Septicemia in acute leukemia

Cesario, Thomas C.; Slater, Lewis M.; Armentrout, Steven A.; Thrupp, Lauri; Tilles, Jeremiah G.

doi:10.1002/mpo.2950050127

Cited by 11 publications

(3 citation statements)

References 14 publications

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“…Tancrede and Andremont (66), however, were able to predict the bacterial serotype or biotype most likely to cause septicemia in leukemia patients by identifying in fecal surveillance cultures the numerically predominant serotype or biotype among the indigenous bacterial species. The GI tract has been demonstrated to be a reservoir for bacteria causing life-threatening infections in cancer patients undergoing chemotherapy (15,20), bone marrow recipients (40), and those with AIDS (69,70).…”

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T lymphocytes in host defense against bacterial translocation from the gastrointestinal tract

1994

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Flow cytofluorometric analyses of lymphocytes harvested from the mesenteric lymph node (MLN), mucosal epithelium, and lamina propria of C57BL/6 mice demonstrate that expression of a/Il or y/6 T-cell receptors (TCR) and CD4 or CD8 molecules by T lymphocytes in the intestinal immune system varies depending upon their anatomic location. The MLN contained equivalent numbers of CD4+ and CD8+ T cells, the vast majority of which were a/I TCR positive (a/Il TCR+). The lamina propria T cells were predominantly CD4+ and a/8l TCR+, while the intestinal intraepithelial lymphocytes consisted of equivalent numbers of a/Il and y/ T cells, the majority of which were CD8+. There were no significant changes in these T-cell phenotypic profiles when the mice were antibiotic decontaminated or monoassociated with Escherichia coli. Mice were depleted of CD4+ T cells and/or CD8+ T cells in vivo by intraperitoneal injections of monoclonal antibody GK 1.5 (rat anti-mouse CD4) and/or monoclonal antibody 2.43 (rat anti-mouse CD8). T-cell depletion was confirmed in the MLN, lamina propria, and the intestinal epithelium by flow cytometry. E. coli C25 translocation from the gastrointestinal (GI) tract to the MLN was significantly increased in mice depleted of CD4+ T cells, CD8+ T cells, or both. T-cell-deficient athymic beige/nude mice also exhibited greater levels of E. coli C25 translocation to the MLN than beige/het euthymic littermates. SalmoneUa typhimurium translocation also was increased following CD4+ and CD8+ T-cell depletion in mice monoassociated with S. typhimurium. Depletion of CD4+ and/or CD8+ T cells also increased the translocation to the MLN of certain indigenous GI flora bacteria. These results confirm that T-cell-mediated immunity is involved in the host defense against bacterial translocation from the GI tract.

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T lymphocytes in host defense against bacterial translocation from the gastrointestinal tract

1994

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“…immunocompromised patients such as cancer patients undergoing chemotherapy (2,4,12), bone marrow recipients (9), and patients with AIDS (13,14). Under certain conditions, indigenous bacteria readily pass through the epithelial cells lining the intestines and are carried in the lymph to the mesenteric lymph node (MLN) complex and possibly to post-MLN complex sites.…”

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Bacterial translocation from the gastrointestinal tract to various segments of the mesenteric lymph node complex

1994

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Escherichia coli and Proteus mirabilis translocate to different segments of the mesenteric lymph node (MLN) complex at levels reflecting their population levels in the regions of the gastrointestinal tract that provide lymph to these various MLN segments. Salmonella typhimurium, however, translocates to all segments of the MLN complex equally regardless of regional intestinal population levels.The gastrointestinal (GI) tract serves as a reservoir for bacteria that can cause life-threatening infections, especially in * Corresponding author. Mailing address:

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“…Our research is focused on the contribution of T cells in the defense of the host against infection by the indigenous bacteria normally inhabiting the gut. The massive populations of indigenous bacteria colonizing the GI tract are the predominant cause of opportunistic infections in debilitated patients (10,14,18,29,52,54,55). Determining the role of T cells in the host defense against opportunistic bacterial infections by members of the indigenous GI microflora is of particular importance in this era of AIDS and selective immunosuppressive therapies.…”

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Adoptive transfer of T lymphocytes to T-cell-depleted mice inhibits Escherichia coli translocation from the gastrointestinal tract

et al. 1995

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Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal (GI) tract to extraintestinal sites, such as the mesenteric lymph node (MLN), spleen, liver, kidneys, and blood. Previously, we reported that depletion of CD4 ؉ and/or CD8 ؉ T cells promotes bacterial translocation from the GI tract to the MLN. In the present study, CD4 ؉ and/or CD8 ؉ T cells, harvested from donor mice, were adoptively transferred to mice previously depleted of T cells by thymectomy plus intraperitoneal injection of rat antimouse T-cell monoclonal antibodies. The adoptively transferred CD4 ؉ and/or CD8 ؉ T cells inhibited the translocation of Escherichia coli from the GI tract. Migration of the adoptively transferred T cells to the spleens and MLNs of the recipient mice was determined by utilizing Thy 1.1 ؉ donor cells adoptively transferred into mice whose cells express the Thy 1.2 marker. These results provide further evidence of the importance of T cells in the host immune defense against bacterial translocation from the GI tract. The gastrointestinal (GI) tract serves as a reservoir for bacteria causing life-threatening infections in debilitated patients, especially in immunocompromised patients such as those with cancer undergoing chemotherapy (10, 14, 52), bone marrow recipients (28), and AIDS patients (54, 55). The passage of indigenous bacteria from the GI lumen through the mucosal epithelium to extraintestinal sites such as the mesenteric lymph node (MLN) complex, spleen, liver, kidneys, and blood is defined as bacterial translocation (8). Bacterial translocation from the GI tract is promoted when (i) the host immune defenses are compromised, (ii) the mucosal epithelial barrier is damaged, or (iii) there is intestinal bacterial overgrowth (4-9, 19, 33, 34, 37, 41, 42, 51). These mechanisms can act synergistically to promote the systemic spread of translocating bacteria to cause septicemia. For example, if immunosuppression is coupled with intestinal bacterial overgrowth, bacteria translocate not only to the MLN but also to post-MLN sites such as the spleen, liver, kidneys, and blood to cause lethal sepsis (9). Our prior studies suggest a role for T-cell-mediated immunity in the host defense against bacterial translocation from the GI tract. Translocation of indigenous GI bacteria to the MLN, liver, spleen, and kidneys occurs spontaneously in athymic (nu/ nu) nude mice but not in heterozygous (nu/ϩ) mice or in thymus-grafted nude (nu/nu) mice (41). Neonatal thymectomy of euthymic (ϩ/ϩ) mice also promotes the translocation of bacteria to extraintestinal sites (42). Recently, we demonstrated that depletion of CD4 ϩ and/or CD8 ϩ T cells in vivo with specific monoclonal antibodies (MAbs) promotes the translocation of bacteria from the GI tract to the MLN (24). To confirm the importance of T cells in the immune defense against bacterial translocation, CD4 ϩ and/or CD8 ϩ T cells, harvested from donor mice, were adoptively transferred to mice previously depleted of T cells by thymectomy plus intraperit...

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Septicemia in acute leukemia

Cited by 11 publications

References 14 publications

T lymphocytes in host defense against bacterial translocation from the gastrointestinal tract

T lymphocytes in host defense against bacterial translocation from the gastrointestinal tract

Bacterial translocation from the gastrointestinal tract to various segments of the mesenteric lymph node complex

Adoptive transfer of T lymphocytes to T-cell-depleted mice inhibits Escherichia coli translocation from the gastrointestinal tract

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