The Experts below are selected from a list of 5598 Experts worldwide ranked by ideXlab platform

Julia K Gittler - One of the best experts on this subject based on the ideXlab platform.

  • progressive activation of th2 th22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis
    The Journal of Allergy and Clinical Immunology, 2012
    Co-Authors: Julia K Gittler, Avner Shemer, Mayte Suarezfarinas, Judilyn Fuentesduculan, Kara J Gulewicz, Claire Q F Wang, Hiroshi Mitsui, Irma Cardinale, Cristina De Guzman Strong
    Abstract:

    Background Atopic dermatitis (AD) is a common Disease with an increasing prevalence. The primary pathogenesis of the Disease is still elusive, resulting in the lack of specific treatments. AD is currently considered a Biphasic Disease, with T H 2 predominating in acute Disease and a switch to T H 1 characterizing chronic Disease. Elucidation of the molecular factors that participate in the onset of new lesions and maintenance of chronic Disease is critical for the development of targeted therapeutics. Objectives We sought to characterize the mechanisms underlying the onset and maintenance of AD. Methods We investigated intrapersonal sets of transcriptomes from nonlesional skin and acute and chronic lesions of 10 patients with AD through genomic, molecular, and cellular profiling. Results Our study associated the onset of acute lesions with a striking increase in a subset of terminal differentiation proteins, specifically the cytokine-modulated S100A7, S100A8, and S100A9. Acute Disease was also associated with significant increases in gene expression levels of major T H 22 and T H 2 cytokines and smaller increases in IL-17 levels. A lesser induction of T H 1-associated genes was detected in acute Disease, although some were significantly upregulated in chronic Disease. Further significant intensification of major T H 22 and T H 2 cytokines was observed between acute and chronic lesions. Conclusions Our data identified increased S100A7, S100A8, and S100A9 gene expression with AD initiation and concomitant activation of T H 2 and T H 22 cytokines. Our findings support a model of progressive activation of T H 2 and T H 22 immune axes from the acute to chronic phases, expanding the prevailing view of pathogenesis with important therapeutic implications.

  • progressive activation of t h 2 t h 22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis
    The Journal of Allergy and Clinical Immunology, 2012
    Co-Authors: Julia K Gittler, Avner Shemer, Mayte Suarezfarinas, Judilyn Fuentesduculan, Kara J Gulewicz, Claire Q F Wang, Hiroshi Mitsui, Irma Cardinale, Cristina De Guzman Strong
    Abstract:

    Background Atopic dermatitis (AD) is a common Disease with an increasing prevalence. The primary pathogenesis of the Disease is still elusive, resulting in the lack of specific treatments. AD is currently considered a Biphasic Disease, with T H 2 predominating in acute Disease and a switch to T H 1 characterizing chronic Disease. Elucidation of the molecular factors that participate in the onset of new lesions and maintenance of chronic Disease is critical for the development of targeted therapeutics. Objectives We sought to characterize the mechanisms underlying the onset and maintenance of AD. Methods We investigated intrapersonal sets of transcriptomes from nonlesional skin and acute and chronic lesions of 10 patients with AD through genomic, molecular, and cellular profiling. Results Our study associated the onset of acute lesions with a striking increase in a subset of terminal differentiation proteins, specifically the cytokine-modulated S100A7, S100A8, and S100A9. Acute Disease was also associated with significant increases in gene expression levels of major T H 22 and T H 2 cytokines and smaller increases in IL-17 levels. A lesser induction of T H 1-associated genes was detected in acute Disease, although some were significantly upregulated in chronic Disease. Further significant intensification of major T H 22 and T H 2 cytokines was observed between acute and chronic lesions. Conclusions Our data identified increased S100A7, S100A8, and S100A9 gene expression with AD initiation and concomitant activation of T H 2 and T H 22 cytokines. Our findings support a model of progressive activation of T H 2 and T H 22 immune axes from the acute to chronic phases, expanding the prevailing view of pathogenesis with important therapeutic implications.

Lucille London - One of the best experts on this subject based on the ideXlab platform.

  • differential role for t cells in the development of fibrotic lesions associated with reovirus 1 l induced bronchiolitis obliterans organizing pneumonia versus acute respiratory distress syndrome
    American Journal of Respiratory Cell and Molecular Biology, 2003
    Co-Authors: Elizabeth I Majeski, Russell A Harley, Stephen C Bellum, Steven D London, Lucille London
    Abstract:

    Bronchiolitis obliterans organizing pneumonia (BOOP) and Acute Respiratory Distress Syndrome (ARDS) are two pulmonary Diseases with fibrotic components. BOOP is characterized by perivascular/peribronchiolar leukocyte infiltration leading to the development of intra-alveolar fibrosis. ARDS is a Biphasic Disease that includes an acute phase, consisting of severe leukocyte infiltration, edema, hemorrhage, and the formation of hyaline membranes, and a chronic phase, which is characterized by persistent intra-alveolar and interstitial fibrosis. CBA/J mice infected with 1 × 106 plaque-forming units (pfu) reovirus 1/L develop follicular bronchiolitis and intra-alveolar fibrosis similar to BOOP. In contrast, CBA/J mice infected with 1 × 107 pfu reovirus 1/L develop histologic characteristics of ARDS including diffuse alveolar damage, hyaline membranes, and intra-alveolar fibrosis. In this report, we demonstrate a differential role for T lymphocytes in the development of fibrosis associated with BOOP versus ARDS. ...

