PMID- 8558061
OWN - NLM
STAT- MEDLINE
DCOM- 19960226
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 59
IP  - 1
DP  - 1996 Jan
TI  - Activation and regulation of chemokines in allergic airway inflammation.
PG  - 13-7
AB  - Allergic airway inflammation is characterized by peribronchial eosinophil 
      accumulation with the submucosa surrounding the airway. The initial induction of 
      immunoglobulin E (IgE)-mediated mast cell degranulation, up-regulation of 
      adhesion molecules, and the production of inflammatory and chemotactic cytokines, 
      leading to the infiltration of specific leukocyte subsets, is orchestrated in a 
      sequential manner. The activation and degranulation of local mast cell 
      populations is an immediate airway response mediated both by antigen-specific, 
      surface bound IgE and by cytokine-induced activational pathways. Subsequently the 
      infiltration and activation of effector leukocytes (neutrophils and eosinophils) 
      mediated by the persistent activation of allergen-specific T cells leads to 
      pathological manifestations within the lung and airway. The development of 
      appropriate animal models to dissect the critical mechanisms involved in 
      antigen-induced airway pathology is crucial for the development of efficacious 
      therapies. We have utilized a model of allergic airway inflammation induced by 
      intratracheal challenge with parasite (Schistosoma mansoni) egg antigen in 
      presensitized mice. This model has proven useful in the assessment of eosinophil 
      recruitment and has identified key cytokines involved in leukocyte elicitation. 
      These cytokines include interleukin-4 and elicitation. These cytokines include 
      interleukin-4 and tumor necrosis factor, which appear to act as early response 
      mediators, as well as C-C chemokines, macrophage inflammatory protein-1a, and 
      RANTES, which act directly on eosinophil recruitment. In addition, we have found 
      that both C-X-C and C-C chemokines are expressed in pulmonary-derived mast cells, 
      suggesting an important contribution to leukocyte responses in the allergic 
      airway.
FAU - Lukacs, N W
AU  - Lukacs NW
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor, USA.
FAU - Strieter, R M
AU  - Strieter RM
FAU - Chensue, S W
AU  - Chensue SW
FAU - Kunkel, S L
AU  - Kunkel SL
LA  - eng
GR  - HL02401/HL/NHLBI NIH HHS/United States
GR  - HL31693/HL/NHLBI NIH HHS/United States
GR  - HL35276/HL/NHLBI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Chemokines)
SB  - IM
MH  - Animals
MH  - Asthma/*metabolism/*pathology
MH  - Chemokines/metabolism/*physiology
MH  - Humans
MH  - Hypersensitivity/*metabolism/*pathology
RF  - 34
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - 10.1002/jlb.59.1.13 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1996 Jan;59(1):13-7. doi: 10.1002/jlb.59.1.13.