Regulation of human beta-defensin-2 by Mycobacterium bovis bacillus Calmette-Guérin (BCG): involvement of PKC, JNK, and PI3K in human lung epithelial cell line (A549).

Human beta-defensin (HBD)-2 is an inducible antimicrobial peptide that plays an important role in innate immunity. Induction of this peptide by mycobacteria in epithelial cells has been reported. However, the mechanism(s) by which Mycobacterium bovis bacillus Calmette-Guérin (BCG) triggers gene transcription of HBD-2 remains poorly understood.

Expression and secretion of cathelicidin LL-37 in human epithelial cells after infection by Mycobacterium bovis Bacillus Calmette-Guérin.

The antimicrobial cathelicidin LL-37 is considered to play an important role in the innate immune response to tuberculosis infection. However, little is known about the induction and secretion of this antimicrobial peptide in A549 epithelial cells after infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG), the world's most widely used tuberculosis vaccine. In this study, we investigated the effect of M.

Mycobacterium bovis Bacillus Calmette-Guérin (BCG) stimulates IL-10 production via the PI3K/Akt and p38 MAPK pathways in human lung epithelial cells.

Infection of human cells with mycobacteria has been shown to result in the production of anti-inflammatory cytokines. However, the signaling pathways that regulate the Mycobacterium bovis BCG-induced interleukin (IL)-10 production are currently unknown. In the present study, we investigated the involvement of phosphatidylinoditol 3-kinase (PI3K)/Akt and the p38 MAPK signaling pathways in the secretion of IL-10 in human lung epithelial cells (A549) after infection with M.

Sphingosine kinase, phosphatidylinositol 3-kinase, Akt, NF-kappaB, and p300 are required for CCL5 production in Mycobacterium bovis Bacillus Calmette-Guérin (BCG)-infected epithelial cells.

CCL5 is a key in limiting mycobacterial infection. Although NF-kappaB has been implicated, signaling cascades involved in CCL5 production by epithelial cells following infection with Mycobacterium bovis BCG are still not defined. Here we show that using pharmacological inhibition of sphingosine kinase (SPK), striking inhibition of M.

Mycobacterium bovis bacillus Calmette-Guerin induces CCL5 secretion via the Toll-like receptor 2-NF-kappaB and -Jun N-terminal kinase signaling pathways.

In response to Mycobacterium bovis bacillus Calmette-Guérin (BCG), CC chemokines are secreted from host cells to attract components of the innate and adaptive immune systems to the site of infection. Toll-like receptor 2 (TLR2) has been shown to recognize M. bovis BCG and to initiate signaling pathways that result in enhanced secretion of CC chemokines.

Mycobacterium bovis-mediated induction of human beta-defensin-2 in epithelial cells is controlled by intracellular calcium and p38MAPK.

Induction of human beta defensin-2 (HBD-2) by mycobacteria has been reported. However, the molecular mechanism(s) by which mycobacteria up-regulates HBD-2 gene expression in epithelial cells remains poorly understood. In this work, we provide evidence that the induction of HBD-2 mRNA in response to Mycobacterium bovis bacillus Calmette-Guerin (BCG) was inhibited in a dose-dependent manner by pretreatment with a cell-permeable BAPTA-AM, which chelates intracellular calcium.

Mycobacterium bovis Bacillus Calmette-Guérin (BCG) stimulates human beta-defensin-2 gene transcription in human epithelial cells.

Antimicrobial peptides produced by epithelial cells represent essential elements of innate immunity. Human beta-defensin-2 (hbetaD-2) is a major inducible antimicrobial peptide which plays an important role in host defense. The goal of this study was to determine the effect of Mycobacterium bovis bacillus Calmette-Guérin (BCG) on hbetaD-2 gene expression in epithelial cells, and to characterize further the signaling pathways involved in hbetaD-2 induction in response to M.

Mycobacterium bovis BCG induces CXC chemokine ligand 8 secretion via the MEK-dependent signal pathway in human epithelial cells.

Current knowledge of the cellular signaling by Mycobacterium bovis bacillus Calmette-Guerin (BCG) in epithelial cells is still limited. In this study, we provide evidence that the signaling events induced by M. bovis BCG in these cells included phosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK).

Role of type I interferon in the bacillus Calmette-Guérin-induced expression of CXCL10 from human monocytes.

Background: The proinflammatory chemokine CXCL10, in addition to its chemotactic properties, is also involved in the stimulation of natural killer and T-cell migration in Mycobacterium tuberculosis infection. In this study, our experiments were designed to determine the role of interferon (IFN)-alphabeta in the production of CXCL10 by human monocytes infected with Mycobacterium bovis bacillus Calmette-Guerin (BCG).

Methods: The concentrations of CXCL10 in culture supernatants of monocytes infected with M.