  • differential role for t cells in the development of fibrotic lesions associated with reovirus 1 l induced bronchiolitis obliterans organizing pneumonia versus acute respiratory distress syndrome
    American Journal of Respiratory Cell and Molecular Biology, 2003
    Co-Authors: Elizabeth I Majeski, Russell A Harley, Stephen C Bellum, Steven D London, Lucille London
    Abstract:

    Bronchiolitis obliterans organizing pneumonia (BOOP) and Acute Respiratory Distress Syndrome (ARDS) are two pulmonary Diseases with fibrotic components. BOOP is characterized by perivascular/peribronchiolar leukocyte infiltration leading to the development of intra-alveolar fibrosis. ARDS is a Biphasic Disease that includes an acute phase, consisting of severe leukocyte infiltration, edema, hemorrhage, and the formation of hyaline membranes, and a chronic phase, which is characterized by persistent intra-alveolar and interstitial fibrosis. CBA/J mice infected with 1 x 10(6) plaque-forming units (pfu) reovirus 1/L develop follicular bronchiolitis and intra-alveolar fibrosis similar to BOOP. In contrast, CBA/J mice infected with 1 x 10(7) pfu reovirus 1/L develop histologic characteristics of ARDS including diffuse alveolar damage, hyaline membranes, and intra-alveolar fibrosis. In this report, we demonstrate a differential role for T lymphocytes in the development of fibrosis associated with BOOP versus ARDS. Neonatally thymectomized CBA/J mice infected with 1 x 10(7) pfu (ARDS) reovirus 1/L still develop the hallmark characteristics of ARDS, including a severe viral pneumonia with cellular infiltrates comprised mainly of macrophages and neutrophils, hyaline membrane formation, and hemorrhage during the acute phase of the Disease and persistent intra-alveolar fibrosis during the chronic phase of the Disease. In contrast, neonatally thymectomized CBA/J mice infected with 1 x 10(6) pfu (BOOP) reovirus 1/L do not develop intra-alveolar fibrosis associated with BOOP. Therefore, while T cells are necessary for the development of intraluminal fibrosis associated with BOOP, they are not necessary for the development of intraluminal fibrosis associated with ARDS. Furthermore, we suggest that interferon-gamma plays a key role in the fibrotic process and that elevated levels of interferon-gamma are associated with a continuum from least to more severe fibrosis.

Cristina De Guzman Strong - One of the best experts on this subject based on the ideXlab platform.

  • progressive activation of th2 th22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis
    The Journal of Allergy and Clinical Immunology, 2012
    Co-Authors: Julia K Gittler, Avner Shemer, Mayte Suarezfarinas, Judilyn Fuentesduculan, Kara J Gulewicz, Claire Q F Wang, Hiroshi Mitsui, Irma Cardinale, Cristina De Guzman Strong
    Abstract:

    Background Atopic dermatitis (AD) is a common Disease with an increasing prevalence. The primary pathogenesis of the Disease is still elusive, resulting in the lack of specific treatments. AD is currently considered a Biphasic Disease, with T H 2 predominating in acute Disease and a switch to T H 1 characterizing chronic Disease. Elucidation of the molecular factors that participate in the onset of new lesions and maintenance of chronic Disease is critical for the development of targeted therapeutics. Objectives We sought to characterize the mechanisms underlying the onset and maintenance of AD. Methods We investigated intrapersonal sets of transcriptomes from nonlesional skin and acute and chronic lesions of 10 patients with AD through genomic, molecular, and cellular profiling. Results Our study associated the onset of acute lesions with a striking increase in a subset of terminal differentiation proteins, specifically the cytokine-modulated S100A7, S100A8, and S100A9. Acute Disease was also associated with significant increases in gene expression levels of major T H 22 and T H 2 cytokines and smaller increases in IL-17 levels. A lesser induction of T H 1-associated genes was detected in acute Disease, although some were significantly upregulated in chronic Disease. Further significant intensification of major T H 22 and T H 2 cytokines was observed between acute and chronic lesions. Conclusions Our data identified increased S100A7, S100A8, and S100A9 gene expression with AD initiation and concomitant activation of T H 2 and T H 22 cytokines. Our findings support a model of progressive activation of T H 2 and T H 22 immune axes from the acute to chronic phases, expanding the prevailing view of pathogenesis with important therapeutic implications.

