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

  • Mononuclear Phagocytes migrate into the murine cochlea after acoustic trauma
    The Journal of Comparative Neurology, 2005
    Co-Authors: Richard M Ransohoff, Keiko Hirose, Christopher M Discolo, Jodi R Keasler
    Abstract:

    Acoustic injury results in destruction of hair cells and numerous nonsensory cells of the cochlea. How these injured structures undergo repair is not well understood. This study was designed to examine the cochlea for the presence of Mononuclear Phagocytes after tissue injury caused by noise damage. We used octave band noise (8--16 kHz) at three levels (106, 112, and 120 dB) for 2 hours and studied the mice at 1, 3, 7, and 14 days after noise exposure to determine how noise affected hearing thresholds, hair cell number, and tissue injury in the cochlea. Furthermore, we assessed the cochlea for presence of inflammation by performing immunohistochemistry for CD45, common leukocyte antigen. We counted the number of CD45(+) cells that were present in the cochlea at the above-mentioned time points after noise. CD45 is present on all bone marrow-derived white blood cells and is not otherwise expressed in the inner ear. We found that, after noise exposure, there is a large increase in CD45(+) cells. These marrow-derived cells are concentrated in the spiral ligament and spiral limbus, areas that are known to be susceptible to acoustic injury. It is possible that this inflammatory response plays a role in propagating cellular damage in these areas. Immunohistochemistry demonstrates that these cochlear cells are derived from the monocyte/macrophage lineage and serve a phagocytic function in the inner ear.

  • Mononuclear Phagocytes migrate into the murine cochlea after acoustic trauma
    The Journal of Comparative Neurology, 2005
    Co-Authors: Keiko Hirose, Christopher M Discolo, Jodi R Keasler, Richard M Ransohoff
    Abstract:

    Acoustic injury results in destruction of hair cells and numerous nonsensory cells of the cochlea. How these injured structures undergo repair is not well understood. This study was designed to examine the cochlea for the presence of Mononuclear Phagocytes after tissue injury caused by noise damage. We used octave band noise (8–16 kHz) at three levels (106, 112, and 120 dB) for 2 hours and studied the mice at 1, 3, 7, and 14 days after noise exposure to determine how noise affected hearing thresholds, hair cell number, and tissue injury in the cochlea. Furthermore, we assessed the cochlea for presence of inflammation by performing immunohistochemistry for CD45, common leukocyte antigen. We counted the number of CD45+ cells that were present in the cochlea at the above-mentioned time points after noise. CD45 is present on all bone marrow-derived white blood cells and is not otherwise expressed in the inner ear. We found that, after noise exposure, there is a large increase in CD45+ cells. These marrow-derived cells are concentrated in the spiral ligament and spiral limbus, areas that are known to be susceptible to acoustic injury. It is possible that this inflammatory response plays a role in propagating cellular damage in these areas. Immunohistochemistry demonstrates that these cochlear cells are derived from the monocyte/macrophage lineage and serve a phagocytic function in the inner ear. J. Comp. Neurol. 489:180–194, 2005. © 2005 Wiley-Liss, Inc.

  • ccr1 ccr5 Mononuclear Phagocytes accumulate in the central nervous system of patients with multiple sclerosis
    American Journal of Pathology, 2001
    Co-Authors: Corinna Trebst, Hans T Lassmann, Finn Sellebjerg, Martha K. Cathcart, J Hesselgesser, Richard Horuk, Pia Kivisakk, Torben Lykke Sorensen, Richard M Ransohoff
    Abstract:

    Mononuclear Phagocytes (monocytes, macrophages, and microglia) are considered central to multiple sclerosis (MS) pathogenesis. Molecular cues that mediate Mononuclear phagocyte accumulation and activation in the central nervous system (CNS) of MS patients may include chemokines RANTES/CCL5 and macrophage inflammatory protein-1α/CCL3. We analyzed expression of CCR1 and CCR5, the monocyte receptors for these chemokines, on circulating and cerebrospinal fluid CD14+ cells, and in MS brain lesions. Approximately 70% of cerebrospinal fluid monocytes were CCR1+/CCR5+, regardless of the presence of CNS pathology, compared to less than 20% of circulating monocytes. In active MS lesions CCR1+/CCR5+ monocytes were found in perivascular cell cuffs and at the demyelinating edges of evolving lesions. Mononuclear Phagocytes in early demyelinating stages comprised CCR1+/CCR5+ hematogenous monocytes and CCR1−/CCR5− resident microglial cells. In later stages, phagocytic macrophages were uniformly CCR1−/CCR5+. Cultured in vitro, adherent monocytes/macrophages up-regulated CCR5 and down-regulated CCR1 expression, compared to freshly-isolated monocytes. Taken together, these findings suggest that monocytes competent to enter the CNS compartment derive from a minority CCR1+/CCR5+ population in the circulating pool. In the presence of ligand, these cells will be retained in the CNS. During further activation in lesions, infiltrating monocytes down-regulate CCR1 but not CCR5, whereas microglia up-regulate CCR5.

