The Experts below are selected from a list of 33 Experts worldwide ranked by ideXlab platform

Peter J Barnes - One of the best experts on this subject based on the ideXlab platform.

  • defective phagocytosis in airways disease
    Chest, 2012
    Co-Authors: Louise E Donnelly, Peter J Barnes
    Abstract:

    Maintaining an airway clear of inhaled particles, pathogens, and cellular debris is paramount for lung homeostasis. In healthy individuals, the Phagocytes of the innate immune system act as sentinels to patrol the airway and ensure sterility. However, in airways diseases, including asthma, COPD, and cystic fibrosis, there is a propensity for bacterial colonization that may contribute to disease worsening. Evidence suggests that this may be due to Dysfunctional phagocytosis. In patients with COPD, phagocytosis of several bacterial species and removal of apoptotic cells (efferocytosis) by alveolar macrophages are significantly reduced; however, these cells can remove inert beads normally. Attenuated phagocytosis is also apparent in monocyte-derived macrophages from the same patients, suggesting an inherent defect in these cells. Reduced expression of cell surface recognition receptors has been suggested as one mechanism for these observations; however, the literature is currently contradictory and requires further clarification. In cystic fibrosis, a similar defect is also observed in both airway neutrophils and macrophages, leading to ineffective bacterial uptake and subsequent killing. In asthma and other airways diseases, there are also reports of defective phagocytosis of bacterial pathogens, although the relevance to disease pathophysiology is not understood. Oxidative stress is emerging as a common mechanism that may be altering both macrophage and neutrophil functions that can be reversed by various antioxidant strategies. The identification of this and other mechanisms underlying Phagocyte Dysfunction may present novel therapeutic opportunities for the treatment of many of these intractable diseases and improve patient morbidity and mortality.

Joachim R Kalden - One of the best experts on this subject based on the ideXlab platform.

  • impaired phagocytosis of apoptotic cell material by monocyte derived macrophages from patients with systemic lupus erythematosus
    Arthritis & Rheumatism, 1998
    Co-Authors: Martin Herrmann, Reinhard E Voll, Otmar Zoller, M Hagenhofer, Botond B Ponner, Joachim R Kalden
    Abstract:

    OBJECTIVE: To investigate whether the established impaired Phagocyte function in systemic lupus erythematosus (SLE) patients also affects apoptotic cell clearance. Accumulation of apoptotic waste as a source for autoantigens that induce and maintain autoimmune responses is discussed. METHODS: Apoptosis was detected by morphology and propidium iodide staining. In vitro phagocytosis of autologous apoptotic cells in cultured peripheral blood mononuclear cells was evaluated microscopically. Cross-feeding experiments were performed to investigate phagocytosis of heterologous apoptotic cells by in vitro-differentiated macrophages. Furthermore, the effect of annexin V on the phagocytosis of apoptotic cells was investigated. RESULTS: Reduced clearance of apoptotic cells in SLE patients was observed. The defective clearance appeared to reflect Phagocyte Dysfunction and not an abnormal execution of apoptosis. A similar picture was seen when in vitro-differentiated macrophages from control populations were treated with annexin V. CONCLUSION: Noninflammatory engulfment phagocytosis of apoptotic cells is decreased in SLE patients. Persistently circulating apoptotic waste may encounter inflammatory removal pathways and serve as immunogen for the induction of autoreactive lymphocytes and as antigen for immune complex formation.

Louise E Donnelly - One of the best experts on this subject based on the ideXlab platform.

  • defective phagocytosis in airways disease
    Chest, 2012
    Co-Authors: Louise E Donnelly, Peter J Barnes
    Abstract:

