PMID- 16603479
OWN - NLM
STAT- MEDLINE
DCOM- 20060629
LR  - 20191026
IS  - 1091-7691 (Electronic)
IS  - 0895-8378 (Linking)
VI  - 18
IP  - 7
DP  - 2006 Jun
TI  - Inhibition of pan neurotrophin receptor p75 attenuates diesel particulate-induced 
      enhancement of allergic airway responses in C57/B16J mice.
PG  - 483-91
AB  - Recent investigations have linked neurotrophins, including nerve growth factor 
      (NGF), neurotrophin-3 (NT-3), and brain-derived neurotrophic factor (BDNF), to 
      allergic airways diseases. Antibody blockade of NGF attenuates airway resistance 
      in allergic mice. Diesel exhaust particle (DEP) exposure has been linked to 
      asthma exacerbation in many cities with vehicular traffic congestion. We tested 
      the hypothesis that DEP-induced enhancement of the hallmark features of allergic 
      airway disease in a murine model is dependent on the function of the pan 
      neurotrophin receptor p75. Ovalbumin (OVA)-sensitized C57B1/6J mice were 
      intranasally instilled with an antibody against the p75 receptor or saline alone 
      1 h before OVA challenge. The mice were then exposed nose-only to the PM2.5 
      fraction of SRM2975 DEP or air alone for 5 h beginning 1 h after OVA challenge. 
      Two days later, air-exposed OVA-allergic mice developed a small but insignificant 
      increase in methacholine-induced airflow obstruction relative to air-exposed, 
      vehicle-sensitized mice. DEP-exposed OVA-allergic mice had a significantly 
      greater degree of airway obstruction than all other groups. Instillation of 
      anti-p75 significantly attenuated the DEP-induced increase in airway obstruction 
      in OVA-allergic mice to levels similar to non-sensitized mice. The DEP-induced 
      exacerbation of allergic airway responses may, in part, be mediated by 
      neurotrophins.
FAU - Farraj, Aimen K
AU  - Farraj AK
AD  - Experimental Toxicology Division, U.S. Environmental Protection Agency, Research 
      Triangle Park, North Carolina 27711, USA. farraj.aimen@epa.gov
FAU - Haykal-Coates, Najwa
AU  - Haykal-Coates N
FAU - Ledbetter, Allen D
AU  - Ledbetter AD
FAU - Evansky, Paul A
AU  - Evansky PA
FAU - Gavett, Stephen H
AU  - Gavett SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - England
TA  - Inhal Toxicol
JT  - Inhalation toxicology
JID - 8910739
RN  - 0 (Interleukin-13)
RN  - 0 (Interleukin-5)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Vehicle Emissions)
RN  - 0W5ETF9M2K (Methacholine Chloride)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Animals
MH  - Asthma/*etiology/prevention & control
MH  - Bronchoalveolar Lavage Fluid/cytology
MH  - Immunoglobulin E/blood
MH  - Interleukin-13/biosynthesis
MH  - Interleukin-4/biosynthesis
MH  - Interleukin-5/biosynthesis
MH  - Lung/pathology
MH  - Male
MH  - Methacholine Chloride/pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Ovalbumin/immunology
MH  - Receptor, Nerve Growth Factor/antagonists & inhibitors/*physiology
MH  - Vehicle Emissions/*toxicity
EDAT- 2006/04/11 09:00
MHDA- 2006/06/30 09:00
CRDT- 2006/04/11 09:00
PHST- 2006/04/11 09:00 [pubmed]
PHST- 2006/06/30 09:00 [medline]
PHST- 2006/04/11 09:00 [entrez]
AID - M1101U1722X053N4 [pii]
AID - 10.1080/08958370600602439 [doi]
PST - ppublish
SO  - Inhal Toxicol. 2006 Jun;18(7):483-91. doi: 10.1080/08958370600602439.