  • ccr1 ccr5 Mononuclear Phagocytes accumulate in the central nervous system of patients with multiple sclerosis
    American Journal of Pathology, 2001
    Co-Authors: Corinna Trebst, Hans T Lassmann, Finn Sellebjerg, Martha K. Cathcart, J Hesselgesser, Richard Horuk, Pia Kivisakk, Torben Lykke Sorensen, Richard M Ransohoff
    Abstract:

    Mononuclear Phagocytes (monocytes, macrophages, and microglia) are considered central to multiple sclerosis (MS) pathogenesis. Molecular cues that mediate Mononuclear phagocyte accumulation and activation in the central nervous system (CNS) of MS patients may include chemokines RANTES/CCL5 and macrophage inflammatory protein-1α/CCL3. We analyzed expression of CCR1 and CCR5, the monocyte receptors for these chemokines, on circulating and cerebrospinal fluid CD14+ cells, and in MS brain lesions. Approximately 70% of cerebrospinal fluid monocytes were CCR1+/CCR5+, regardless of the presence of CNS pathology, compared to less than 20% of circulating monocytes. In active MS lesions CCR1+/CCR5+ monocytes were found in perivascular cell cuffs and at the demyelinating edges of evolving lesions. Mononuclear Phagocytes in early demyelinating stages comprised CCR1+/CCR5+ hematogenous monocytes and CCR1−/CCR5− resident microglial cells. In later stages, phagocytic macrophages were uniformly CCR1−/CCR5+. Cultured in vitro, adherent monocytes/macrophages up-regulated CCR5 and down-regulated CCR1 expression, compared to freshly-isolated monocytes. Taken together, these findings suggest that monocytes competent to enter the CNS compartment derive from a minority CCR1+/CCR5+ population in the circulating pool. In the presence of ligand, these cells will be retained in the CNS. During further activation in lesions, infiltrating monocytes down-regulate CCR1 but not CCR5, whereas microglia up-regulate CCR5.

Steffen Jung - One of the best experts on this subject based on the ideXlab platform.

  • securing the immune tightrope Mononuclear Phagocytes in the intestinal lamina propria
    Nature Reviews Immunology, 2010
    Co-Authors: Chen Varol, Ehud Zigmond, Steffen Jung
    Abstract:

    Several distinct populations of dendritic cells and macrophages are found in the intestinal lamina propria; these cells have crucial roles in both tolerogenic and inflammatory-type immune responses at the mucosa. This Review describes the recent findings that have increased our understanding of the origin and functions of intestinal Mononuclear Phagocytes.

  • securing the immune tightrope Mononuclear Phagocytes in the intestinal lamina propria
    Nature Reviews Immunology, 2010
    Co-Authors: Chen Varol, Ehud Zigmond, Steffen Jung
    Abstract:

    The intestinal landscape comprises the host's own tissue and immune cells, as well as a diverse intestinal microbiota. Intricate regulatory mechanisms have evolved to maintain peaceful coexistence at this site, the breakdown of which can result in devastating inflammatory bowel diseases (IBDs). Mononuclear Phagocytes promote both innate and adaptive immune responses in the gut and, as such, are essential for the maintenance of intestinal homeostasis. Here, we review the origins and functions of the Mononuclear Phagocytes found in the intestinal lamina propria, highlighting the problems that have arisen from their classification. Understanding these cells in their physiological context will be important for developing new therapies for IBDs.

