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Dermatophagoides pteronyssinus

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Dermatophagoides pteronyssinus is a species of dust mite. It is a small arthropod that commonly lives in household dust. The core function of this product is to serve as a laboratory reference material for research and testing purposes.

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20 protocols using dermatophagoides pteronyssinus

1

Allergic Sensitization Evaluation in Infants

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Rhinitis was defined as having symptoms of sneezing, runny and/or blocked nose that lasted for at least four weeks in single or multiple episodes (each episode lasting at least two weeks) This definition was based on the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines [4 (link)]. Wheeze was defined as presence of wheeze symptoms (noisy breathing with a high-pitched, whistling sound heard from the chest, not the mouth). Eczema was defined as physician-diagnosed eczema in the first 18 months. At the 18 month visit, subjects were assessed via skin prick test (SPT) for the presence of allergic sensitization to a panel of food (milk, peanut, egg) and house dust mites allergens (Dermatophagoides pteronyssinus, Dermatophagoides farinae) from Greer Laboratories (Lenoir, NC, USA) and Blomia tropicalis (extract obtained from in-house laboratory) [18 (link)]. Wheal size of at least 3mm larger than the negative control (saline) was inferred as a positive reaction.
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2

Allergic Airway Inflammation Asthma Treatment

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Example 3

Splenocytes were isolated from DO11.10 mice and ˜1×106CD4T cells were transferred to pure BALB/c mice by intravenous injection. For 3 days from the next day, 100 μg of a mixture of HDM (Dermatophagoidesfarinae 50 μg, Dermatophagoidespteronyssinus 50 μg, Greer Laboratories, Inc., USA) and OVA (Sigma-Aldrich Co., USA) was administered intranasally to the mice. From day 2 after administration, the mice were treated with 200 μg of each of the inventive compounds or PBS (for control mice) three times daily through the intraperitoneal route. After the mice were euthanized on day 11, the numbers of total cells and eosinophils in the airways were checked. The treatment schedule with the Formula 5 (KB 1517) and Formula 10 (KB 1518) (200 μg each) in house dust mite (HDM)-induced allergic airway inflammation mouse models is shown in FIG. 8. The results are shown in FIGS. 4 and 5.

As can be seen from FIGS. 4 and 5, the numbers of total cells and eosinophils in the airways of the mice treated with the inventive compounds of Formula 5 (KB-1517) and Formula 10 (KB-1518) (200 μg each) were significantly reduced than those in the untreated controls. These results lead to the conclusion that the inventive quinolinone derivatives can be used to fundamentally prevent and treat allergic diseases such as asthma atopic dermatitis.

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3

Allergen Sensitivity Threshold Determination

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AAs and ACs had positive SPT to standardized HDM [Dermatophagoides pteronyssinus; Greer Laboratories, 10,000 allergy units (AU) per ml] and/or cat hair extract [Felis catis; Greer Laboratories, 10,000 bioequivalent allergy units (BAU) per ml]. The threshold level of allergen sensitivity was determined by quantitative SPT using serial threefold dilutions of extract. The lowest concentration of extract eliciting a positive skin prick test (3-mm wheal diameter) was used as the allergen dose administered during SAC (9 ). The same stock of allergen was used for both SPT and SAC.
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4

Murine Model of Allergic Airway Inflammation

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To prime mice to HDM allergen and elicit allergic lung inflammation, animals were sensitized to HDM on day 0 by the intranasal administration of 100 μg of HDM allergen (Dermatophagoides pteronyssinus, Greer Laboratories) in 30 μl of PBS and then challenged on days 7 and 14 by intranasal treatment with 50 μg of HDM (30 μl total volume). HDM allergen preparations used throughout this study contained minimal levels of LPS. Control groups comprised mice receiving 30 μl of PBS on days 0, 7, and 14. To determine the level of mucosal inflammation, bronchoalveolar lavage fluid (BALF) and lung tissue were harvested 48 h after the last challenge on day 16. To examine the proinflammatory properties of MWCNT and their effect on allergic airway inflammation, mice were additionally challenged with a single 50 μg dose of MWCNT (30 μl of 1.67 mg/ml suspension) administered oropharyngeally 24 h prior to harvest, as illustrated in Figure 1.
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5

