Mechanisms of cell accumulation induced by Mycobacterium bovis BCG

Menezes-de-Lima-Júnior, O; G, Henriques M das

doi:10.1590/s0074-02761997000800033

Cited by 6 publications

(3 citation statements)

References 31 publications

(27 reference statements)

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“…In animal models of mycobacterial infection, a drastic expansion of the ␥␦ T cell population is observed in the blood and tissue sites (34 -36). In this study we used a model of pleural mycobacteria infection, which allows an evaluation of early inflammatory cell recruitment induced by infection (37,38). Within 24 h of infection, significantly increased numbers of neutrophils, eosinophils, monocytes, and lymphocytes are recovered from the pleural cavity (37,38).…”

Section: ␥␦ T Cell Migration and Mcp-1 Synthesis Induced By Bcgmentioning

confidence: 99%

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Penido

Vieira‐de‐Abreu

Bozza

et al. 2003

The Journal of Immunology

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γδ T lymphocytes are involved in a great variety of inflammatory and infectious responses. However, the mechanisms by which γδ T lymphocytes migrate to inflamed sites are poorly understood. In this study we investigate the role of monocyte chemotactic protein (MCP)-1 in regulating γδ T cell migration after LPS or Mycobacterium bovis bacille Calmette-Guérin (BCG) challenge. LPS-induced γδ T cell influx was significantly inhibited by either pretreatment with dexamethasone or vaccinia virus Lister 35-kDa chemokine binding protein, vCKBP, a CC chemokine neutralizing protein, suggesting a role for CC chemokines in this phenomenon. LPS stimulation increased the expression of MCP-1 mRNA and protein at the inflammation site within 6 h. It is noteworthy that LPS was unable to increase MCP-1 production or γδ T cell recruitment in C3H/HeJ, indicative of the involvement of Toll-like receptor 4. γδ T cells express MCP-1 receptor CCR2. Pretreatment with anti-MCP-1 mAb drastically inhibited LPS-induced in vivo γδ T cell mobilization. Indeed, MCP-1 knockout mice were unable to recruit γδ T cells to the pleural cavity after LPS stimulation, effect that could be restored by coadministration of MCP-1. In addition, BCG-induced γδ lymphocyte accumulation was significantly reduced in MCP-1 knockout mice when compared with wild-type mice. In conclusion, our results indicate that LPS-induced γδ T lymphocyte migration is dependent on Toll-like receptor 4 and sensitive to both dexamethasone and CC chemokine-binding protein inhibition. Moreover, by using MCP-1 neutralizing Abs and genetically deficient mice we show that LPS- and BCG-induced γδ T lymphocyte influx to the pleural cavity of mice is mainly orchestrated by the CC chemokine MCP-1.

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Section: ␥␦ T Cell Migration and Mcp-1 Synthesis Induced By Bcgmentioning

confidence: 99%

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Penido

Vieira‐de‐Abreu

Bozza

et al. 2003

The Journal of Immunology

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“…In fact, selectins seem to be involved in leukocyte migration during a mycobacterially induced immune response (16). Recently, using an experimental model of pulmonary tuberculosis, Schreiber and coworkers (25) demonstrated that although the initial lymphocyte accumulation in lung granuloma 21 days after M. tuberculosis infection is dependent on selectin ligands, chronic-phase cell-mediated immune responses depend not on selectins but probably on organized neolymphoid structures within the lungs.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of T-Lymphocyte Accumulation during Experimental Pleural Infection Induced byMycobacterium bovisBCG

et al. 2008

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“…Furthermore, an experimental pleurisy was used to con® rm the anti-adhesion eOE ect of Lm-3 in-vivo. Pleurisy is known to be a delayed in¯ammation composed chie¯y of lymphocytes 3 days after induction (in comparison with the dominant granulocytes in the initial stage) and adhesion molecules are involved in the cell accumulation (Widstrom & Nilsson 1982 ;Menezes-de-Lima-Ju! nior & Henriques 1997).…”

Section: Discussionmentioning

confidence: 99%

Ruscogenin glycoside (Lm-3) isolated fromLiriope muscariinhibits lymphocyte adhesion to extracellular matrix

Liu

Chen

et al. 2002

Journal of Pharmacy and Pharmacology

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We examined the effects of ruscogenin glycoside (Lm-3), isolated from Liriope muscari, on lymphocyte adhesion to extracellular matrix. Adhesion of Jurkat cells activated by anti-CD3 to type I collagen was inhibited by Lm-3 in a concentration- and time-dependent manner. Lm-3 also inhibited the cell attachment to fibronectin and laminin. However, the saponin did not influence anti-CD3-induced cell proliferation and Mn2+-induced adhesion. Protein kinase C activator, phorbol 12,13-dibutyrate, significantly enhanced, while its inhibitor, chlorpromazine, almost completely blocked, the adhesion of anti-CD3-activated Jurkat cells to collagen. Against phorbol 12,13-dibutyrate-activated Jurkat cells, Lm-3 treatment, either before or after activation, significantly inhibited the cell adhesion to collagen. Lm-3 also inhibited the adhesion activated by both anti-CD3 and phorbol 12,13-dibutyrate. Similar inhibition by Lm-3 of the phorbol 12,13-dibutyrate-induced adhesion to collagen was also observed in lymphocytes freshly isolated from mice with contact dermatitis. Furthermore, Lm-3 significantly decreased the leucocyte accumulation in an animal model of experimental pleurisy. These results suggest that the blockade of lymphocyte adhesion to extracellular matrix through interference with the protein kinase C pathway may be one of the mechanisms by which Lm-3 exerts anti-inflammatory activity.

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Mechanisms of cell accumulation induced by Mycobacterium bovis BCG

Cited by 6 publications

References 31 publications

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on γδ T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide orMycobacterium bovisBacille Calmette-Guérin

Mechanisms of T-Lymphocyte Accumulation during Experimental Pleural Infection Induced byMycobacterium bovisBCG

Ruscogenin glycoside (Lm-3) isolated fromLiriope muscariinhibits lymphocyte adhesion to extracellular matrix

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