Mast Cell Chemotactic Activity of RANTES

Mattoli, Sabrina; Ackerman, V.P.; Vittori, Enza; Marini, Maurizio

doi:10.1006/bbrc.1995.1505

Cited by 63 publications

(43 citation statements)

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“…3 We observed that, compared to vehicle treatment, CP55,940 treatment of sickle mice for 3 weeks significantly decreased the cytokines released from skin biopsies (IL-1α, IL-6, TNF-α, MCP-1; P<0.01, Figure 2H). Consistent with decreased mast cell activation, treatment with CP55,940 lowered the levels of granulocte macrophage colony-stimulating factor (GM-CSF) and regulated on activation, normal T-cell expressed and secreted (RANTES), two chemokines involved in mast cell recruitment and function, 24,25 by at least 35% (P<0.01). GM-CSF plays a critical role in regulating leukocyte counts, which are often elevated in SCA.…”

Section: Cannabinoids Attenuate Mast Cell Activation In Sickle Cell Amentioning

confidence: 93%

Cannabinoid receptor-specific mechanisms to alleviate pain in sickle cell anemia via inhibition of mast cell activation and neurogenic inflammation

et al. 2015

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Sickle cell anemia is a manifestation of a single point mutation in hemoglobin, but inflammation and pain are the insignia of this disease which can start in infancy and continue throughout life. Earlier studies showed that mast cell activation contributes to neurogenic inflammation and pain in sickle mice. Morphine is the common analgesic treatment but also remains a major challenge due to its side effects and ability to activate mast cells. We, therefore, examined cannabinoid receptor-specific mechanisms to mitigate mast cell activation, neurogenic inflammation and hyperalgesia, using HbSS-BERK sickle and cannabinoid receptor-2-deleted sickle mice. We show that cannabinoids mitigate mast cell activation, inflammation and neurogenic inflammation in sickle mice via both cannabinoid receptors 1 and 2. Thus, cannabinoids influence systemic and neural mechanisms, ameliorating the disease pathobiology and hyperalgesia in sickle mice. This study provides 'proof of principle' for the potential of cannabinoid/cannabinoid receptor-based therapeutics to treat several manifestations of sickle cell anemia.

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Section: Cannabinoids Attenuate Mast Cell Activation In Sickle Cell Amentioning

confidence: 93%

Cannabinoid receptor-specific mechanisms to alleviate pain in sickle cell anemia via inhibition of mast cell activation and neurogenic inflammation

et al. 2015

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“…The factors that stimulate mast cell migration remain largely undefined, although recent reports have implicated stem cell factor, C3a and C5a, RANTES, interleukin-8 (IL-8), and serum amyloid A protein to be involved [2][3][4][5][6][7][8]. Other potential candidates for acting as mast cell chemotaxins are members of the transforming growth factor-␤ (TGF-␤) family, which include TGF-␤1, -␤2, -␤3, activins, and bone morphogenetic proteins [reviewed in ref .…”

Section: Introductionmentioning

confidence: 99%

Human mast cell migration in response to members of the transforming growth factor-β family

Olsson

Piek

Dijke

et al. 2000

Journal of Leukocyte Biology

113

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“…The increase in the number of mast cells at the local tissue may result from their proliferation and directional movement. There are various kinds of cytokines (6 -11) and chemoattractants (12)(13)(14)(15)(16)(17)(18)(19) which not only induce chemotactic movement of mast cells but also promote their other functional abilities. Much is known that cross-linking of IgE bound to Fc⑀RI by specific Ag mediates rapid release of biologically active chemical mediators and production of proinflammatory cytokines.…”

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confidence: 99%

Stem Cell Factor Has a Suppressive Activity to IgE-Mediated Chemotaxis of Mast Cells

Sawada

Shimizu

Tamatani

et al. 2005

The Journal of Immunology

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Stem cell factor (SCF), which is well known as a cytokine capable of amplifying development and functions of mast cells, is mainly released from fibroblasts in the peripheral tissue. To investigate whether SCF controlled chemotactic migration of mast cells induced by IgE-specific Ag, murine bone marrow-derived cultured mast cells (BMCMC) and human cord blood-derived cultured mast cells (HuCMC) were preincubated with SCF. Although BMCMC and HuCMC sensitized with IgE directly moved toward specific Ag, preincubation for even 1 h with an optimal dose of SCF suppressed the IgE-mediated chemotactic movement. No or little inhibitory effect of SCF was detected in BMCMC derived from c-kit receptor-defect WBB6F1-W/Wv mice. In contrast, preincubation of BMCMC and HuCMC with SCF enhanced β-hexosaminidase release and Ca2+ mobilization in response to Ag after sensitization with IgE. Using the real-time record of chemotactic migration, BMCMC preincubated with SCF manifested motionless without degranulation. These results suggest that locally produced SCF may have an inhibitory effect on chemotaxis of mast cells, contributing to their accumulation and enhancement of functions at the peripheral site in allergic and nonallergic conditions.

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Mast Cell Chemotactic Activity of RANTES

Cited by 63 publications

References 0 publications

Cannabinoid receptor-specific mechanisms to alleviate pain in sickle cell anemia via inhibition of mast cell activation and neurogenic inflammation

Cannabinoid receptor-specific mechanisms to alleviate pain in sickle cell anemia via inhibition of mast cell activation and neurogenic inflammation

Human mast cell migration in response to members of the transforming growth factor-β family

Stem Cell Factor Has a Suppressive Activity to IgE-Mediated Chemotaxis of Mast Cells

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