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Mauro M. Teixeira - One of the best experts on this subject based on the ideXlab platform.

  • role of the chemokines CCL3 mip 1α and ccl5 rantes in sponge induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Brunolima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Bruno-lima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1 α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Guilherme Bruno-lima Jr., Amanda E.i. Proudfoot, Silvia P. Andrade, Mauro M. Teixeira
    Abstract:

    OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS: CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

Lucíola S. Barcelos - One of the best experts on this subject based on the ideXlab platform.

  • role of the chemokines CCL3 mip 1α and ccl5 rantes in sponge induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Brunolima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Bruno-lima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1 α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Guilherme Bruno-lima Jr., Amanda E.i. Proudfoot, Silvia P. Andrade, Mauro M. Teixeira
    Abstract:

    OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS: CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

Amanda E.i. Proudfoot - One of the best experts on this subject based on the ideXlab platform.

  • role of the chemokines CCL3 mip 1α and ccl5 rantes in sponge induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Brunolima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Bruno-lima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1 α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Guilherme Bruno-lima Jr., Amanda E.i. Proudfoot, Silvia P. Andrade, Mauro M. Teixeira
    Abstract:

    OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS: CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

Amanda M. Coelho - One of the best experts on this subject based on the ideXlab platform.

  • role of the chemokines CCL3 mip 1α and ccl5 rantes in sponge induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Brunolima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Bruno-lima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1 α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Guilherme Bruno-lima Jr., Amanda E.i. Proudfoot, Silvia P. Andrade, Mauro M. Teixeira
    Abstract:

    OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS: CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

Remo C. Russo - One of the best experts on this subject based on the ideXlab platform.

  • role of the chemokines CCL3 mip 1α and ccl5 rantes in sponge induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Brunolima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Amanda E.i. Proudfoot, Silvia P. Andrade, Guilherme Bruno-lima, Mauro M. Teixeira
    Abstract:

    Abstract Objective We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. Methods Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. Results CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3 −/− mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5 −/− mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. Conclusion Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.

  • Role of the chemokines CCL3/MIP-1 α and CCL5/RANTES in sponge-induced inflammatory angiogenesis in mice
    Microvascular Research, 2009
    Co-Authors: Lucíola S. Barcelos, Amanda M. Coelho, Remo C. Russo, Rodrigo Guabiraba, Adriano L.s. Souza, Guilherme Bruno-lima Jr., Amanda E.i. Proudfoot, Silvia P. Andrade, Mauro M. Teixeira
    Abstract:

    OBJECTIVE: We examined the potential contribution of CCL3 and CCL5 to inflammatory angiogenesis in mice. METHODS: Polyester-polyurethane sponges were implanted in mice and blood vessel counting and hemoglobin, myeloperoxidase and N-acetylglucosaminidase measurements used as indexes for vascularization, neutrophil and macrophage accumulation, respectively. RESULTS: CCL3 and CCL5 were expressed throughout the observation period. Exogenous CCL3 enhanced angiogenesis in WT, but angiogenesis proceeded normally in CCL3(-/-) mice, suggesting that endogenous CCL3 is not critical for sponge-induced angiogenesis in mice. CCL5 expression was detected at day 1, but levels significantly increased thereafter. Exogenous CCL5 reduced angiogenesis in WT mice possible via CCR5 as CCL5 was without an effect in CCR5(-/-) mice. Treatment of WT with the CCR1/CCR5 antagonist, Met-RANTES, prevented neutrophil and macrophage accumulation, but enhanced sponge vascularization. CONCLUSION: Thus, endogenous CCL3 appears not to play a role in driving sponge-induced inflammatory angiogenesis in mice. The effects of CCL5 were anti-angiogenic and appeared to be mediated via activation of CCR5.