Roles of Intracellular Calcium and NF-κB in the Bacillus Calmette- Guérin-Induced Secretion of Interleukin-8 from Human Monocytes

Méndez-Samperio, Patricia; Palma, Janet; Vázquez, Abraham

doi:10.1006/cimm.2001.1816

Cited by 18 publications

(10 citation statements)

References 35 publications

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“…30 Additionally, others 31,32 have shown that the Ca 2C / calmodulin pathway has also been involved in LPSinduced TNF-a production. In the present study, we observed that, M. bovis BCG induction of TNF-a was dependent on the intracellular calcium influx.…”

Section: Discussionmentioning

confidence: 99%

Activation of ERK1/2 and TNF-α production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection

Méndez-Samperio¹,

Trejo²,

Miranda³

2006

Journal of Infection

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Section: Discussionmentioning

confidence: 99%

Activation of ERK1/2 and TNF-α production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection

Méndez-Samperio¹,

Trejo²,

Miranda³

2006

Journal of Infection

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“…Both the Ca 2ϩ /CaM/CaMK and cAMP/PKA pathways have been implicated in signal transduction cascades leading to production of inflammatory cytokines such as TNF-␣ (10, 24) and IL-8 (25). However, as discussed above, the cAMP/PKA pathway has also been shown to inhibit TNF-␣ production (26) and IL-12 production (27).…”

Section: Tnf-␣ Production Is Dependent On the Cam/camk And Camp/ Pka mentioning

confidence: 99%

Increased Mitogen-Activated Protein Kinase Activity and TNF-α Production Associated with Mycobacterium smegmatis- but Not Mycobacterium avium-Infected Macrophages Requires Prolonged Stimulation of the Calmodulin/Calmodulin Kinase and Cyclic AMP/Protein Kinase A Pathways

Yadav

Roach

Schorey

2004

The Journal of Immunology

100

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Previous studies have shown the mitogen-activated protein kinases (MAPKs) to be activated in macrophages upon infection with Mycobacterium, and that expression of TNF-α and inducible NO synthase by infected macrophages was dependent on MAPK activation. Additional analysis demonstrated a diminished activation of p38 and extracellular signal-regulated kinase (ERK)1/2 in macrophages infected with pathogenic strains of Mycobacterium avium compared with infections with the fast-growing, nonpathogenic Mycobacterium smegmatis and Mycobacterium phlei. However, the upstream signals required for MAPK activation and the mechanisms behind the differential activation of the MAPKs have not been defined. In this study, using bone marrow-derived macrophages from BALB/c mice, we determined that ERK1/2 activation was dependent on the calcium/calmodulin/calmodulin kinase II pathway in both M. smegmatis- and M. avium-infected macrophages. However, in macrophages infected with M. smegmatis but not M. avium, we observed a marked increase in cAMP production that remained elevated for 8 h postinfection. This M. smegmatis-induced cAMP production was also dependent on the calmodulin/calmodulin kinase pathway. Furthermore, stimulation of the cAMP/protein kinase A pathway in M. smegmatis-infected cells was required for the prolonged ERK1/2 activation and the increased TNF-α production observed in these infected macrophages. Our studies are the first to demonstrate an important role for the calmodulin/calmodulin kinase and cAMP/protein kinase A pathways in macrophage signaling upon mycobacterial infection and to show how cAMP production can facilitate macrophage activation and subsequent cytokine production.

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“…In cardiac myocytes, the stimulation of p38 MAPK by MKK6 activates the transcription factor nuclear factor (NF)-kB, to induce IL-6 gene expression and release (Craig et al, 2000). Activation of both NF-kB and p38 MAPK is also found in monocytes following infection with M. tuberculosis (Ghosh, 1999;Mendez-Samperio et al, 2001. But whether the involvement of MKK3/6, p38 MAPK and NF-kB results in the induction of IL-6 in M. tuberculosis H37Rv-infected monocytes is not known.…”

Section: Introductionmentioning

confidence: 99%

Mycobacterium tuberculosisH37Rv induces monocytic release of interleukin-6 via activation of mitogen-activated protein kinases: inhibition byN-acetyl-l-cysteine

Natarajan

Narayanan

2007

FEMS Immunol Med Microbiol

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The release of proinflammatory cytokines after mycobacterial infection is a host immune response that may be propitious or deleterious to the host. Elevated levels of interleukin (IL)-6 are present in plasma of patients with active tuberculosis infection. The aim of this study was to investigate the role of mitogen-activated protein kinases in the secretion of interleukin-6 in THP-1 cells and human primary monocytes that were infected with Mycobacterium tuberculosis H37Rv, and its regulation by N-acetyl-L-cysteine, a potential antimycobacterial agent. Exposure of THP-1 human monocytes to M. tuberculosis H37Rv induced rapidly, in a timedependent manner, the phosphorylation of mitogen-activated protein kinase kinase 3/6 and p38 mitogen-activated protein kinase, accompanied by an upregulation of interleukin-6. Using highly specific inhibitors of mitogen-activated protein kinase kinase-1, p38 mitogen-activated protein kinase and nuclear factor-kB, we found that extracellular-signal regulated kinase 1/2, p38 mitogenactivated protein kinase and nuclear factor-kB were essential for M. tuberculosis H37Rv-induced interleukin-6 production in human primary monocytes. Pretreatment with N-acetyl-L-cysteine reduced, in a dose-dependent manner, M. tuberculosis H37Rv-induced activation of mitogen-activated protein kinase kinase 3/6 and interleukin-6 production in THP-1 cells.

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Roles of Intracellular Calcium and NF-κB in the Bacillus Calmette- Guérin-Induced Secretion of Interleukin-8 from Human Monocytes

Cited by 18 publications

References 35 publications

Activation of ERK1/2 and TNF-α production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection

Activation of ERK1/2 and TNF-α production are mediated by calcium/calmodulin, and PKA signaling pathways during Mycobacterium bovis infection

Increased Mitogen-Activated Protein Kinase Activity and TNF-α Production Associated with Mycobacterium smegmatis- but Not Mycobacterium avium-Infected Macrophages Requires Prolonged Stimulation of the Calmodulin/Calmodulin Kinase and Cyclic AMP/Protein Kinase A Pathways

Mycobacterium tuberculosisH37Rv induces monocytic release of interleukin-6 via activation of mitogen-activated protein kinases: inhibition byN-acetyl-l-cysteine

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