Abstract
Bloodstream infection (BSI) is the major cause of mortality in acute lymphocytic leukemia (ALL). Causative pathogens in BSI originate from the gut microbiota due to an increase in intestinal permeability, a process known as bacterial translocation (BT). The gut microbiota in physiological conditions is controlled by a large number of immune cells as part of the gut-associated lymphoid tissue (GALT).The aim of the current study was to investigate the mechanism of bacterial translocation in leukemia by identifying and characterizing alterations in the GALT in leukemic mouse model. Our studies revealed a severe impairment of the GALT characterized by a loss of lymphatic cells in ALL, which eventually led to BSI. We identified differentially expressed genes in the intraepithelium and the lamina propria, which may contribute to BT and to the impairment of lymphocyte migration.
Highlights
Hematological malignancies are the most common cancers during childhood, and leukemia comprises of 30% of all pediatric cancers
Bloodstream infection (BSI) is a severe and life-threatening complication commonly occurring in leukemia
We investigated the structure of the gut-associated lymphoid tissue (GALT), the mechanisms of bacterial translocation (BT) and their contributions to the development of BSI in leukemia
Summary
Hematological malignancies are the most common cancers during childhood, and leukemia comprises of 30% of all pediatric cancers. Acute lymphocytic leukemia (ALL) is the most frequently occurring pediatric leukemia, comprising 80% of childhood leukemias, with the incidence highest between 2–5 years of age [1]. The gut-associated lymphoid tissue (GALT) is the largest immunological organ in the body [7]. It is primarily located in the lamina propria (LP) [8] and includes scattered lymphoid cells in the mucosal epithelium (intraepithelial lymphocytes, IEL) [9]. The highest number of immune cells in the body can be found in the GALT in order to ensure the integrity of the intestinal barrier against microbial translocation. The GALT helps to maintain homeostasis with the gut microbiota to preserve its regulatory functions [6]
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