inflammation and tissue destruction (Pettipher et al, 1986;Chandrasekhar et al, 1990). The finding that intra-articular injection of IL-1 induces release of substance P. presumably from afferent nerve fibres, into the synovial fluid (O'Byrne et al, 1990a,b) suggests that cytokines themselves could evoke signs of neurogenic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Herbert

Holzer

1994

British J Pharmacology

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This study examined the effect of interleukin‐1β (IL‐1β) on the capsaicin‐induced increase in cutaneous blood flow of anaesthetized rats as measured by laser Doppler flowmetry. The substances were administered by intraplantar subcutaneous injection of 10 μl‐volumes, saline being injected into one hindpaw and IL‐1β into the other. IL‐1β (0.5–500 pg) was without effect on blood flow on its own but dose‐dependently enhanced the hyperaemic response to intraplantar capsaicin (0.3 μg) up to 180% (P < 0.05) of the response seen in saline‐treated paws. Il‐1β‐(163–171), a fragment devoid of proinflammatory activity, failed to enhance capsaicin‐induced hyperaemia when given at a dose of 50 pg. Indomethacin (10 mg kg−1, i.p.) did not alter the capsaicin‐induced vasodilatation but prevented IL‐1β (50 pg) from augmenting the hyperaemic response to capsaicin. The hyperaemia evoked by intraplantar calcitonin gene‐related peptide (0.038–3.8 ng) was not altered by IL‐1β (50 pg). These data indicate that IL‐1β enhances the cutaneous hyperaemic response to afferent nerve stimulation with capsaicin in a prostaglandin‐dependent manner. This proinflammatory action of the cytokine appears to arise from sensitization of afferent nerve endings.

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Section: Discussionmentioning

confidence: 99%

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Herbert

Holzer

1994

British J Pharmacology

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“…In this regard, we investigate here the effects of 3,4-DHPEA-EA, a hydrolysis product of oleuropein, in a mouse model of CII-induced arthritis. Although T-cell and antibody responses against CII are a crucial event for the initiation of CIA (Holmdahl et al, 1989), it has been demonstrated that several cytokines also appear to direct cell-to-cell communication in a cascade fashion during the progression of CIA such as IL-1 (Hom et al, 1992), TNF- (Dong et al, 2010), and IL-6 (Ferraccioli et al, 2010). In addition, it has been demonstrated that monocyte chemotactic protein-1, MIP-, MIP-1 , and regulated on activation normal T cell expressed and secreted are differentially chemotactic for lymphocyte subsets and are expressed in tissue from the inflamed joints of patients with rheumatoid arthritis (Koch et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Oleuropein an Olive Oil Compound in Acute and Chronic Inflammation Models: Facts and Perspectives

Britti¹,

Impellizzeri²,

Procopio³

et al. 2012

Olive Germplasm - The Olive Cultivation, Table Olive and Olive Oil Industry in Italy

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“…The synovium is chronically hypoxic in RA and probably also in CIA: biochemical evidence of anaerobic metabolism suggests that blood flow is insufficient to meet the high metabolic demands of inflamed synovial tissue (41). In that regard, the cytokines mentioned above are known to be involved in the development and maintenance of CIA (42)(43)(44). Thus, hypoxia, various cytokines, oxygen radicals, and nitric oxide may act in concert to stimulate angiogenesis in CIA synovitis through up-regulation of VEGF.…”

Section: Discussionmentioning

confidence: 99%

Vascular Endothelial Growth Factor Expression and Regulation of Murine Collagen-Induced Arthritis

Kasama

Kobayashi

et al. 2000

The Journal of Immunology

130

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We have examined the expression and function of the angiogenic factor, vascular endothelial growth factor (VEGF) during the evolution of type II collagen-induced arthritis (CIA). Biologically active VEGF was expressed along a time course that paralleled the expression of two specific VEGF receptors, Flk-1 and Flt-1, and the progression of joint disease. Moreover, levels of VEGF expression correlated with the degree of neovascularization, as defined by vWF levels, and arthritis severity. Macrophage- and fibroblast-like cells, which infiltrated inflamed sites and were then activated by other inflammatory mediators, are probably important sources of VEGF and may thus regulate angiogenesis during the development of CIA. Administration of anti-VEGF antiserum to CIA mice before the onset of arthritis delayed the onset, reduced the severity, and diminished the vWF content of arthritic joints. By contrast, administration of anti-VEGF antiserum after the onset of the disease had no effect on the progression or ultimate severity of the arthritis. These data suggest that VEGF plays a crucial role during an early stage of arthritis development, affecting both neovascularization and the progression of experimentally induced synovitis.

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Interleukin-1 enhances the development of type II collagen-induced arthritis only in susceptible and not in resistant mice

Cited by 34 publications

References 42 publications

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Oleuropein an Olive Oil Compound in Acute and Chronic Inflammation Models: Facts and Perspectives

Vascular Endothelial Growth Factor Expression and Regulation of Murine Collagen-Induced Arthritis

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