  • the inflammatory versus constitutive trafficking of Mononuclear Phagocytes into the alveolar space of mice is associated with drastic changes in their gene expression profiles
    Journal of Immunology, 2005
    Co-Authors: Mrigank Srivastava, Steffen Jung, Jochen Wilhelm, Ludger Fink, Frank Buhling, Tobias Welte, Rainer M Bohle, Werner Seeger, Jurgen Lohmeyer, Ulrich A Maus
    Abstract:

    Mononuclear Phagocytes enter the lungs both constitutively to maintain alveolar macrophage and dendritic cell homeostasis, as well as during lung inflammation, where the role of these cells is less well defined. We used a transgenic mouse strain (CX3CR1(+/GFP)) that harbors a GFP label in circulating monocytes to identify and sort these cells from the vascular and alveolar compartments under both constitutive and acute lung inflammatory conditions. Using nylon arrays combined with real-time RT-PCR for gene expression profiling, we found that flow-sorted, highly purified Mononuclear Phagocytes recruited to acutely inflamed mouse lungs showed strongly up-regulated mRNA levels of the neutrophil chemoattractants KC, MIP-2, and IP-10, which contrasted with alveolar Mononuclear Phagocytes that immigrated in steady state. Similar observations were made for the lysosomal cathepsins B, L, and K being strongly up-regulated in Mononuclear Phagocytes upon recruitment to inflamed lungs but not during constitutive alveolar immigration. Inflammatory elicited Mononuclear Phagocytes also demonstrated significantly increased mRNA levels of the cytokine TNF-alpha and the PRR-associated molecules CD14, TLR4, and syndecan-4. Together, inflammatory elicited Mononuclear Phagocytes exhibit strongly increased neutrophil chemoattractants, lysosomal proteases, and LPS signaling mRNA transcripts, suggesting that these cells may play a major role in acute lung inflammatory processes.

Ehud Zigmond - One of the best experts on this subject based on the ideXlab platform.

  • securing the immune tightrope Mononuclear Phagocytes in the intestinal lamina propria
    Nature Reviews Immunology, 2010
    Co-Authors: Chen Varol, Ehud Zigmond, Steffen Jung
    Abstract:

    Several distinct populations of dendritic cells and macrophages are found in the intestinal lamina propria; these cells have crucial roles in both tolerogenic and inflammatory-type immune responses at the mucosa. This Review describes the recent findings that have increased our understanding of the origin and functions of intestinal Mononuclear Phagocytes.

  • securing the immune tightrope Mononuclear Phagocytes in the intestinal lamina propria
    Nature Reviews Immunology, 2010
    Co-Authors: Chen Varol, Ehud Zigmond, Steffen Jung
    Abstract:

    The intestinal landscape comprises the host's own tissue and immune cells, as well as a diverse intestinal microbiota. Intricate regulatory mechanisms have evolved to maintain peaceful coexistence at this site, the breakdown of which can result in devastating inflammatory bowel diseases (IBDs). Mononuclear Phagocytes promote both innate and adaptive immune responses in the gut and, as such, are essential for the maintenance of intestinal homeostasis. Here, we review the origins and functions of the Mononuclear Phagocytes found in the intestinal lamina propria, highlighting the problems that have arisen from their classification. Understanding these cells in their physiological context will be important for developing new therapies for IBDs.

Corinna Trebst - One of the best experts on this subject based on the ideXlab platform.

  • ccr1 ccr5 Mononuclear Phagocytes accumulate in the central nervous system of patients with multiple sclerosis
    American Journal of Pathology, 2001
    Co-Authors: Corinna Trebst, Hans T Lassmann, Finn Sellebjerg, Martha K. Cathcart, J Hesselgesser, Richard Horuk, Pia Kivisakk, Torben Lykke Sorensen, Richard M Ransohoff
    Abstract:

    Mononuclear Phagocytes (monocytes, macrophages, and microglia) are considered central to multiple sclerosis (MS) pathogenesis. Molecular cues that mediate Mononuclear phagocyte accumulation and activation in the central nervous system (CNS) of MS patients may include chemokines RANTES/CCL5 and macrophage inflammatory protein-1α/CCL3. We analyzed expression of CCR1 and CCR5, the monocyte receptors for these chemokines, on circulating and cerebrospinal fluid CD14+ cells, and in MS brain lesions. Approximately 70% of cerebrospinal fluid monocytes were CCR1+/CCR5+, regardless of the presence of CNS pathology, compared to less than 20% of circulating monocytes. In active MS lesions CCR1+/CCR5+ monocytes were found in perivascular cell cuffs and at the demyelinating edges of evolving lesions. Mononuclear Phagocytes in early demyelinating stages comprised CCR1+/CCR5+ hematogenous monocytes and CCR1−/CCR5− resident microglial cells. In later stages, phagocytic macrophages were uniformly CCR1−/CCR5+. Cultured in vitro, adherent monocytes/macrophages up-regulated CCR5 and down-regulated CCR1 expression, compared to freshly-isolated monocytes. Taken together, these findings suggest that monocytes competent to enter the CNS compartment derive from a minority CCR1+/CCR5+ population in the circulating pool. In the presence of ligand, these cells will be retained in the CNS. During further activation in lesions, infiltrating monocytes down-regulate CCR1 but not CCR5, whereas microglia up-regulate CCR5.

