Abstract
Background. Experiments were designed to determine expression of type II (iNOS) and type III (ecNOS) nitric oxide synthase in lung parenchyma and systemic endothelial cells with rejection and/or infection of single lung allografts. Methods. After single lung allotransplantation, dogs were maintained on standard triple immunosuppressive therapy for 5 days and then placed into one of three groups. Group I (n=4) was maintained on immunosuppressants, group II (n=7) immunosuppression was withdrawn to allow acute rejection of the allograft, and group III (n=6) infection was induced by bronchoscopic inoculation of Escherichia coli. Results. At postoperative days 7-9, no histological evidence of rejection or infection was observed in transplanted lungs of group I. In lungs of group II, rejection ranged from mild to severe; in lungs of group III, infection was severe. Some animals had both rejection and infection (n=8) and were studied separately. Plasma levels of nitric oxide increased comparably with rejection and/or infection compared to preoperative values. Expression of mRNA for ecNOS decreased significantly in lung parenchyma but not in aortic endothelial cells from dogs of groups II and III. However, expression of mRNA for iNOS increased with both rejection and/or infection in both lung parenchyma and aortic endothelial cells. Conclusions. iNOS is induced locally within the graft and systemically in aortic endothelial cells with rejection and/or infection of lung allografts. Plasma levels of nitric oxide are elevated with both rejection and infection and may not be useful in the differential diagnosis of these processes after lung transplantation.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 567-572 |
| Number of pages | 6 |
| Journal | Transplantation |
| Volume | 66 |
| Issue number | 5 |
| DOIs | |
| State | Published - Sep 15 1998 |
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ASJC Scopus subject areas
- Transplantation
- Immunology
Cite this
Alterations in mRNA for inducible and endothelial nitric oxide synthase and plasma nitric oxide with rejection and/or infection of allotransplanted lungs. / Wang, Xiaofang; Lewis, Debra A.; Kim, Hae Kyoon; Tazelaar, Henry D.; Park, Young Sik; McGregor, Christopher G A; Miller, Virginia M.
In: Transplantation, Vol. 66, No. 5, 15.09.1998, p. 567-572.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Alterations in mRNA for inducible and endothelial nitric oxide synthase and plasma nitric oxide with rejection and/or infection of allotransplanted lungs
AU - Wang, Xiaofang
AU - Lewis, Debra A.
AU - Kim, Hae Kyoon
AU - Tazelaar, Henry D.
AU - Park, Young Sik
AU - McGregor, Christopher G A
AU - Miller, Virginia M
PY - 1998/9/15
Y1 - 1998/9/15
N2 - Background. Experiments were designed to determine expression of type II (iNOS) and type III (ecNOS) nitric oxide synthase in lung parenchyma and systemic endothelial cells with rejection and/or infection of single lung allografts. Methods. After single lung allotransplantation, dogs were maintained on standard triple immunosuppressive therapy for 5 days and then placed into one of three groups. Group I (n=4) was maintained on immunosuppressants, group II (n=7) immunosuppression was withdrawn to allow acute rejection of the allograft, and group III (n=6) infection was induced by bronchoscopic inoculation of Escherichia coli. Results. At postoperative days 7-9, no histological evidence of rejection or infection was observed in transplanted lungs of group I. In lungs of group II, rejection ranged from mild to severe; in lungs of group III, infection was severe. Some animals had both rejection and infection (n=8) and were studied separately. Plasma levels of nitric oxide increased comparably with rejection and/or infection compared to preoperative values. Expression of mRNA for ecNOS decreased significantly in lung parenchyma but not in aortic endothelial cells from dogs of groups II and III. However, expression of mRNA for iNOS increased with both rejection and/or infection in both lung parenchyma and aortic endothelial cells. Conclusions. iNOS is induced locally within the graft and systemically in aortic endothelial cells with rejection and/or infection of lung allografts. Plasma levels of nitric oxide are elevated with both rejection and infection and may not be useful in the differential diagnosis of these processes after lung transplantation.
AB - Background. Experiments were designed to determine expression of type II (iNOS) and type III (ecNOS) nitric oxide synthase in lung parenchyma and systemic endothelial cells with rejection and/or infection of single lung allografts. Methods. After single lung allotransplantation, dogs were maintained on standard triple immunosuppressive therapy for 5 days and then placed into one of three groups. Group I (n=4) was maintained on immunosuppressants, group II (n=7) immunosuppression was withdrawn to allow acute rejection of the allograft, and group III (n=6) infection was induced by bronchoscopic inoculation of Escherichia coli. Results. At postoperative days 7-9, no histological evidence of rejection or infection was observed in transplanted lungs of group I. In lungs of group II, rejection ranged from mild to severe; in lungs of group III, infection was severe. Some animals had both rejection and infection (n=8) and were studied separately. Plasma levels of nitric oxide increased comparably with rejection and/or infection compared to preoperative values. Expression of mRNA for ecNOS decreased significantly in lung parenchyma but not in aortic endothelial cells from dogs of groups II and III. However, expression of mRNA for iNOS increased with both rejection and/or infection in both lung parenchyma and aortic endothelial cells. Conclusions. iNOS is induced locally within the graft and systemically in aortic endothelial cells with rejection and/or infection of lung allografts. Plasma levels of nitric oxide are elevated with both rejection and infection and may not be useful in the differential diagnosis of these processes after lung transplantation.
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U2 - 10.1097/00007890-199809150-00003
DO - 10.1097/00007890-199809150-00003
M3 - Article
C2 - 9753333
AN - SCOPUS:0032531068
VL - 66
SP - 567
EP - 572
JO - Transplantation
JF - Transplantation
SN - 0041-1337
IS - 5
ER -