Sensitized CD8+ T cells fail to control organism burden but accelerate the onset of lung injury during Pneumocystis carinii pneumonia

被引:29
作者
Gigliotti, Francis
Crow, Elliott L.
Bhagwat, Samir P.
Wright, Terry W.
机构
[1] Univ Rochester, Sch Med & Dent, Dept Pediat, Rochester, NY 14642 USA
[2] Univ Rochester, Sch Med & Dent, Dept Microbiol & Immunol, Rochester, NY 14642 USA
关键词
D O I
10.1128/IAI.00668-06
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
While CD8(+) cells have been shown to contribute to lung injury during Pneumocystis carinii pneumonia (PCP), there are conflicting reports concerning the ability of CD8(+) cells to kill P. carinii. To address these two issues, we studied the effect of the presence of CD8(+) cells in two mouse models of PCP. In the reconstituted SCID mouse model, depletion of CD8(+) cells in addition to CD4(+) cells after reconstitution did not result in increased numbers of P. carinii cysts compared to the numbers of cysts in mice with only CD4(+) cells depleted. This result was observed regardless of whether the mice were reconstituted with naive or P. carinii-sensitized lymphocytes. In contrast, reconstitution with sensitized lymphocytes resulted in more rapid onset of lung injury that was dependent on the presence of CD8(+) cells. The course of organism replication over a 6-week period was also examined in the CD4(+)-T-cell-depleted and CD4(+)- and CD8(+)-T-cell-depleted mouse model of PCP. Again, the organism burdens were identical at all times regardless of whether CD8(+) cells were present. Thus, in the absence of CD4(+) T cells, CD8(+) T cells are a key contributor to the inflammatory lung injury associated with PCP. However, we were unable to demonstrate an in vivo effect of these cells on the course of P. carinii infection.
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页码:6310 / 6316
页数:7
相关论文
共 18 条
[1]   MECHANICS OF RESPIRATION IN UNANESTHETIZED GUINEA PIGS [J].
AMDUR, MO ;
MEAD, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1958, 192 (02) :364-368
[2]   Role of CD8+ lymphocytes in host defense against Pneumocystis carinii in mice [J].
Beck, JM ;
Newbury, RL ;
Palmer, BE ;
Warnock, ML ;
Byrd, PK ;
Kaltreider, HB .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1996, 128 (05) :477-487
[3]   LUNG-MECHANICS IN ORALLY IMMUNIZED MICE AFTER AEROLIZED EXPOSURE TO INFLUENZA-VIRUS [J].
BERGMANN, KC ;
LACHMANN, B ;
NOACK, K .
RESPIRATION, 1984, 46 (02) :218-221
[4]   A 4TH-ORDER NONLINEAR ITERATIVE METHOD IN BANACH-SPACES [J].
CHEN, D ;
ARGYROS, IK .
APPLIED MATHEMATICS LETTERS, 1993, 6 (04) :97-98
[5]   Passive immunization of neonatal mice against Pneumocystis carinii f. sp muris enhances control of infection without stimulating inflammation [J].
Empey, KM ;
Hollifield, M ;
Schuer, K ;
Gigliotti, F ;
Garvy, BA .
INFECTION AND IMMUNITY, 2004, 72 (11) :6211-6220
[6]   Pneumocystis carinii host origin defines the antibody specificity and protective response induced by immunization [J].
Gigliotti, F ;
Harmsen, AG .
JOURNAL OF INFECTIOUS DISEASES, 1997, 176 (05) :1322-1326
[7]   Glycoprotein A is the immunodominant antigen of Pneumocystis carinii in mice following immunization [J].
Gigliotti, F ;
McCool, T .
PARASITOLOGY RESEARCH, 1996, 82 (01) :90-91
[8]   REQUIREMENT FOR CD4+ CELLS IN RESISTANCE TO PNEUMOCYSTIS-CARINII PNEUMONIA IN MICE [J].
HARMSEN, AG ;
STANKIEWICZ, M .
JOURNAL OF EXPERIMENTAL MEDICINE, 1990, 172 (03) :937-945
[9]  
Kolls JK, 1999, J IMMUNOL, V162, P2890
[10]   Molecular characterization of KEX1, a kexin-like protease in mouse Pneumocystis carinii [J].
Lee, LH ;
Gigliotti, F ;
Wright, TW ;
Simpson-Haidaris, PJ ;
Weinberg, GA ;
Haidaris, CG .
GENE, 2000, 242 (1-2) :141-150