PMID- 22441537
OWN - NLM
STAT- MEDLINE
DCOM- 20120726
LR  - 20131121
IS  - 1423-0216 (Electronic)
IS  - 1021-7401 (Linking)
VI  - 19
IP  - 4
DP  - 2012
TI  - 3,4-methylenedioxymethamphetamine (ecstasy) decreases inflammation and airway 
      reactivity in a murine model of asthma.
PG  - 209-19
LID - 10.1159/000334098 [doi]
AB  - OBJECTIVE: 3,4-Methylenedioxymethamphetamine (MDMA), or ecstasy, is a synthetic 
      drug used recreationally, mainly by young people. It has been suggested that MDMA 
      has a Th cell skewing effect, in which Th1 cell activity is suppressed and Th2 
      cell activity is increased. Experimental allergic airway inflammation in 
      ovalbumin (OVA)-sensitized rodents is a useful model to study Th2 response; 
      therefore, based on the Th2 skewing effect of MDMA, we studied MDMA in a model of 
      allergic lung inflammation in OVA-sensitized mice. METHODS: We evaluated cell 
      trafficking in the bronchoalveolar lavage fluid, blood and bone marrow; cytokine 
      production; L-selectin expression and lung histology. We also investigated the 
      effects of MDMA on tracheal reactivity in vitro and mast cell degranulation. 
      RESULTS: We found that MDMA given prior to OVA challenge in OVA-sensitized mice 
      decreased leukocyte migration into the lung, as revealed by a lower cell count in 
      the bronchoalveolar lavage fluid and lung histologic analysis. We also showed 
      that MDMA decreased expression of both Th2-like cytokines (IL-4, IL-5 and IL-10) 
      and adhesion molecules (L-selectin). Moreover, we showed that the 
      hypothalamus-pituitary-adrenal axis is partially involved in the MDMA-induced 
      reduction in leukocyte migration into the lung. Finally, we showed that MDMA 
      decreased tracheal reactivity to methacholine as well as mast cell degranulation 
      in situ. CONCLUSIONS: Thus, we report here that MDMA given prior to OVA challenge 
      in OVA-sensitized allergic mice is able to decrease lung inflammation and airway 
      reactivity and that hypothalamus-pituitary-adrenal axis activation is partially 
      involved. Together, the data strongly suggest an involvement of a neuroimmune 
      mechanism in the effects of MDMA on lung inflammatory response and cell 
      recruitment to the lungs of allergic animals.
CI  - Copyright (c) 2012 S. Karger AG, Basel.
FAU - Stankevicius, Daniel
AU  - Stankevicius D
AD  - Department of Pharmacology, Institute of Biomedical Sciences, University of Sao 
      Paulo, Sao Paulo, Brazil.
FAU - Ferraz-de-Paula, Viviane
AU  - Ferraz-de-Paula V
FAU - Ribeiro, Alison
AU  - Ribeiro A
FAU - Pinheiro, Milena Lobao
AU  - Pinheiro ML
FAU - Ligeiro de Oliveira, Ana P
AU  - Ligeiro de Oliveira AP
FAU - Damazo, Amilcar S
AU  - Damazo AS
FAU - Lapachinske, Silvio F
AU  - Lapachinske SF
FAU - Moreau, Regina L M
AU  - Moreau RL
FAU - Tavares de Lima, Wothan
AU  - Tavares de Lima W
FAU - Palermo-Neto, Joao
AU  - Palermo-Neto J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120321
PL  - Switzerland
TA  - Neuroimmunomodulation
JT  - Neuroimmunomodulation
JID - 9422763
RN  - 0 (Cytokines)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Animals
MH  - Asthma/*immunology
MH  - Bone Marrow Cells
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Cell Movement/drug effects
MH  - Cytokines/drug effects/metabolism
MH  - Disease Models, Animal
MH  - Inflammation/*immunology
MH  - Leukocyte Count
MH  - Leukocytes/*drug effects
MH  - Lung/cytology/*drug effects
MH  - Male
MH  - Mast Cells/drug effects
MH  - Mice
MH  - N-Methyl-3,4-methylenedioxyamphetamine/immunology/*pharmacology
MH  - Th2 Cells/*drug effects/physiology
MH  - Trachea/drug effects
EDAT- 2012/03/24 06:00
MHDA- 2012/07/27 06:00
CRDT- 2012/03/24 06:00
PHST- 2011/07/29 00:00 [received]
PHST- 2011/09/28 00:00 [accepted]
PHST- 2012/03/24 06:00 [entrez]
PHST- 2012/03/24 06:00 [pubmed]
PHST- 2012/07/27 06:00 [medline]
AID - 000334098 [pii]
AID - 10.1159/000334098 [doi]
PST - ppublish
SO  - Neuroimmunomodulation. 2012;19(4):209-19. doi: 10.1159/000334098. Epub 2012 Mar 
      21.