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Inflammatory Pathologies (inflammatory + pathology)

Distribution by Scientific Domains

Medical Sciences	60%
Life Sciences	40%

Selected Abstracts

Association between atmospheric ozone levels and damage to human nasal mucosa in Florence, Italy

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 3 2003
Stefania Pacini
Abstract We evaluated the effects of urban air pollutants on human nasal mucosa over an 8-month period on 102 subjects living in Florence, Tuscany, Italy. A group of subjects living in a city with a lower level of pollution (Sassari, Sardinia, Italy) was also analyzed. Nasal mucosa cells were harvested by brushing, a noninvasive procedure. Half of the cells were used for genotoxicity studies using the alkaline comet assay, and half for morphological studies. The levels of DNA damage in the nasal mucosa were considerably higher (+73%) in the subjects living in Florence than in Sassari. High levels of atmospheric ozone in Florence air correlated with DNA damage, and to the prevalence of inflammatory pathologies of the upper respiratory tract, although the ozone concentrations were below the Italian recommended attention level. Furthermore, higher levels of DNA damage were correlated with a dysfunction in the ability to maintain a normal epithelial cell structure. These data suggest an association between ozone air levels and damage in the upper respiratory tract. It remains unclear whether ozone itself or other associated pollutants are responsible for the observed alterations. Environ. Mol. Mutagen. 42:127,135, 2003. © 2003 Wiley-Liss, Inc. [source]

PET/CT in the assessment of previously treated skull base malignancies,

HEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 1 2010
Richard J. Harvey MD
Abstract Background Altered anatomy, radiotherapy, hardware, and reconstructive materials distort the posttreatment ventral skull base. The diagnostic characteristics of positron emission tomography/CT (PET/CT) studies in those with suspected recurrent malignancy were assessed. Methods A retrospective review was undertaken of patients with head and neck cancer who had PET/CT for ventral skull base disease. Results Thirty-four PET/CTs were performed for suspected recurrent malignancy in the skull base (mean age, 59.6 ± 10.7 years; female 38%). The group comprised mainly minor salivary (35.3%), squamous (32.3%), and neuroectodermal (23.6%) tumors. Mean clinical follow-up after PET/CT was 256 ± 173 days. Sensitivity was 100% but specificity was 40%. Standard uptake values (SUVs) for true positives were higher than for those without disease (p = .03). Conclusions PET/CT is a highly sensitive test for malignant disease. The mucosal lining of the reconstructed skull base is a common source for inflammatory pathologies that may lead to false-positive PET/CT. Defining SUV thresholds for malignancy may improve specificity. © 2009 Wiley Periodicals, Inc. Head Neck, 2010 [source]

Regulatory T cells in human disease and their potential for therapeutic manipulation

IMMUNOLOGY, Issue 1 2006
Leonie S. Taams
Summary Regulatory T cells are proposed to play a central role in the maintenance of immunological tolerance in the periphery, and studies in many animal models demonstrate their capacity to inhibit inflammatory pathologies in vivo. At a recent meeting [Clinical Application of Regulatory T Cells, 7,8 April 2005, Horsham, UK, organized by the authors of this review, in collaboration with the British Society for Immunology and Novartis] evidence was discussed that certain human autoimmune, infectious and allergic diseases are associated with impaired regulatory T-cell function. In contrast, evidence from several human cancer studies and some infections indicates that regulatory T cells may impair the development of protective immunity. Importantly, certain therapies, both those that act non-specifically to reduce inflammation and antigen-specific immunotherapies, may induce or enhance regulatory T-cell function. The purpose of this review was to summarize current knowledge on regulatory T-cell function in human disease, and to assess critically how this can be tailored to suit the therapeutic manipulation of immunity. [source]

CXCL12 chemokine up-regulates bone resorption and MMP-9 release by human osteoclasts: CXCL12 levels are increased in synovial and bone tissue of rheumatoid arthritis patients

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2004
Francesco Grassi
Chemokines are involved in a number of inflammatory pathologies and some of them show a pivotal role in the modulation of osteoclast development. Therefore, we evaluated the role of CXCL12 chemokine on osteoclast differentiation and function and we analyzed its expression on synovial and bone tissue biopsies from rheumatoid arthritis (RA) patients. Osteoclasts were obtained by 7 days in vitro differentiation with RANKL and M-CSF of CD11b positive cells in the presence or absence of CXCL12. The total number of osteoclast was analyzed by Tartrate-resistant acid phosphatase (TRAP)-staining and bone-resorbing activity was assessed by pit assay. MMP-9 and TIMP-1 release was evaluated by ELISA assay. CXCL12 expression on biopsies from RA patients was analyzed by immunohistochemistry. Osteoclasts obtained in the presence of CXCL12 at 10 nM concentration displayed a highly significant increase in bone-resorbing activity as measured by pit resorption assay, while the total number of mature osteoclasts was not affected. The increased resorption is associated with overexpression of MMP-9. Immunostaining for CXCL12 on synovial and bone tissue biopsies from both rheumatoid arthritis (RA) and osteoarthritis (OA) samples revealed a strong increase in the expression levels under inflammatory conditions. CXCL12 chemokine showed a clear activating role on mature osteoclast by inducing bone-resorbing activity and specific MMP-9 enzymatic release. Moreover, since bone and synovial biopsies from RA patients showed an elevated CXCL12 expression, these findings may provide useful tools for achieving a full elucidation of the complex network that regulates osteoclast function in course of inflammatory diseases. J. Cell. Physiol. 199: 244,251, 2004© 2003 Wiley-Liss, Inc. [source]

IL-23 and the Th17 pathway promote inflammation and impair antifungal immune resistance

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 10 2007
Teresa Zelante
Abstract Although inflammation is an essential component of the protective response to fungi, its dysregulation may significantly worsen fungal diseases. We found here that the IL-23/IL-17 developmental pathway acted as a negative regulator of the Th1-mediated immune resistance to fungi and played an inflammatory role previously attributed to uncontrolled Th1 cell responses. Both inflammation and infection were exacerbated by a heightened Th17 response against Candida albicans and Aspergillus fumigatus, two major human fungal pathogens. IL-23 acted as a molecular connection between uncontrolled fungal growth and inflammation, being produced by dendritic cells in response to a high fungal burden and counter-regulating IL-12p70 production. Both IL-23 and IL-17 subverted the inflammatory program of neutrophils, which resulted in severe tissue inflammatory pathology associated with infection. Our data are the first demonstrating that the IL-23/IL-17 pathway promotes inflammation and susceptibility in an infectious disease model. As IL-23-driven inflammation promotes infection and impairs antifungal resistance, modulation of the inflammatory response represents a potential strategy to stimulate protective immune responses to fungi. See accompanying commentary: http://dx.doi.org/10.1002/eji.200737804 [source]