    Maintaining an airway clear of inhaled particles, pathogens, and cellular debris is paramount for lung homeostasis. In healthy individuals, the Phagocytes of the innate immune system act as sentinels to patrol the airway and ensure sterility. However, in airways diseases, including asthma, COPD, and cystic fibrosis, there is a propensity for bacterial colonization that may contribute to disease worsening. Evidence suggests that this may be due to Dysfunctional phagocytosis. In patients with COPD, phagocytosis of several bacterial species and removal of apoptotic cells (efferocytosis) by alveolar macrophages are significantly reduced; however, these cells can remove inert beads normally. Attenuated phagocytosis is also apparent in monocyte-derived macrophages from the same patients, suggesting an inherent defect in these cells. Reduced expression of cell surface recognition receptors has been suggested as one mechanism for these observations; however, the literature is currently contradictory and requires further clarification. In cystic fibrosis, a similar defect is also observed in both airway neutrophils and macrophages, leading to ineffective bacterial uptake and subsequent killing. In asthma and other airways diseases, there are also reports of defective phagocytosis of bacterial pathogens, although the relevance to disease pathophysiology is not understood. Oxidative stress is emerging as a common mechanism that may be altering both macrophage and neutrophil functions that can be reversed by various antioxidant strategies. The identification of this and other mechanisms underlying Phagocyte Dysfunction may present novel therapeutic opportunities for the treatment of many of these intractable diseases and improve patient morbidity and mortality.

Martin Herrmann - One of the best experts on this subject based on the ideXlab platform.

  • impaired phagocytosis of apoptotic cell material by monocyte derived macrophages from patients with systemic lupus erythematosus
    Arthritis & Rheumatism, 1998
    Co-Authors: Martin Herrmann, Reinhard E Voll, Otmar Zoller, M Hagenhofer, Botond B Ponner, Joachim R Kalden
    Abstract:

    OBJECTIVE: To investigate whether the established impaired Phagocyte function in systemic lupus erythematosus (SLE) patients also affects apoptotic cell clearance. Accumulation of apoptotic waste as a source for autoantigens that induce and maintain autoimmune responses is discussed. METHODS: Apoptosis was detected by morphology and propidium iodide staining. In vitro phagocytosis of autologous apoptotic cells in cultured peripheral blood mononuclear cells was evaluated microscopically. Cross-feeding experiments were performed to investigate phagocytosis of heterologous apoptotic cells by in vitro-differentiated macrophages. Furthermore, the effect of annexin V on the phagocytosis of apoptotic cells was investigated. RESULTS: Reduced clearance of apoptotic cells in SLE patients was observed. The defective clearance appeared to reflect Phagocyte Dysfunction and not an abnormal execution of apoptosis. A similar picture was seen when in vitro-differentiated macrophages from control populations were treated with annexin V. CONCLUSION: Noninflammatory engulfment phagocytosis of apoptotic cells is decreased in SLE patients. Persistently circulating apoptotic waste may encounter inflammatory removal pathways and serve as immunogen for the induction of autoreactive lymphocytes and as antigen for immune complex formation.

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

  • impaired phagocytosis of apoptotic cell material by monocyte derived macrophages from patients with systemic lupus erythematosus
    Arthritis & Rheumatism, 1998
    Co-Authors: Martin Herrmann, Reinhard E Voll, Otmar Zoller, M Hagenhofer, Botond B Ponner, Joachim R Kalden
    Abstract:

    OBJECTIVE: To investigate whether the established impaired Phagocyte function in systemic lupus erythematosus (SLE) patients also affects apoptotic cell clearance. Accumulation of apoptotic waste as a source for autoantigens that induce and maintain autoimmune responses is discussed. METHODS: Apoptosis was detected by morphology and propidium iodide staining. In vitro phagocytosis of autologous apoptotic cells in cultured peripheral blood mononuclear cells was evaluated microscopically. Cross-feeding experiments were performed to investigate phagocytosis of heterologous apoptotic cells by in vitro-differentiated macrophages. Furthermore, the effect of annexin V on the phagocytosis of apoptotic cells was investigated. RESULTS: Reduced clearance of apoptotic cells in SLE patients was observed. The defective clearance appeared to reflect Phagocyte Dysfunction and not an abnormal execution of apoptosis. A similar picture was seen when in vitro-differentiated macrophages from control populations were treated with annexin V. CONCLUSION: Noninflammatory engulfment phagocytosis of apoptotic cells is decreased in SLE patients. Persistently circulating apoptotic waste may encounter inflammatory removal pathways and serve as immunogen for the induction of autoreactive lymphocytes and as antigen for immune complex formation.