Infection of human monocytes with Mycobacterium bovis BCG induces production of CC-chemokines

Méndez-Samperio, Patricia; Vázquez, Abraham; Ayala, H

doi:10.1016/s0163-4453(03)00010-0

Cited by 14 publications

(14 citation statements)

References 34 publications

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“…Furthermore, it has been demonstrated that anti-CCL5 antibodies decrease the sizes of pulmonary granuloma lesions in M. bovis BCGinfected mice, suggesting a functional role for CCL5 in murine mycobacterial granulomas (28). Our results have provided evidence that in vitro, M. bovis BCG stimulates human monocytes to produce CC chemokines and that mobilization of intracellular Ca 2ϩ and the CD40 molecule are critical for the induction of CCL5 (25). However, the effects of JNK and NF-B on TLR2-mediated CCL2 or CCL5 pro-duction in epithelial cells are mostly unknown.…”

supporting

confidence: 58%

Mycobacterium bovisBacillus Calmette-Guérin Induces CCL5 Secretion via the Toll-Like Receptor 2-NF-κB and -Jun N-Terminal Kinase Signaling Pathways

Méndez-Samperio¹,

Trejo²,

Pérez³

2008

Clin Vaccine Immunol

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supporting

confidence: 58%

Mycobacterium bovisBacillus Calmette-Guérin Induces CCL5 Secretion via the Toll-Like Receptor 2-NF-κB and -Jun N-Terminal Kinase Signaling Pathways

Méndez-Samperio¹,

Trejo²,

Pérez³

2008

Clin Vaccine Immunol

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“…This suggested that immunization with tuberculosis germs might be critical for the induction of DP monocytes. To test this hypothesis, we examined whether the cytokines and chemokines known to be induced by the recombinant Mycobacterium bovis bacillus Calmette-Guerin (BCG) [32][33][34] can induce DP monocytes in vitro. PBMCs from F344 rats were stimulated with IL-12, RANTES, or GM-CSF for 24 hours and then the percentage of DP monocytes was measured.…”

Section: Induction Of Dp Monocytes In Nontransgenic Fw-wt Ratsmentioning

confidence: 99%

CD4+/CD8+ macrophages infiltrating at inflammatory sites: a population of monocytes/macrophages with a cytotoxic phenotype

Baba

Ishizu

Iwasaki

et al. 2006

Blood

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We found a population of nonlymphoid cells expressing both CD4 and CD8 in peripheral blood mononuclear cells (PBMCs) of human T-cell leukemia virus type-I pX transgenic rats with autoimmune diseases. These cells, which showed a monocytic phenotype, were also found in wild-type rats, and their number increased by adjuvant-assisted immunization. GM-CSF increased the number of these double-positive (DP) monocytes in PBMCs. Consistent with the idea that DP monocytes differentiate into DP macrophages at sites of inflammation, we found infiltration of DP macrophages at the site of myosin-induced myocarditis in wild-type rats; these cells exhibited a T-helper 1 (Th1)-type cytokine/ chemokine profile and expressed high levels of Fas ligand, perforin, granzyme B, and NKR-P2 (rat orthologue of human NKG2D). Adoptive transfer of GFP-positive spleen cells confirmed hematogenous origin of DP macrophages. DP monocytes had a cytotoxic phenotype similar to DP macrophages, indicating that this phenotypic specialization occurred before entry into a tissue. In line with this, DP monocytes killed tumor cells in vitro. Combined evidence indicates that certain inflammatory stimuli that induce GM-CSF trigger the expansion of a population of DP monocytes with a cytotoxic phenotype and that these cells differentiate into macrophages at inflammatory sites. Interestingly, human PBMCs also contain DP

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“…We examined the early interactions between M. leprae and monocytes isolated from the blood of M. leprae-naïve healthy donors. As a positive control in our studies, we used Mycobacterium bovis bacillus Calmette-Guérin (BCG), which is a potent stimulant of innate immune response (25,43) used widely as a vaccine for tuberculosis in humans.…”

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confidence: 99%

Mycobacterium lepraeActively Modulates the Cytokine Response in Naïve Human Monocytes

et al. 2010

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Leprosy is a chronic but treatable infectious disease caused by the intracellular pathogen Mycobacterium leprae. Host immunity to M. leprae determines the diversity of clinical manifestations seen in patients, from tuberculoid leprosy with robust production of Th1-type cytokines to lepromatous disease, characterized by elevated levels of Th2-type cytokines and a suboptimal proinflammatory response. Previous reports have indicated that M. leprae is a poor activator of macrophages and dendritic cells in vitro. To understand whether M. leprae fails to elicit an optimal Th1 immune response or actively interferes with its induction, we have examined the early interactions between M. leprae and monocytes from healthy human donors. We found that, in naïve monocytes, M. leprae induced high levels of the negative regulatory molecules MCP-1 and interleukin-1 (IL-1) receptor antagonist (IL-1Ra), while suppressing IL-6 production through phosphoinositide-3 kinase (PI3K)-dependent mechanisms. In addition, low levels of proinflammatory cytokines were observed in association with reduced activation of nuclear factor-B (NF-B) and delayed activation of IL-1␤-converting enzyme, ICE (caspase-1), in monocytes stimulated with M. leprae compared with Mycobacterium bovis BCG stimulation. Interestingly, although in itself a weak stimulator of cytokines, M. leprae primed the cells for increased production of tumor necrosis factor alpha and IL-10 in response to a strongly inducing secondary stimulus. Taken together, our results suggest that M. leprae plays an active role to control the release of cytokines from monocytes by providing both positive and negative regulatory signals via multiple signaling pathways involving PI3K, NF-B, and caspase-1.

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Infection of human monocytes with Mycobacterium bovis BCG induces production of CC-chemokines

Cited by 14 publications

References 34 publications

Mycobacterium bovisBacillus Calmette-Guérin Induces CCL5 Secretion via the Toll-Like Receptor 2-NF-κB and -Jun N-Terminal Kinase Signaling Pathways

Mycobacterium bovisBacillus Calmette-Guérin Induces CCL5 Secretion via the Toll-Like Receptor 2-NF-κB and -Jun N-Terminal Kinase Signaling Pathways

CD4+/CD8+ macrophages infiltrating at inflammatory sites: a population of monocytes/macrophages with a cytotoxic phenotype

Mycobacterium lepraeActively Modulates the Cytokine Response in Naïve Human Monocytes

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