Serum amyloid A protein stimulates CCL20 production in rheumatoid synoviocytes

Migita, Kiyoshi; Koga, Tomohiro; Torigoshi, Takafumi; Maeda, Yümi; Miyashita, Taichiro; Izumi, Yuichi; Aiba, Yoshihiro; Komori, Atsumasa; Nakamura, Minoru; Motokawa, Satoru; Ishibashi, Hiromi

doi:10.1093/rheumatology/kep089

Cited by 23 publications

(18 citation statements)

References 37 publications

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“…JNK pathway is known to be involved in chemokines expression such as MIP-1, MIP-1β, and MIP-3α [45–47]. These chemokines are also known to be produced by activated astrocytes [48].…”

Section: Resultsmentioning

confidence: 99%

“…For example, treatment with a JNK inhibitor inhibits production of CCL-2 (MCP-1) and CCL-4 (MIP-1β) in IL-1β- or TNF-α-stimulated trimester decidual cells [47]. JNK pathway is also involved in CCL-20 production in keratinocytes and Rheumatoid arthritis synoviocytes after inflammatory stimuli [45,46]. Furthermore, MCP-1 is produced by astrocytes via JNK-mediated pathway after SNL and involved in NP and central sensitization (hyperactivity of dorsal horn neurons) [16].…”

Section: Discussionmentioning

confidence: 99%

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Analgesic Effect of Acupuncture Is Mediated via Inhibition of JNK Activation in Astrocytes after Spinal Cord Injury

Lee

Choi

et al. 2013

PLoS ONE

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Acupuncture (AP) has been used worldwide to relieve pain. However, the mechanism of action of AP is poorly understood. Here, we found that AP relieved neuropathic pain (NP) by inhibiting Jun-N-terminal kinase (JNK) activation in astrocytes after spinal cord injury (SCI). After contusion injury which induces the below-level (L4-L5) NP, Shuigou (GV26) and Yanglingquan (GB34) acupoints were applied. At 31 d after injury, both mechanical allodynia and thermal hyperalgesia were significantly alleviated by AP applied at GV26 and GB34. Immunocytochemistry revealed that JNK activation was mainly observed in astrocytes after injury. AP inhibited JNK activation in astrocytes at L4-L5 level of spinal cord. The level of p-c-Jun known, a downstream molecule of JNK, was also decreased by AP. In addition, SCI-induced GFAP expression, a marker for astrocytes, was decreased by AP as compared to control groups. Especially, the number of hypertrophic, activated astrocytes in laminae I–II of dorsal horn at L4-5 was markedly decreased by AP treatment when compared with vehicle and simulated AP-treated groups. When animals treated with SP600125, a specific JNK inhibitor, after SCI, both mechanical allodynia and thermal hyperalgesia were significantly attenuated by the inhibitor, suggesting that JNK activation is likely involved in SCI-induced NP. Also, the expression of chemokines which is known to be mediated through JNK pathway was significantly decreased by AP and SP600125 treatment. Therefore, our results indicate that analgesic effect of AP is mediated in part by inhibiting JNK activation in astrocytes after SCI.

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“…JNK pathway is known to be involved in chemokines expression such as MIP-1, MIP-1β, and MIP-3α [45–47]. These chemokines are also known to be produced by activated astrocytes [48].…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Analgesic Effect of Acupuncture Is Mediated via Inhibition of JNK Activation in Astrocytes after Spinal Cord Injury

Lee

Choi

et al. 2013

PLoS ONE

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“…For example, SAA3 induces expression of CCL20 (MIP-3␣) (45). CCL20 is a ligand for CCR6, which is expressed on IL-17A ϩ ␥␦ T cells (39).…”

Section: Discussionmentioning

confidence: 99%

Pivotal role of IL-6 in the hyperinflammatory responses to subacute ozone in adiponectin-deficient mice

Kasahara¹,

Kim

Mathews³

et al. 2014

American Journal of Physiology-Lung Cellular and Molecular Phys

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Adiponectin is an adipose-derived hormone with anti-inflammatory activity. Following subacute ozone exposure (0.3 ppm for 24-72 h), neutrophilic inflammation and IL-6 are augmented in adiponectin-deficient (Adipo(-/-)) mice. The IL-17/granulocyte colony-stimulating factor (G-CSF) axis is required for this increased neutrophilia. We hypothesized that elevated IL-6 in Adipo(-/-) mice contributes to their augmented responses to ozone via effects on IL-17A expression. Therefore, we generated mice deficient in both adiponectin and IL-6 (Adipo(-/-)/IL-6(-/-)) and exposed them to ozone or air. In ozone-exposed mice, bronchoalveolar lavage (BAL) neutrophils, IL-6, and G-CSF, and pulmonary Il17a mRNA expression were greater in Adipo(-/-) vs. wild-type mice, but reduced in Adipo(-/-)/IL-6(-/-) vs. Adipo(-/-) mice. IL-17A(+) F4/80(+) cells and IL-17A(+) γδ T cells were also reduced in Adipo(-/-)/IL-6(-/-) vs. Adipo(-/-) mice exposed to ozone. Only BAL neutrophils were reduced in IL-6(-/-) vs. wild-type mice. In wild-type mice, IL-6 was expressed in Gr-1(+)F4/80(-)CD11c(-) cells, whereas in Adipo(-/-) mice F4/80(+)CD11c(+) cells also expressed IL-6, suggesting that IL-6 is regulated by adiponectin in these alveolar macrophages. Transcriptomic analysis identified serum amyloid A3 (Saa3), which promotes IL-17A expression, as the gene most differentially augmented by ozone in Adipo(-/-) vs. wild-type mice. After ozone, Saa3 mRNA expression was markedly greater in Adipo(-/-) vs. wild-type mice but reduced in Adipo(-/-)/IL-6(-/-) vs. Adipo(-/-) mice. In conclusion, our data support a pivotal role of IL-6 in the hyperinflammatory condition observed in Adipo(-/-) mice after ozone exposure and suggest that this role of IL-6 involves its ability to induce Saa3, IL-17A, and G-CSF.

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“…Interaction of SAA with FPRL1 stimulates endothelial cell proliferation, migration and angiogenesis, as well as synovitis [66,67]. It has been reported that SAA in part acts via the induction of MIP3a/CCL20 chemokine production by RA synovial fibroblasts [68 ]. MIP-3a/CCL20, as well as its receptor, CCR6, have been implicated in RA-associated inflammation and angiogenesis [44,69].…”

Section: Other Angiogenic Mediatorsmentioning

confidence: 99%

Angiogenesis and vasculogenesis in rheumatoid arthritis

Szekanecz

Besenyei

Simonyi

et al. 2010

Current Opinion in Rheumatology

129

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Serum amyloid A protein stimulates CCL20 production in rheumatoid synoviocytes

Abstract: These findings suggest that SAA may be implicated in the recruitment of lymphocytes, including CCR6-expressing Th17 cells, in RA synovium by up-regulating CCL20 production in synoviocytes.

Cited by 23 publications

References 37 publications

Analgesic Effect of Acupuncture Is Mediated via Inhibition of JNK Activation in Astrocytes after Spinal Cord Injury

Analgesic Effect of Acupuncture Is Mediated via Inhibition of JNK Activation in Astrocytes after Spinal Cord Injury

Pivotal role of IL-6 in the hyperinflammatory responses to subacute ozone in adiponectin-deficient mice

Angiogenesis and vasculogenesis in rheumatoid arthritis

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