In vitro and in vivo analyses of the PTGDR involvement in allergic asthma andresponse to the treatment with corticosteroids

  1. Marcos-Vadillo E 1
  2. Marqués-García F 1
  3. García-Sánchez A 2
  4. Isidoro-García M 1
  5. Cornejo-García JA 3
  6. Moreno-Rodilla E 4
  7. Estravis M 5
  8. Dávila I 4
  9. Sanz C 6
  1. 1 Hospital Universitario de Salamanca
    info

    Hospital Universitario de Salamanca

    Salamanca, España

    ROR https://ror.org/0131vfw26

  2. 2 IBSAL, Institute of Biomedical Research of Salamanca. Department of Biomedical and Diagnostic Sciences, University of Salamanca
  3. 3 Research Laboratory, IBIMA, Regional University Hospital of Malaga, UMA
  4. 4 IBSAL, Institute of Biomedical Research of Salamanca. Department of Biomedical and Diagnostic Sciences, University of Salamanca. Department of Immunoallergy. Salamanca University Hospital
  5. 5 Instituto de Investigación Biomédica de Salamanca
    info

    Instituto de Investigación Biomédica de Salamanca

    Salamanca, España

    ROR https://ror.org/03em6xj44

  6. 6 Universidad de Salamanca
    info

    Universidad de Salamanca

    Salamanca, España

    ROR https://ror.org/02f40zc51

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Actas:
Allergy

ISSN: 0105-4538,  1398-9995

Año de publicación: 2018

Volumen: 73

Número: s105

Páginas: 516-517

Congreso: European Academy of Allergy and Clinical Immunology Congress

Tipo: Aportación congreso

GOOGLE SCHOLAR

Resumen

Background:The prostaglandin D2 receptor (PTGDR) has beenrelated to allergic asthma. We aim to verify the implication ofPTGDR in allergic asthma using a cell and a murine model, and toanalyze the effect of a corticosteroid treatment.Method:Four groups of Balb/c mice were defined: control andasthmatic, with and without treatment. Asthmatic groups were sensi-tized with intraperitoneal ovalbumin (OVA) and provoked with intra-nasal OVA (0.1% OVA three times a week for 12 weeks). Treatedgroups received 0.2 mg/kg dexamethasone before each challenge.RNA was extracted from lung tissue andPTGDRexpression was ana-lyzed by qRT‐PCR. Kruskal‐Wallis test was performed through theSPSS 19.0 program. To deeper analyze the involved mechanism,A549 cells were transfected withPTGDRexpression vectors for12 hours. Cell culture cytokines levels were analysed using Bio‐PlexSystem.Results:In the murine model, OVA stimulation caused an increasein the expression ofPTGDR,while corticosteroid treatment reducedit. Control groups, without and with dexamethasone, presented amedian of 2.17 (RI=3.25) and 1.02 (RI=0.89), respectively. Asthmaticgroups, without and with dexamethasone, presented a median of84.45 (RI=77.96) and 36.08 (RI=26.32), respectively (P= 0.013).Overexpression ofPTGDRin pulmonary cells associated to a general-ized increase of cytokine expression.Conclusion:In a mouse model we confirmed the involvement ofPTGDRin allergic asthma by the increase of its expression levelsafter ovalbumin sensitization. We also identified a reduction ofPTGDRlevels in response to dexamethasone treatment. Thein vitromodel suggests thatPTGDRinduces an inflammatory response,increasing the cytokines levels