Intranasal House Dust Mite Allergy Model

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After sedation with isoflurane (5% induction, 2–3% maintenance dose), mice were administered house dust mite (HDM) extract (Dermatophagoides pteronyssinus; Greer Laboratories, Lenoir, NC) intranasally in PBS (40μg/25μl PBS) 5 times/week for 3 weeks as previously described (29 (link)) with control mice received PBS intranasally at the same time-points. For memory generation and secondary challenge, mice exposed to HDM for 3 wks were “rested” (no further manipulation) for 4–8 weeks, then challenged intranasally with 2 doses of HDM (40μg/25μl PBS) 24hrs apart. Airway hyper-responsiveness was measured 24 hours after the final HDM challenge.
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6

HDM-Induced Allergic Responses in Mice

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Mice received 5-fold increasing doses (0.2, 1, 5 or 25 µg) of HDM (Dermatophagoides pteronyssinus, Greer Laboratories) in 10 µl saline once daily for 7 consecutive days or 5 days/week followed by 2 days of rest for a total of 2 or 4 weeks, as specified. For the in vivo recall protocol, mice were exposed to 0.2 µg HDM for 10 consecutive days, then rested for 4 weeks, and re-exposed to saline, 0.02 or 0.2 µg HDM for 3 consecutive days. To evaluate very early events, mice received only one administration of 0.2 or 100 µg HDM, or 4 µg recombinant murine GM-CSF.
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7

Intraperitoneal Allergen Sensitization

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For intraperitoneal sensitization OVA (salt free albumin egg, Serva, Heidelberg, Germany), HDM (mite, house dust, Dermatophagoides pteronyssinus, Greer Laboratories, Lenoir, N.C., USA), and CRA (cockroach, german, Blattella germanica, Greer Laboratories, Lenoir, N.C., USA) were solubilised in 100 µl phosphate buffered saline and absorbed to 100 µl Al(OH)3 (Imject Alum, Rockford, USA). For challenge, allergens were solubilised in 50 µl phosphate buffered saline (PBS, BioWhittaker Europe, Verviers, Belgium) and administered via intratracheal application.
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8

Longitudinal Allergen Skin Prick Testing

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SPT was conducted at ages 18 months, 3, 5 and 8 years to major relevant allergens in Singapore, which included cow's milk, egg, peanut and house dust mites, Dermatophagoides pteronyssinus, Dermatophagoides farina (Greer Laboratories, Lenoir, NC, USA) and Blomia tropicalis. SPT was defined as positive at a timepoint if any of the allergens tested positive at the timepoint with an average wheal size of at least 3 mm.
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9

HDM-induced Allergic Asthma in Mice

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Female C57BL/6 mice at 8–10 weeks of age and free of murine-specific pathogens were obtained from the Orient Bio Inc. (Seongnam, Korea). In addition, Cas9 RNA-guided endonuclease (RGEN) PI3K-δ KO mice (Macrogen, Inc., Seoul, Korea) were used, and they were interbred and maintained up to 8–10 weeks of age in pathogen-free condition at Macrogen, Inc. They were housed throughout the experiments in a laminar flow cabinet and maintained on standard laboratory chow ad libitum. All experimental animals used in this study were under a protocol approved by the Institutional Animal Care and Use Committee of Chonbuk National University (CBU 2014-00054). Each animal experiment was performed using 6 mice per group. When using Cas9 RGEN PI3K-δ KO mice, 4 mice were allocated to each experimental group. For the HDM-induced asthma model, mice were sensitized intratracheally with HDM extract (100 μg, Dermatophagoides pteronyssinus; GREER laboratories, Lenoir, NC, USA) on days 1 and 7. On day 14 after the initial sensitization, the mice were challenged intratracheally with 100 μg of HDM extract in saline (or with saline as a control). Bronchoalveolar lavage (BAL) was performed 48 hours after the challenge as previously described.11 (link)
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10

Allergen-Induced Airway Inflammation in Mice

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Mice were sensitized to house dust mite (HDM; Dermatophagoides pteronyssinus, Greer Laboratories Inc. Lenoir, NC, USA) to elicit allergen-induced airway inflammation (Figure S1). We followed an established acute exposure model, which included five consecutive daily intranasal exposures (25 μg of crude extract in 35 μL normal saline) followed by a single intranasal sensitization 7 days later [19 (link),20 (link),21 (link)]. Disease induced by this acute exposure model has been previously demonstrated to manifest primary phenotypes of airway hyperresponsiveness [22 (link)]. Control groups were instilled intranasally with 35 µL of saline solution. HDM and saline sensitized mice were exposed to GDI engine exhaust on the day following the final intranasal sensitisation.
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