  • progressive activation of t h 2 t h 22 cytokines and selective epidermal proteins characterizes acute and chronic atopic dermatitis
    The Journal of Allergy and Clinical Immunology, 2012
    Co-Authors: Julia K Gittler, Avner Shemer, Mayte Suarezfarinas, Judilyn Fuentesduculan, Kara J Gulewicz, Claire Q F Wang, Hiroshi Mitsui, Irma Cardinale, Cristina De Guzman Strong
    Abstract:

    Background Atopic dermatitis (AD) is a common Disease with an increasing prevalence. The primary pathogenesis of the Disease is still elusive, resulting in the lack of specific treatments. AD is currently considered a Biphasic Disease, with T H 2 predominating in acute Disease and a switch to T H 1 characterizing chronic Disease. Elucidation of the molecular factors that participate in the onset of new lesions and maintenance of chronic Disease is critical for the development of targeted therapeutics. Objectives We sought to characterize the mechanisms underlying the onset and maintenance of AD. Methods We investigated intrapersonal sets of transcriptomes from nonlesional skin and acute and chronic lesions of 10 patients with AD through genomic, molecular, and cellular profiling. Results Our study associated the onset of acute lesions with a striking increase in a subset of terminal differentiation proteins, specifically the cytokine-modulated S100A7, S100A8, and S100A9. Acute Disease was also associated with significant increases in gene expression levels of major T H 22 and T H 2 cytokines and smaller increases in IL-17 levels. A lesser induction of T H 1-associated genes was detected in acute Disease, although some were significantly upregulated in chronic Disease. Further significant intensification of major T H 22 and T H 2 cytokines was observed between acute and chronic lesions. Conclusions Our data identified increased S100A7, S100A8, and S100A9 gene expression with AD initiation and concomitant activation of T H 2 and T H 22 cytokines. Our findings support a model of progressive activation of T H 2 and T H 22 immune axes from the acute to chronic phases, expanding the prevailing view of pathogenesis with important therapeutic implications.

Elizabeth I Majeski - One of the best experts on this subject based on the ideXlab platform.

  • differential role for t cells in the development of fibrotic lesions associated with reovirus 1 l induced bronchiolitis obliterans organizing pneumonia versus acute respiratory distress syndrome
    American Journal of Respiratory Cell and Molecular Biology, 2003
    Co-Authors: Elizabeth I Majeski, Russell A Harley, Stephen C Bellum, Steven D London, Lucille London
    Abstract:

    Bronchiolitis obliterans organizing pneumonia (BOOP) and Acute Respiratory Distress Syndrome (ARDS) are two pulmonary Diseases with fibrotic components. BOOP is characterized by perivascular/peribronchiolar leukocyte infiltration leading to the development of intra-alveolar fibrosis. ARDS is a Biphasic Disease that includes an acute phase, consisting of severe leukocyte infiltration, edema, hemorrhage, and the formation of hyaline membranes, and a chronic phase, which is characterized by persistent intra-alveolar and interstitial fibrosis. CBA/J mice infected with 1 × 106 plaque-forming units (pfu) reovirus 1/L develop follicular bronchiolitis and intra-alveolar fibrosis similar to BOOP. In contrast, CBA/J mice infected with 1 × 107 pfu reovirus 1/L develop histologic characteristics of ARDS including diffuse alveolar damage, hyaline membranes, and intra-alveolar fibrosis. In this report, we demonstrate a differential role for T lymphocytes in the development of fibrosis associated with BOOP versus ARDS. ...

  • differential role for t cells in the development of fibrotic lesions associated with reovirus 1 l induced bronchiolitis obliterans organizing pneumonia versus acute respiratory distress syndrome
    American Journal of Respiratory Cell and Molecular Biology, 2003
    Co-Authors: Elizabeth I Majeski, Russell A Harley, Stephen C Bellum, Steven D London, Lucille London
    Abstract:

