Neutrophil Recruitment by Interleukin-17 into Rat Airways <i>In Vivo</i>

Hoshino, Hiroshi; Lötvall, Jan; Skoogh, Bengt-Eric; Lindén, Anders

doi:10.1164/ajrccm.159.5.9806008

Cited by 87 publications

(72 citation statements)

References 34 publications

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“…When compared with its family member IL-17, IL-17B is about 10 time less potent in inducing PMN infiltration (Ref. 16 and data not shown).…”

Section: Discussionmentioning

confidence: 97%

“…More recently, IL-17 has been implicated in allergic skin immune responses (14), neutrophil recruitment during airway inflammation (15,16), cardiac and renal allograft rejection (17)(18)(19), and granulopoiesis (21,22). In addition, it has been found to up-regulate nitric oxide production in human osteoarthritic cartilage and inflammatory cytokine production by rheumatoid arthritis synoviocytes (23,24), to stimulate osteoclastogenesis and the expression of several genes associated with inflammation and cartilage degradation in human chondrocytes (25)(26)(27)(28), and to induce ICAM-1 expression in human bronchial epithelial cells (29).…”

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confidence: 99%

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A Novel Cytokine Receptor-Ligand Pair

Shi¹,

Ullrich²,

Zhang³

et al. 2000

Journal of Biological Chemistry

199

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As part of a large scale effort to discover novel secreted proteins, a cDNA encoding a novel cytokine was identified. Alignments of the sequence of the new protein, designated IL-17B, suggest it to be a homolog of the recently described T cell-derived cytokine, IL-17. By Northern analysis, EST distribution and real-time quantitative polymerase chain reaction analysis, mRNA was detected in many cell types. A novel type I transmembrane protein, identified in an EST data base by homology to IL-17R, was found to bind specifically IL-17B, as determined by surface plasmon resonance analysis, flow cytometry, and co-immunoprecipitation experiments. Readily detectable transcription of IL-17BR was restricted to human kidney, pancreas, liver, brain, and intestines and only a few of the many cell lines tested. By using a rodent ortholog of IL-17BR as a probe, IL-17BR message was found to be drastically up-regulated during intestinal inflammation elicited by indomethacin treatment in rats. In addition, intraperitoneal injection of IL-17B purified from Chinese hamster ovary cells caused marked neutrophil migration in normal mice, in a specific and dose-dependent manner. Together these results suggest that IL-17B may be a novel proinflammatory cytokine acting on a restricted set of target cell types. They also demonstrate the strength of genomic approaches in the unraveling of novel biological pathways.

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“…When compared with its family member IL-17, IL-17B is about 10 time less potent in inducing PMN infiltration (Ref. 16 and data not shown).…”

Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

A Novel Cytokine Receptor-Ligand Pair

Shi¹,

Ullrich²,

Zhang³

et al. 2000

Journal of Biological Chemistry

199

View full text Add to dashboard Cite

show abstract

“…This hypothesis was initially based merely on plain experimental studies that documented the neutrophil mobilising potential of IL-17A protein in animal airway models in vivo plus models of human bronchial epithelial and venous endothelial cells in vitro [15][16][17]. In essence, the results of these early experimental studies indicated that IL-17A recruits and accumulates neutrophils indirectly into the airways by inducing the transcription and release of neutrophil mobilising cytokines from structural airway cells ( fig.…”

Section: Original Hypothesis On Neutrophil Accumulationmentioning

confidence: 99%

Interleukin-17 cytokine signalling in patients with asthma

Lindén

Dahlén

2014

Eur Respir J

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Asthma remains a global health problem and, therefore, more effective pharmacotherapy is needed. This is particularly true for chronic and severe asthma. In these clinical phenotypes, chronic inflammation involving neutrophils is likely to play a pathogenic role, making it interesting to target cytokine signalling involved in the accumulation of neutrophils. Therefore, it is of interest that the archetype T-helper 17 cell cytokine interleukin (IL)-17A, perhaps also IL-17F, controls neutrophil accumulation, mucus secretion, macrophage mobilisation and smooth muscle reactivity in various experimental airway models. However, much less is known about the involvement of signalling via IL-17 cytokines in humans with asthma. Existing evidence suggests that these cytokines are released from several types of immune cells in asthma and, for IL-17A, there is a local increase associated with disease severity, with the mobilisation of neutrophils and smooth muscle cells locally in the airways. Even though the causative role of IL-17 cytokines remains unclear, there is potential for clinical utility in targeting IL-17A specifically in patients with moderate-to-severe asthma and high reversibility. There is a need for new and well-powered clinical investigations of signalling via IL-17 cytokines in this clinical phenotype. @ERSpublications There is potential utility for drugs targeting IL-17 cytokine signalling in a sub-group of patients with asthma

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“…The intracellular pathways leading to this type of response appear to involve MAP kinases, even though there is conflicting data on the specific type of MAP kinase involved in human bronchial epithelial cells (74,75). Of particular interest in the context of neutrophilic airway inflammation is the fact that hIL-17 stimulates human venous endothelial cells, bronchial fibroblasts and macrophages to release IL-6 and IL-8 as well, even though the functional significance of these effects remains to be proven (46,76,77).…”

Section: Stimulation With Il-17 Causes Expression Of Neutrophilmobilimentioning

confidence: 99%