Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0206061 (interstitial pneumonia)
 6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferon-gamma knockout (IFN-gamma KO) mice were infected with Sarcocystis neurona merozoites to characterize the immunopathology associated with infection. By day 14 postinfection (PI), mice developed splenomegaly and lymphadenopathy, characterized by marked lymphoid hyperplasia with increased numbers of germinal centers. Additional histopathologic changes included increased extramedullary hematopoiesis, multifocal mixed inflammatory infiltrates in the liver, perivascular infiltrate of the liver and lung, and interstitial pneumonia. The total number of B-cell splenocytes (P < 0.05) and the percentage of B-cells increased on day 14 PI in the spleen and on day 28 PI in the lymph nodes (P < 0.05). By day 28 PI, the number of B-cell splenocytes decreased significantly. A non-subset-specific decrease in percentages of CD4 lymphocytes throughout all lymphoid organs was observed on day 14 PI. However, total CD4 and CD44/CD4 splenocytes increased significantly by day 28 PI. Early-activation CD8 lymphocytes were reduced in the blood and spleen, whereas memory CD8 lymphocyte percentages and total numbers were significantly increased. On the basis of the results, we propose that S. neurona-infected IFN-gamma KO mice are immunocompromised and unable to clear the infection. Thus, they develop B-cell exhaustion and a delayed, but sustained, increased number of memory CD4 and CD8 lymphocytes due to chronic antigen stimulation.
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PMID:Immunopathologic effects associated with Sarcocystis neurona-infected interferon-gamma knockout mice. 1462 40

Idiopathic pulmonary fibrosis (IPF) is the most common and severe form of idiopathic interstitial pneumonia. A recently proposed pathogenic model suggests that the concurrent action of cell senescence, exposure to cigarette smoke and mechanical stress due to respiratory lung movements lead to a localized exhaustion of tissue renewal capacity with eventual alveolar loss and abnormal lung remodeling. In this study we have compared the distribution of IPF lesions, as shown by TC radiological images, with the hypothetical distribution of maximal mechanical stress obtained by a simplified mathematical model. The geometry and distribution of stress as determined by our simulation are closely similar to those demonstrated in vivo in the lungs of patients with idiopathic pulmonary fibrosis using high resolution CT scan radiological imaging. These data argue in favor of the recently proposed contribution of mechanical stress to progressive damage and remodeling of lung parenchyma in IPF. The parameters of the model can be tuned on the age of the patients.
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PMID:Heterogeneous distribution of mechanical stress in human lung: a mathematical approach to evaluate abnormal remodeling in IPF. 2366 8