|
|
 Previous Article | Table of Contents | Next Article 
Increased Mucosal B-Lymphocyte Apoptosis During Polymicrobial Sepsis
Is a Fas Ligand But Not an Endotoxin-Mediated Process
Alfred Ayala,
Ying Xin Xu,
Carol A. Ayala,
Diane E. Sonefeld,
Shannon M. Karr,
Tracy A. Evans, and
Irshad H. Chaudry
From the Center for Surgical Research and Department of Surgery,
Brown University School of Medicine and Rhode Island Hospital,
Providence, RI.
Sepsis is reported to induce an increase in the rate of apoptosis
(Ao), in immature lymphoid cells residing in hematopoietic tissues such as the thymus and bone marrow. Alternatively, secondary lymphoid tissue, such as the spleen exhibit little innate
(unstimulated) Ao. However, it is unknown whether or not
polymicrobial sepsis has any effects on the frequency of Ao
in mucosal lymphoid tissue and what, if any, are the functional
consequences of such a change. To assess this, Peyer's patch cells
were harvested from C3H/HeN (endotoxin-sensitive) mice killed 12 or 24 hours after the onset of polymicrobial sepsis (cecal ligation and
puncture [CLP]). The results indicate that the percentage of cells
that were Ao+ as determined by flow cytometry were
markedly increased at 24 hours, but not at 12 hours post-CLP. This
correlates well with evidence of increased DNA fragmentation as well as
histological changes observed both at a light and transmission electron
microscopic level of the Peyer's patch Ao. Phenotypically,
these changes were restricted to the B220+ (B-cell)
population that also exhibited a marked increase of Fas/Apo-1 antigen
expression. The functional consequence of this increased apoptosis
appears to be associated with the endogenous stimulation (activation)
of IgA production by mucosal B lymphocytes and increased nuclear c-Rel
expression. Furthermore, we found that Peyer's patch lymphocytes
isolated from C3H/HeJ-Faslgld
(endotoxin-tolerant/Fas ligand- [FasL] deficient) as opposed to
C3H/HeJ (endotoxin-tolerant) inbred mice did not exhibit increased Ao after CLP. These findings indicate that increased B-cell
Ao appears to be a FasL-Fas antigen-mediated process, but
is not due to endotoxin sensitivity. In conclusion, we speculate that the increased Fas-associated apoptosis detected in mucosal B cells (as
opposed to splenic or bone marrow B cells) may be due to increased luminal antigens other than endotoxin, released due to gut barrier integrity breakdown during sepsis.
Blood, Vol. 91 No. 4 (February 15), 1998:
pp. 1362-1372
© 1998 by The American Society of Hematology.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
M. Miksa, R. Wu, W. Dong, H. Komura, D. Amin, Y. Ji, Z. Wang, H. Wang, T. S. Ravikumar, K. J. Tracey, et al.
Immature Dendritic Cell-Derived Exosomes Rescue Septic Animals Via Milk Fat Globule Epidermal Growth Factor VIII
J. Immunol.,
November 1, 2009;
183(9):
5983 - 5990.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A Ogawa, T Tagawa, H Nishimura, T Yajima, T Abe, T Arai, M Taniguchi, K Takeda, S Akira, Y Nimura, et al.
Toll-like receptors 2 and 4 are differentially involved in Fas dependent apoptosis in Peyer's patch and the liver at an early stage after bile duct ligation in mice
Gut,
January 1, 2006;
55(1):
105 - 113.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. D. Bowman, J. L. Sondeen, B. Zhao, V. G. Coppes, J. J. Nelson, M. A. Dubick, and G. M. Vaughan
A temporal study of gene expression in rat lung following fixed-volume hemorrhage
Physiol Genomics,
November 17, 2005;
23(3):
275 - 286.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. E. Wesche, J. L. Lomas-Neira, M. Perl, C.-S. Chung, and A. Ayala
Leukocyte apoptosis and its significance in sepsis and shock
J. Leukoc. Biol.,
August 1, 2005;
78(2):
325 - 337.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. A. Efron, A. Martins, D. Minnich, K. Tinsley, R. Ungaro, F. R. Bahjat, R. Hotchkiss, M. Clare-Salzler, and L. L. Moldawer
Characterization of the Systemic Loss of Dendritic Cells in Murine Lymph Nodes During Polymicrobial Sepsis
J. Immunol.,
September 1, 2004;
173(5):
3035 - 3043.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. G. R. WEAVER, M. S. ROUSE, J. M. STECKELBERG, and A. D. BADLEY
Improved survival in experimental sepsis with an orally administered inhibitor of apoptosis
FASEB J,
August 1, 2004;
18(11):
1185 - 1191.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L Ohman, L Franzen, U Rudolph, L Birnbaumer, and E H. Hornquist
Regression of Peyer's patches in G{alpha}i2 deficient mice prior to colitis is associated with reduced expression of Bcl-2 and increased apoptosis
Gut,
September 1, 2002;
51(3):
392 - 397.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
C.-S. Chung, W. Wang, I. H. Chaudry, and A. Ayala
Increased apoptosis in lamina propria B cells during polymicrobial sepsis is FasL but not endotoxin mediated
Am J Physiol Gastrointest Liver Physiol,
May 1, 2001;
280(5):
G812 - G818.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. C. Reddy, G. H. Chen, M. W. Newstead, T. Moore, X. Zeng, K. Tateda, and T. J. Standiford
Alveolar Macrophage Deactivation in Murine Septic Peritonitis: Role of Interleukin 10
Infect. Immun.,
March 1, 2001;
69(3):
1394 - 1401.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Fukuzuka, C. K. Edwards III, M. Clare-Salzler, E. M. Copeland III, L. L. Moldawer, and D. W. Mozingo
Glucocorticoid-induced, caspase-dependent organ apoptosis early after burn injury
Am J Physiol Regulatory Integrative Comp Physiol,
April 1, 2000;
278(4):
R1005 - R1018.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. S. Hotchkiss, K. W. Tinsley, J.-J. Hui, K. C. Chang, P. E. Swanson, A. M. Drewry, T. G. Buchman, and I. E. Karl
p53-Dependent and -Independent Pathways of Apoptotic Cell Death in Sepsis
J. Immunol.,
April 1, 2000;
164(7):
3675 - 3680.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C.-S. Chung, Y. X. Xu, W. Wang, I. H. Chaudry, and A. Ayala
Is Fas Ligand or Endotoxin Responsible for Mucosal Lymphocyte Apoptosis in Sepsis?
Arch Surg,
November 1, 1998;
133(11):
1213 - 1220.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
