Mast cell inhibitor treatment

GL Gang Liu
TH Tatt Jhong Haw
MS Malcolm R. Starkey
AP Ashleigh M. Philp
SP Stelios Pavlidis
CN Christina Nalkurthi
PN Prema M. Nair
HG Henry M. Gomez
IH Irwan Hanish
AH Alan CY. Hsu
EH Elinor Hortle
SP Sophie Pickles
JR Joselyn Rojas-Quintero
RE Raul San Jose Estepar
JM Jacqueline E. Marshall
RK Richard Y. Kim
AC Adam M. Collison
JM Joerg Mattes
SI Sobia Idrees
AF Alen Faiz
NH Nicole G. Hansbro
RF Ryutaro Fukui
YM Yusuke Murakami
HC Hong Sheng Cheng
NT Nguan Soon Tan
SC Sanjay H. Chotirmall
JH Jay C. Horvat
PF Paul S. Foster
BO Brian GG. Oliver
FP Francesca Polverino
AI Antonio Ieni
FM Francesco Monaco
GC Gaetano Caramori
SS Sukhwinder S. Sohal
KB Ken R. Bracke
PW Peter A. Wark
IA Ian M. Adcock
KM Kensuke Miyake
DS Don D. Sin
PH Philip M. Hansbro
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Mice (female, 6–8 weeks old, n = 8) were exposed to CS for 8 weeks, control mice were exposed to normal air. Some mice were treated with 50 mg/kg disodium cromoglycate (DSCG, cat# 15826-37-6, Sigma) intranasally from weeks 6 to 8 of CS exposure, and control mice received equal volumes of vehicle. BALF was collected for assessment of inflammatory cell influx, lungs were perfused, formalin-fixed, paraffin-embedded and sectioned (3.5 μm thickness) for histology, stained with H&E for emphysema analysis, and lung function was assessed using the flexiVent system27,28,42,46. Proteins were extracted from mouse lungs and mMCP6 levels were measured by immunoblot41.

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