    Bronchiolitis obliterans organizing pneumonia (BOOP) and Acute Respiratory Distress Syndrome (ARDS) are two pulmonary Diseases with fibrotic components. BOOP is characterized by perivascular/peribronchiolar leukocyte infiltration leading to the development of intra-alveolar fibrosis. ARDS is a Biphasic Disease that includes an acute phase, consisting of severe leukocyte infiltration, edema, hemorrhage, and the formation of hyaline membranes, and a chronic phase, which is characterized by persistent intra-alveolar and interstitial fibrosis. CBA/J mice infected with 1 x 10(6) plaque-forming units (pfu) reovirus 1/L develop follicular bronchiolitis and intra-alveolar fibrosis similar to BOOP. In contrast, CBA/J mice infected with 1 x 10(7) pfu reovirus 1/L develop histologic characteristics of ARDS including diffuse alveolar damage, hyaline membranes, and intra-alveolar fibrosis. In this report, we demonstrate a differential role for T lymphocytes in the development of fibrosis associated with BOOP versus ARDS. Neonatally thymectomized CBA/J mice infected with 1 x 10(7) pfu (ARDS) reovirus 1/L still develop the hallmark characteristics of ARDS, including a severe viral pneumonia with cellular infiltrates comprised mainly of macrophages and neutrophils, hyaline membrane formation, and hemorrhage during the acute phase of the Disease and persistent intra-alveolar fibrosis during the chronic phase of the Disease. In contrast, neonatally thymectomized CBA/J mice infected with 1 x 10(6) pfu (BOOP) reovirus 1/L do not develop intra-alveolar fibrosis associated with BOOP. Therefore, while T cells are necessary for the development of intraluminal fibrosis associated with BOOP, they are not necessary for the development of intraluminal fibrosis associated with ARDS. Furthermore, we suggest that interferon-gamma plays a key role in the fibrotic process and that elevated levels of interferon-gamma are associated with a continuum from least to more severe fibrosis.

Robert E Johnston - One of the best experts on this subject based on the ideXlab platform.

  • the role of the blood brain barrier during venezuelan equine encephalitis virus infection
    Journal of Virology, 2011
    Co-Authors: Alexandra Schafer, Christopher B Brooke, Alan C Whitmore, Robert E Johnston
    Abstract:

    : Venezuelan equine encephalitis (VEE) virus is a mosquito-borne alphavirus associated with sporadic outbreaks in human and equid populations in the Western Hemisphere. After the bite of an infected mosquito, the virus initiates a Biphasic Disease: a peripheral phase with viral replication in lymphoid and myeloid tissues, followed by a neurotropic phase with infection of central nervous system (CNS) neurons, causing neuropathology and in some cases fatal encephalitis. The mechanisms allowing VEE virus to enter the CNS are currently poorly understood. Previous data have shown that the virus gains access to the CNS by infecting olfactory sensory neurons in the nasal mucosa of mice. However, at day 5 after inoculation, the infection of the brain is multifocal, indicating that virus particles are able to cross the blood-brain barrier (BBB). To better understand the role of the BBB during VEE virus infection, we used a well-characterized mouse model system. Using VEE virus replicon particles (VRP), we modeled the early events of neuroinvasion, showing that the replication of VRP in the nasal mucosa induced the opening of the BBB, allowing peripherally administered VRP to invade the brain. Peripheral VEE virus infection was characterized by a Biphasic opening of the BBB. Further, inhibition of BBB opening resulted in a delayed viral neuroinvasion and pathogenesis. Overall, these results suggest that VEE virus initially enters the CNS through the olfactory pathways and initiates viral replication in the brain, which induces the opening of the BBB, allowing a second wave of invading virus from the periphery to enter the brain.

  • mechanism of neuroinvasion of venezuelan equine encephalitis virus in the mouse
    Virology, 1995
    Co-Authors: Peter C Charles, Eric Walters, Frank L Margolis, Robert E Johnston
    Abstract:

    Venezuelan equine encephalitis virus (VEE) causes a Biphasic Disease in mice following subcutaneous inoculation in the footpad. In the initial phase, virus replicates primarily in the lymphoid tissues and induces a high titer viremia. Subsequently, the virus invades the central nervous system (CNS) from the circulation, and an encephalitis ensues. At the earliest times that VEE specific in situ hybridization signal was observed in the CNS, it was in areas of the brain involved in olfaction, leading to the hypothesis that virus may invade the brain from the circulation through the olfactory system. The results presented in this paper define the route of CNS invasion in experimental murine VEE Disease initiated by subcutaneous inoculation. Virus circulating in the blood appears to seed specific areas of the peripheral nervous system during the viremic lymphoid phase of the illness. Virus replication within olfactory and dental tissues is followed by centripetal spread of virus along neural pathways. Virus enters the brain in a pattern reflecting the proximity of the peripheral invasion site to the CNS. Specifically, virus is first found in the brain within the structures of the olfactory system, followed by areas innervated by the trigeminal nerve. Virus later disseminates along fiber tracts and connected circuits within the brain, resulting in a disseminated meningoencephalitis. Surgical or chemical interruption of the olfactory system at the level of the olfactory neuroepithelium or the main olfactory bulb inhibited entry of VEE into the CNS through the olfactory nerve. However, the olfactory route is not absolutely required for CNS invasion, as virus invaded the CNS of olfactory ablated animals through the trigeminal nerve. These observations are consistent with a model of hematogenous seeding of the peripheral nervous system, followed by invasion of the CNS by direct neural spread.