Rat Thymus Activation Regulated Chemokine ELISA Kit (DEIA-BJ2294)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
Species Reactivity
Rat
Intended Use
Rat Thymus Activation Regulated Chemokine ELISA Kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of the Thymus Activation Regulated Chemokine. This ELISA kit is for research use only, not for therapeutic or diagnostic applications.
Contents of Kit
1. MICROTITER PLATE: 96 wells
2. ENZYME CONJUGATE: 6.0 mL or 10 ml
3. STANDARD A-F: 1 vial each
4. SUBSTRATE A: 6 mL
5. SUBSTRATE B: 6 mL
6. STOP SOLUTION: 6 mL
7. WASH SOLUTION (100 x): 10 mL
8. BALANCE SOLUTION: 3 mL
Storage
All components of this kit are stable at 2-8°C until the kit's expiration date.
Detection Range
100-2500 pg/mL
Sensitivity
1.0 pg/mL

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References


Induction of regional chemokine expression in response to human umbilical cord blood cell infusion in the neonatal mouse ischemia-reperfusion brain injury model

PLOS ONE

Authors: Baba, Nobuyasu; Wang, Feifei; Iizuka, Michiro; Shen, Yuan; Yamashita, Tatsuyuki; Takaishi, Kimiko; Tsuru, Emi; Matsushima, Sachio; Miyamura, Mitsuhiko; Fujieda, Mikiya; Tsuda, Masayuki; Sagara, Yusuke; Maeda, Nagamasa

Regenerative medicine using umbilical cord blood (UCB) cells shows promise for the treatment of cerebral palsy. Although the efficacy of this therapy has been seen in the clinic, the mechanisms by which UCB cells interact and aid in the improvement of symptoms are not clear. We explored the chemokine expression profile in damaged brain tissue in the neonatal mouse ischemia-reperfusion (IR) brain injury model that was infused with human UCB (hUCB) cells. IR brain injury was induced in 9-day-old NOD/SCID mice. hUCB cells were administered 3 weeks post brain injury. Chemokine expression profiles in the brain extract were determined at various time points. Inflammatory chemokines such as CCL1, CCL17, and CXCL12 were transiently upregulated by 24 hours post brain injury. Upregulation of other chemokines, including CCL5, CCL9, and CXCL1 were prolonged up to 3 weeks post brain injury, but most chemokines dissipated over time. There were marked increases in levels of CCL2, CCL12, CCL20, and CX3CL1 in response to hUCB cell treatment, which might be related to the new recruitment and differentiation of neural stem cells, leading to the induction of tissue regeneration. We propose that the chemokine expression profile in the brain shifted from responding to tissue damage to inducing tissue regeneration. hUCB cell administration further enhanced the production of chemokines, and chemokine networks may play an active role in tissue regeneration in neonatal hypoxic-ischemic brain injury.

A CCR4 antagonist ameliorates atopic dermatitis-like skin lesions induced by dibutyl phthalate and a hydrogel patch containing ovalbumin

BIOMEDICINE & PHARMACOTHERAPY

Authors: Matsuo, Kazuhiko; Hatanaka, Shota; Kimura, Yuta; Hara, Yuta; Nishiwaki, Keiji; Quan, Ying-Shu; Kamiyama, Fumio; Oiso, Naoki; Kawada, Akira; Kabashima, Kenji; Nakayama, Takashi

CCR4 is a chemokine receptor highly expressed by Th2 cells, and regarded as a potential therapeutic target for atopic dermatitis (AD). CCL17 and CCL22 are the CCR4 ligands, and thymic stromal lymphopoietin (TSLP) is shown to promote the expression of CCL17 and CCL22 by dendritic cells. Here, by using dibutyl phthalate (DBP), a TSLP inducer, and a hydrogel patch as a transcutaneous delivery device for ovalbumin, we developed a novel murine AD model and investigated the effect of Compound 22, a CCR4 antagonist. We first found that the mRNA expression of TSLP together with CCL17 and CCL22 was increased in the skins treated with DBP. Furthermore, the topical application of ovalbumin and DBP efficiently and rapidly induced AD-like skin lesions in BALB/c mice, which were characterized by ear swelling accompanied by infiltration of eosinophils, mast cells, and CCR4-expressing Th2 cells in the skin lesions, and elevated total IgE levels in the sera. Using this AD model, we demonstrated that cutaneous administration of Compound 22 inhibited Th2 cell infiltration and ameliorated the AD-like skin lesions. These results suggest that our AD model could be useful for studying new therapeutic strategies. Collectively, CCR4 antagonists may be a promising approach for treating AD.

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