Abstract
Following allergen exposure, sensitized Brown Norway rats develop airway hyperresponsiveness (AHR) and eosinophilic inflammation together with an increase in activated T cells (CD25+) in the airways. We tested the hypothesis that CD4+ T cells are involved directly in the acquisition of AHR. Spleen T cells from animals that were injected intraperitoneally on three consecutive days with ovalbumin/Al(OH)3, showed a dose-dependent proliferative response in vitro to ovalbumin, but not to bovine serum albumin, as measured by [3H]thymidine uptake. For total T-cell transfer, spleen cells obtained from donor rats 4 days after sensitization were depleted of adherent cells by a nylon wool column separation. CD4+ and CD8+ T cells were purified by immunomagnetic beads cell separation. Recipient naive rats were injected intravenously with 50 x 106 total T cells, 20 x 106 and 5 x 106 CD4+ cells, and 5 x 106 CD8+ cells, and were exposed to ovalbumin aerosol 24 hr afterwards. After a further 24 hr. airway responsiveness to acetylcholine (ACh) was measured and provocative concentration (PC) values (PC100, PC200 and PC300) (the ACh concentration needed to achieve 100, 200 and 300% increase in lung resistance above baseline) were calculated. Airway responsiveness was significantly increased in recipients of sensitized total T cells compared with recipients of cells from saline-injected donor rats (P < 0.05). There were significantly increased eosinophil major basic protein (MBP)+ cell counts/mm2 in airway submucosal tissue in the hyperreactive rats and a significant correlation was found between the number of MBP+ cells and PC100 (r = 0.75; P < 0.03) in recipients of sensitized total T cells. Purified CD4+ T cells from sensitized donors induced AHR in naive recipients (P < 0.05), while sensitized CD8+ and naive CD4+ cells failed to do so. Our data indicate that T cells may induce AHR through an eosinophilic airway inflammation and that CD4+ T cells may have a direct effect in this process in Brown-Norway rats.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 176-185 |
| Number of pages | 10 |
| Journal | Immunology |
| Volume | 91 |
| Issue number | 2 |
| State | Published - 1997 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
Cite this
Adoptive transfer of allergen-specific CD4+ T cells induces airway inflammation and hyperresponsiveness in Brown-Norway rats. / Haczku, Angela Franciska; Macary, P.; Huang, T. J.; Tsukagoshi, H.; Barnes, P. J.; Kay, A. B.; Kemeny, D. M.; Chung, K. F.; Moqbel, R.
In: Immunology, Vol. 91, No. 2, 1997, p. 176-185.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Adoptive transfer of allergen-specific CD4+ T cells induces airway inflammation and hyperresponsiveness in Brown-Norway rats
AU - Haczku, Angela Franciska
AU - Macary, P.
AU - Huang, T. J.
AU - Tsukagoshi, H.
AU - Barnes, P. J.
AU - Kay, A. B.
AU - Kemeny, D. M.
AU - Chung, K. F.
AU - Moqbel, R.
PY - 1997
Y1 - 1997
N2 - Following allergen exposure, sensitized Brown Norway rats develop airway hyperresponsiveness (AHR) and eosinophilic inflammation together with an increase in activated T cells (CD25+) in the airways. We tested the hypothesis that CD4+ T cells are involved directly in the acquisition of AHR. Spleen T cells from animals that were injected intraperitoneally on three consecutive days with ovalbumin/Al(OH)3, showed a dose-dependent proliferative response in vitro to ovalbumin, but not to bovine serum albumin, as measured by [3H]thymidine uptake. For total T-cell transfer, spleen cells obtained from donor rats 4 days after sensitization were depleted of adherent cells by a nylon wool column separation. CD4+ and CD8+ T cells were purified by immunomagnetic beads cell separation. Recipient naive rats were injected intravenously with 50 x 106 total T cells, 20 x 106 and 5 x 106 CD4+ cells, and 5 x 106 CD8+ cells, and were exposed to ovalbumin aerosol 24 hr afterwards. After a further 24 hr. airway responsiveness to acetylcholine (ACh) was measured and provocative concentration (PC) values (PC100, PC200 and PC300) (the ACh concentration needed to achieve 100, 200 and 300% increase in lung resistance above baseline) were calculated. Airway responsiveness was significantly increased in recipients of sensitized total T cells compared with recipients of cells from saline-injected donor rats (P < 0.05). There were significantly increased eosinophil major basic protein (MBP)+ cell counts/mm2 in airway submucosal tissue in the hyperreactive rats and a significant correlation was found between the number of MBP+ cells and PC100 (r = 0.75; P < 0.03) in recipients of sensitized total T cells. Purified CD4+ T cells from sensitized donors induced AHR in naive recipients (P < 0.05), while sensitized CD8+ and naive CD4+ cells failed to do so. Our data indicate that T cells may induce AHR through an eosinophilic airway inflammation and that CD4+ T cells may have a direct effect in this process in Brown-Norway rats.
AB - Following allergen exposure, sensitized Brown Norway rats develop airway hyperresponsiveness (AHR) and eosinophilic inflammation together with an increase in activated T cells (CD25+) in the airways. We tested the hypothesis that CD4+ T cells are involved directly in the acquisition of AHR. Spleen T cells from animals that were injected intraperitoneally on three consecutive days with ovalbumin/Al(OH)3, showed a dose-dependent proliferative response in vitro to ovalbumin, but not to bovine serum albumin, as measured by [3H]thymidine uptake. For total T-cell transfer, spleen cells obtained from donor rats 4 days after sensitization were depleted of adherent cells by a nylon wool column separation. CD4+ and CD8+ T cells were purified by immunomagnetic beads cell separation. Recipient naive rats were injected intravenously with 50 x 106 total T cells, 20 x 106 and 5 x 106 CD4+ cells, and 5 x 106 CD8+ cells, and were exposed to ovalbumin aerosol 24 hr afterwards. After a further 24 hr. airway responsiveness to acetylcholine (ACh) was measured and provocative concentration (PC) values (PC100, PC200 and PC300) (the ACh concentration needed to achieve 100, 200 and 300% increase in lung resistance above baseline) were calculated. Airway responsiveness was significantly increased in recipients of sensitized total T cells compared with recipients of cells from saline-injected donor rats (P < 0.05). There were significantly increased eosinophil major basic protein (MBP)+ cell counts/mm2 in airway submucosal tissue in the hyperreactive rats and a significant correlation was found between the number of MBP+ cells and PC100 (r = 0.75; P < 0.03) in recipients of sensitized total T cells. Purified CD4+ T cells from sensitized donors induced AHR in naive recipients (P < 0.05), while sensitized CD8+ and naive CD4+ cells failed to do so. Our data indicate that T cells may induce AHR through an eosinophilic airway inflammation and that CD4+ T cells may have a direct effect in this process in Brown-Norway rats.
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UR - http://www.scopus.com/inward/citedby.url?scp=0030960802&partnerID=8YFLogxK
M3 - Article
C2 - 9227314
AN - SCOPUS:0030960802
VL - 91
SP - 176
EP - 185
JO - Immunology
JF - Immunology
SN - 0019-2805
IS - 2
ER -