INT82448
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Depletion of neutrophils abrogated S-CorNV and S100A8 and S100A9 production | |||||||||||||||
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We further showed that depletion of neutrophils decreased S100A8 and S100A9 expression in S-CorNV corneas compared to control S-CorNV corneas (Figure 3). | |||||||||||||||
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Recently, S100A6, S100A8, and S100A9 were found to be extensively expressed in pterygium tissue removed from patients [41,42]. | |||||||||||||||
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The expression of S100A8/A9 has been investigated in several infection models. | |||||||||||||||
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We show that despite high S100A8/A9 expression in bladder and kidney tissue upon UTI, in this model S100A8/A9 does not contribute to an effective host response against E. | |||||||||||||||
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We anticipate that the S100A8/A9 expression we found originated from infiltrating granulocytes at infected areas. | |||||||||||||||
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Of these S100 proteins, S100A8/A9 are of special interest because S100A8/A9 complexes induce an inflammatory response and S100A8/A9 expression correlates with disease severity in several inflammatory disorders [9], [15]. | |||||||||||||||
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In addition, U. parvum-induced complicated UTI in rats, leads to higher expression of S100A8/A9 complex in bladder tissue compared to bladders from animals with asymptomatic UTI [17]. | |||||||||||||||
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CP-10, a chemotactic peptide, is expressed in lesions of experimental autoimmune encephalomyelitis, neuritis, uveitis and in C6 gliomas. | |||||||||||||||
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Using double labeling experiments, other cells participating in the inflammatory reaction were found to express CP-10, like few lymphoblastic W3/13+ cells in the vicinity of the inflammatory infiltrate. | |||||||||||||||
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It is concluded that this mouse model with infection by the CagA-positive, vac-toxin-producing H. pylori strain 119/95 is suitable for use in the study of lymphoma development and also development of squamous cell papilloma with proliferative features. | |||||||||||||||
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In situ hybridization clearly shows MRP14 to be expressed, in addition to expression in keratinocytes, in the region of the wound populated by inflammatory cells in the wild-type only (Figure 7Ak,l), and indeed, previous experiments suggest that both neutrophils and macrophages express MRP8 and MRP14 [22]. | |||||||||||||||
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Interestingly, another member of the late effector cluster, the intracellular Ca2+-binding protein MRP8 (S100A8) is expressed in a similar temporal and spatial pattern to K6 (Figure 4o and 4p). | |||||||||||||||
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The temporal and spatial coexpression of K6 with MRP8 may highlight a relationship between them and as such reveals another advantage of cluster analysis - the ability to identify potential interactions between genes and genetic pathways within the same cluster. | |||||||||||||||
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Interestingly, another member of the late effector cluster, the intracellular Ca2+-binding protein MRP8 (S100A8) is expressed in a similar temporal and spatial pattern to K6 (Figure 4o and 4p). | |||||||||||||||
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Immunohistochemistry analysis of the S-CorNV corneas showed that S100A8 and S100A9 were deposited in the neovascularized corneas (Figure 2). | |||||||||||||||
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To conclude, we found that S100A8 and S100A9 were involved in the inflammatory CorNV model. | |||||||||||||||
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Considering the above observation that S100A8 and S100A9 proteins are located in both neutrophils and macrophages (Figure 2), we suggest that S100A8 (and S100A9) produced by neutrophils attracted more neutrophils in turn, thus forming a positive feedback in certain stages of inflammatory CorNV. | |||||||||||||||
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Thus comparative studies of mice that are deficient in S100A8 or S100A9 (e.g., gene knockout mice of such genes) will help to determine how these two genes take their effects in the development of CorNV under various conditions. | |||||||||||||||
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Subconjunctival injection of anti-S100A8 mAb | |||||||||||||||
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General Comments
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