PMID- 29879991
OWN - NLM
STAT- MEDLINE
DCOM- 20181029
LR  - 20231112
IS  - 1465-993X (Electronic)
IS  - 1465-9921 (Print)
IS  - 1465-9921 (Linking)
VI  - 19
IP  - 1
DP  - 2018 Jun 8
TI  - Is IgE or eosinophils the key player in allergic asthma pathogenesis? Are we 
      asking the right question?
PG  - 113
LID - 10.1186/s12931-018-0813-0 [doi]
LID - 113
AB  - Bronchial asthma (BA) is a chronic inflammatory disease with a marked 
      heterogeneity in pathophysiology and etiology. The heterogeneity of BA may be 
      related to the inducing mechanism(s) (allergic vs non-allergic), the 
      histopathological background (eosinophilic vs non-eosinophilic), and the clinical 
      manifestations, particularly in terms of severity and frequency of exacerbations. 
      Asthma can be divided into at least two different endotypes based on the degree 
      of Th2 inflammation (T2 'high' and T2 'low'). For patients with severe 
      uncontrolled asthma, monoclonal antibodies (mAbs) against immunoglobulin E (IgE) 
      or interleukin (IL)-5 are now available as add-on treatments. Treatment decisions 
      for individual patients should consider the biological background in terms of the 
      "driving mechanisms" of inflammation as this should predict the patients' likely 
      responses to treatment. The question is not whether an anti-IgE or an 
      anti-eosinophilic strategy is more effective, but rather what the mechanism is at 
      the origin of the airway. While IgE is involved early in the inflammatory cascade 
      and can be considered as a cause of allergic asthma, eosinophilia can be 
      considered a consequence of the whole process. This article discusses the 
      different roles of the IgE and IL-5/eosinophil pathways in the pathogenic 
      mechanisms of airway inflammation occurring in allergic asthma, and the possible 
      reasons to choose an anti-IgE mAb or anti-IL-5 treatment.
FAU - Matucci, Andrea
AU  - Matucci A
AD  - Immunoallergology Unit, Azienda Ospedaliero-Universitaria Careggi, Largo 
      Brambilla 3, 50134, Florence, Italy. andrea.matucci@unifi.it.
FAU - Vultaggio, Alessandra
AU  - Vultaggio A
AD  - Immunoallergology Unit, Azienda Ospedaliero-Universitaria Careggi, Largo 
      Brambilla 3, 50134, Florence, Italy.
FAU - Maggi, Enrico
AU  - Maggi E
AD  - Center for Research, Transfer and High Education DENOTHE, University of Florence, 
      Florence, Italy.
FAU - Kasujee, Ismail
AU  - Kasujee I
AD  - Novartis Pharma AG, Basel, Switzerland.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20180608
PL  - England
TA  - Respir Res
JT  - Respiratory research
JID - 101090633
RN  - 0 (Inflammation Mediators)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Asthma/immunology/*metabolism
MH  - Eosinophilia/immunology/*metabolism
MH  - Eosinophils/immunology/*metabolism
MH  - Humans
MH  - Immunoglobulin E/immunology/*metabolism
MH  - Inflammation Mediators/immunology/metabolism
PMC - PMC5992661
OTO - NOTNLM
OT  - Anti-IL-5
OT  - Asthma pathogenesis; anti-IgE
OT  - Eosinophil
OT  - IL-5
OT  - IgE
OT  - Immunoglobulin E
OT  - Interleukin 5
COIS- ETHICS APPROVAL AND CONSENT TO PARTICIPATE: Not applicable. COMPETING INTERESTS: 
      AM and AV have received payment for lectures from Novartis, GlaxoSmithKline, 
      Teva, AstraZeneca and have consultant arrangements with Novartis, 
      GlaxoSmithKline, Teva, AstraZeneca. EM has received research support from 
      Novartis, and has consultant arrangements with Novartis, AstraZeneca; Teva, 
      Sanofi. AP, FS, XJ and IK are full-time employees of Novartis. PUBLISHER'S NOTE: 
      Springer Nature remains neutral with regard to jurisdictional claims in published 
      maps and institutional affiliations.
EDAT- 2018/06/09 06:00
MHDA- 2018/10/30 06:00
PMCR- 2018/06/08
CRDT- 2018/06/09 06:00
PHST- 2017/12/22 00:00 [received]
PHST- 2018/05/14 00:00 [accepted]
PHST- 2018/06/09 06:00 [entrez]
PHST- 2018/06/09 06:00 [pubmed]
PHST- 2018/10/30 06:00 [medline]
PHST- 2018/06/08 00:00 [pmc-release]
AID - 10.1186/s12931-018-0813-0 [pii]
AID - 813 [pii]
AID - 10.1186/s12931-018-0813-0 [doi]
PST - epublish
SO  - Respir Res. 2018 Jun 8;19(1):113. doi: 10.1186/s12931-018-0813-0.