  • ccr1 ccr5 Mononuclear Phagocytes accumulate in the central nervous system of patients with multiple sclerosis
    American Journal of Pathology, 2001
    Co-Authors: Corinna Trebst, Hans T Lassmann, Finn Sellebjerg, Martha K. Cathcart, J Hesselgesser, Richard Horuk, Pia Kivisakk, Torben Lykke Sorensen, Richard M Ransohoff
    Abstract:

    Mononuclear Phagocytes (monocytes, macrophages, and microglia) are considered central to multiple sclerosis (MS) pathogenesis. Molecular cues that mediate Mononuclear phagocyte accumulation and activation in the central nervous system (CNS) of MS patients may include chemokines RANTES/CCL5 and macrophage inflammatory protein-1α/CCL3. We analyzed expression of CCR1 and CCR5, the monocyte receptors for these chemokines, on circulating and cerebrospinal fluid CD14+ cells, and in MS brain lesions. Approximately 70% of cerebrospinal fluid monocytes were CCR1+/CCR5+, regardless of the presence of CNS pathology, compared to less than 20% of circulating monocytes. In active MS lesions CCR1+/CCR5+ monocytes were found in perivascular cell cuffs and at the demyelinating edges of evolving lesions. Mononuclear Phagocytes in early demyelinating stages comprised CCR1+/CCR5+ hematogenous monocytes and CCR1−/CCR5− resident microglial cells. In later stages, phagocytic macrophages were uniformly CCR1−/CCR5+. Cultured in vitro, adherent monocytes/macrophages up-regulated CCR5 and down-regulated CCR1 expression, compared to freshly-isolated monocytes. Taken together, these findings suggest that monocytes competent to enter the CNS compartment derive from a minority CCR1+/CCR5+ population in the circulating pool. In the presence of ligand, these cells will be retained in the CNS. During further activation in lesions, infiltrating monocytes down-regulate CCR1 but not CCR5, whereas microglia up-regulate CCR5.

Runolfur Palsson - One of the best experts on this subject based on the ideXlab platform.

  • Mononuclear Phagocytes orchestrate prolyl hydroxylase inhibition mediated renoprotection in chronic tubulointerstitial nephritis
    Kidney International, 2019
    Co-Authors: Gunnar Schley, Bernd Klanke, Joanna Kalucka, Valentin Schatz, Christoph Daniel, Marleen Mayer, Margarete Goppeltstruebe, Martin Herrmann, Margret Thorsteinsdottir, Runolfur Palsson
    Abstract:

    Prolyl hydroxylase domain enzyme inhibitors (PHDIs) stabilize hypoxia-inducible factors (HIFs), and are protective in models of acute ischemic and inflammatory kidney disease. Whether PHDIs also confer protection in chronic inflammatory kidney disease models remains unknown. Here we investigated long-term effects of PHDI treatment in adenine-induced nephropathy as a model for chronic tubulointerstitial nephritis. After three weeks, renal dysfunction and tubulointerstitial damage, including proximal and distal tubular injury, tubular dilation and renal crystal deposition were significantly attenuated in PHDI-treated (the isoquinoline derivative ICA and Roxadustat) compared to vehicle-treated mice with adenine-induced nephropathy. Crystal-induced renal fibrosis was only partially diminished by treatment with ICA. Renoprotective effects of ICA treatment could not be attributed to changes in adenine metabolism or urinary excretion of the metabolite 2,8-dihydroxyadenine. ICA treatment reduced inflammatory infiltrates of F4/80+ Mononuclear Phagocytes in the kidneys and supported a regulatory, anti-inflammatory immune response. Furthermore, interstitial deposition of complement C1q was decreased in ICA-treated mice fed an adenine-enriched diet. Tubular cell-specific HIF-1α and myeloid cell-specific HIF-1α and HIF-2α expression were not required for the renoprotective effects of ICA. In contrast, depletion of Mononuclear Phagocytes with clodronate largely abolished the nephroprotective effects of PHD inhibition. Thus, our findings indicate novel and potent systemic anti-inflammatory properties of PHDIs that confer preservation of kidney function and structure in chronic tubulointerstitial inflammation and might counteract kidney disease progression.