PMID- 19733592
OWN - NLM
STAT- MEDLINE
DCOM- 20100603
LR  - 20131121
IS  - 1879-0542 (Electronic)
IS  - 0165-2478 (Linking)
VI  - 127
IP  - 1
DP  - 2009 Dec 2
TI  - Allergen-sensitization in vivo enhances mast cell-induced inflammatory responses 
      and supports innate immunity.
PG  - 48-54
LID - 10.1016/j.imlet.2009.08.012 [doi]
AB  - Mast cells are immune cells that play a crucial role in inflammatory reactions 
      related to allergic reactions and the defense against certain parasites and 
      bacteria. In allergy, the binding of immunoglobulin E (IgE) to its high-affinity 
      receptor (FcepsilonRI) sensitizes mast cells. Subsequent cross-linking of 
      IgE-FcepsilonRI by multivalent antigen results in cellular activation and the 
      release of proinflammatory mediators. Recent in vivo and in vitro experiments 
      suggest that IgE not only acts as an allergen sensor, but also induces molecular 
      and biological changes in mast cells. In the present study we examined whether 
      allergen-sensitization in vivo could modify the magnitude of mast cells-induced 
      inflammatory responses. Moreover, we studied changes in peritoneal mast cell 
      number and histamine amount during and after sensitization. We provided evidence 
      that sensitization, at the time of the maximum allergen-specific IgE-titer, 
      increases the intensity of a local inflammatory process generated in a cutaneous 
      anaphylactic reaction. Sensitization also supports innate immunity, improving 
      survival and speeding up the resolution of an acute inflammatory reaction induced 
      by polymicrobial sepsis, while decreasing the amount of histamine in peritoneal 
      mast cells. In addition, our results showed that sensitization induces a late 
      increase in the number and histamine amount of peritoneal mast cells. Thus, our 
      findings clearly demonstrated that sensitization induces changes in mast cells 
      which prepare the cell to induce more intense inflammatory responses. This 
      entails an increased detrimental role in subsequent IgE-dependent allergic 
      reactions and an improved protective function in innate defense against 
      pathogens.
FAU - Salinas, Eva
AU  - Salinas E
AD  - Department of Microbiology, Basic Science Center, Autonomous University of 
      Aguascalientes, Mexico. emsalin@correo.uaa.mx
FAU - Quintanar, J Luis
AU  - Quintanar JL
FAU - Ramirez-Celis, Nora Alejandra
AU  - Ramirez-Celis NA
FAU - Quintanar-Stephano, Andres
AU  - Quintanar-Stephano A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090904
PL  - Netherlands
TA  - Immunol Lett
JT  - Immunology letters
JID - 7910006
RN  - 0 (Allergens)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 5QB0T2IUN0 (Aluminum Hydroxide)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Allergens/*immunology
MH  - Aluminum Hydroxide/administration & dosage
MH  - Animals
MH  - Cell Count
MH  - Histamine Release
MH  - *Immunity, Innate
MH  - Immunization
MH  - Immunoglobulin E/blood
MH  - Male
MH  - Mast Cells/*immunology/*metabolism/pathology
MH  - Ovalbumin/*immunology
MH  - Passive Cutaneous Anaphylaxis/*immunology
MH  - Peritoneal Cavity/pathology
MH  - Rats
MH  - Rats, Wistar
EDAT- 2009/09/08 06:00
MHDA- 2010/06/04 06:00
CRDT- 2009/09/08 06:00
PHST- 2009/06/22 00:00 [received]
PHST- 2009/08/13 00:00 [revised]
PHST- 2009/08/30 00:00 [accepted]
PHST- 2009/09/08 06:00 [entrez]
PHST- 2009/09/08 06:00 [pubmed]
PHST- 2010/06/04 06:00 [medline]
AID - S0165-2478(09)00215-6 [pii]
AID - 10.1016/j.imlet.2009.08.012 [doi]
PST - ppublish
SO  - Immunol Lett. 2009 Dec 2;127(1):48-54. doi: 10.1016/j.imlet.2009.08.012. Epub 
      2009 Sep 4.