PMID- 10988141
OWN - NLM
STAT- MEDLINE
DCOM- 20001012
LR  - 20081121
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 162
IP  - 3 Pt 1
DP  - 2000 Sep
TI  - CD8 depletion-induced late airway response is characterized by eosinophilia, 
      increased eotaxin, and decreased IFN-gamma expression in rats.
PG  - 1123-31
AB  - There is an emerging body of knowledge defining the role of CD8(+) cells in the 
      pathogenesis of allergic asthma. We have previously demonstrated in sensitized 
      Sprague-Dawley (SD) rats that depletion of CD8(+) cells caused an increase in the 
      late airway response (LAR) and cellular infiltration after antigen challenge. To 
      better delineate the mechanism of CD8(+) cell involvement in the development of 
      the LAR and airway inflammation, we investigated the pattern of chemokine and 
      cytokine production after antigen challenge. SD rats were sensitized to ovalbumin 
      (OA) and subsequently treated with anti-CD8 (OX-8) monoclonal antibody (mAb) for 
      the depletion of CD8(+) cells or with control mouse anti-rat IgG(1) mAb as a 
      control procedure. After OA challenge, CD8- depleted SD rats developed an 
      increased LAR when compared with control rats (area under the curve: 16.65 +/- 
      6.6 in CD8- depleted rats versus 5.39 +/- 2.0 in control animals; p < 0.05). 
      Compared with the control animals, the increase in the LAR was accompanied by a 
      significantly increased eosinophilic infiltration of the airways and was 
      associated with increased eotaxin expression (both messenger RNA [mRNA] and 
      protein) in the CD8-depleted group. There were no differences between the groups 
      in RANTES or monocyte chemoattractant protein-1 (MCP-1) expression. In addition, 
      we found a significantly lower interferon gamma (IFN-gamma) mRNA expression in 
      the CD8-depleted rats, without any effects on interleukin (IL)-4 and IL-5 mRNA 
      expression when measured either by semiquantitative reverse 
      transcriptase/polymerase chain reaction (RT-PCR) or by in situ hybridization for 
      the number of cells expressing these cytokines. Taken together, these results 
      suggest that CD8(+) cells from sensitized SD rats exhibit the functional capacity 
      to suppress the LAR, possibly through downregulation of eotaxin expression and 
      increased expression of IFN-gamma mRNA.
FAU - Allakhverdi, Z
AU  - Allakhverdi Z
AD  - CHUM Research Center, Notre-Dame Hospital, University of Montreal, and 
      Meakins-Christie Laboratories and Department of Medicine and Pathology, McGill 
      University, Montreal, Quebec, Canada.
FAU - Lamkhioued, B
AU  - Lamkhioued B
FAU - Olivenstein, R
AU  - Olivenstein R
FAU - Hamid, Q
AU  - Hamid Q
FAU - Renzi, P M
AU  - Renzi PM
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Ccl11 protein, mouse)
RN  - 0 (Ccl11 protein, rat)
RN  - 0 (Chemokine CCL11)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CC)
RN  - 0 (Cytokines)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Airway Resistance/immunology
MH  - Animals
MH  - Asthma/*immunology
MH  - CD8-Positive T-Lymphocytes/*immunology
MH  - Chemokine CCL11
MH  - Chemokines/blood
MH  - *Chemokines, CC
MH  - Cytokines/*blood
MH  - Eosinophilia/*immunology
MH  - Interferon-gamma/*blood
MH  - Male
MH  - Ovalbumin/immunology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Respiratory Hypersensitivity/*immunology
EDAT- 2000/09/16 11:00
MHDA- 2000/10/14 11:01
CRDT- 2000/09/16 11:00
PHST- 2000/09/16 11:00 [pubmed]
PHST- 2000/10/14 11:01 [medline]
PHST- 2000/09/16 11:00 [entrez]
AID - 10.1164/ajrccm.162.3.9910001 [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 2000 Sep;162(3 Pt 1):1123-31. doi: 
      10.1164/ajrccm.162.3.9910001.