PMID- 21677048
OWN - NLM
STAT- MEDLINE
DCOM- 20111017
LR  - 20151119
IS  - 1460-2377 (Electronic)
IS  - 0953-8178 (Linking)
VI  - 23
IP  - 7
DP  - 2011 Jul
TI  - Infliximab alleviates inflammation and ex vivo airway hyperreactivity in 
      asthmatic E3 rats.
PG  - 443-51
LID - 10.1093/intimm/dxr032 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) has been implicated in the pathogenesis of 
      asthma, and neutralization of TNF-alpha is an effective therapy for inflammatory 
      diseases. The present study tested the idea that a TNF-alpha antibody, infliximab, 
      may be useful in the management of asthma. E3 rats were immunized with ovalbumin 
      (OVA)/alum and received infliximab intra-peritoneally. Two weeks later, OVA-PBS 
      was instilled intranasally daily for 7 days. Bronchoalveolar lavage fluids 
      (BALFs), serum and lung homogenates were collected for analysis of cells and 
      inflammatory mediators. Contractile responses of lobar-bronchus segments to 
      agonists were functionally tested. Pulmonary tissues were investigated using 
      histological examination. The results showed that the sensitized 'model E3 rats' 
      exhibited an increase in the total amount of inflammatory cells, primarily 
      eosinophils, in BALF and pulmonary tissue, as well as epithelial damage. Serum 
      levels of IgE increased and so did the levels of nitric oxide, inducible nitric 
      oxide synthase, TNF-alpha and IL-4, IL-5 and IL-13 in lung homogenate and serum. 
      Furthermore, the contractile responses in bronchi induced by endothelin-1, 
      sarafotoxin 6c and bradykinin increased and isoprenaline-induced relaxations 
      decreased. All these changes induced by the sensitization procedure were reduced 
      by the infliximab treatment. The results suggest that infliximab prevents the 
      development of local airway inflammation and antagonizes changes of the bronchial 
      smooth muscle receptor phenotype, thereby blocking the development of airway 
      smooth muscle hyperreactivity of asthmatic rats.
FAU - Cai, Yan
AU  - Cai Y
AD  - Department of Pharmacology, Xi'an Jiaotong University College of Medicine, 
      Shaanxi, People's Republic of China.
FAU - Cao, Yong-Xiao
AU  - Cao YX
FAU - Lu, She-Min
AU  - Lu SM
FAU - Xu, Cang-Bao
AU  - Xu CB
FAU - Cardell, Lars Olaf
AU  - Cardell LO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110615
PL  - England
TA  - Int Immunol
JT  - International immunology
JID - 8916182
RN  - 0 (Anti-Asthmatic Agents)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Cytokines)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - B72HH48FLU (Infliximab)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 3.5.3.1 (Arginase)
SB  - IM
MH  - Animals
MH  - Anti-Asthmatic Agents/*pharmacology/*therapeutic use
MH  - Antibodies, Monoclonal/*pharmacology/*therapeutic use
MH  - Arginase/metabolism
MH  - Asthma/blood/*drug therapy/pathology
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Cytokines/blood
MH  - Disease Models, Animal
MH  - Eosinophils/drug effects/immunology/pathology
MH  - Immunoglobulin E/blood
MH  - Inflammation/*immunology/metabolism/pathology
MH  - Infliximab
MH  - Lung/drug effects/immunology/metabolism/pathology
MH  - Male
MH  - Muscle, Smooth/*drug effects/immunology
MH  - Nitric Oxide/blood
MH  - Nitric Oxide Synthase/metabolism
MH  - Rats
EDAT- 2011/06/17 06:00
MHDA- 2011/10/18 06:00
CRDT- 2011/06/17 06:00
PHST- 2011/06/17 06:00 [entrez]
PHST- 2011/06/17 06:00 [pubmed]
PHST- 2011/10/18 06:00 [medline]
AID - dxr032 [pii]
AID - 10.1093/intimm/dxr032 [doi]
PST - ppublish
SO  - Int Immunol. 2011 Jul;23(7):443-51. doi: 10.1093/intimm/dxr032. Epub 2011 Jun 15.