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

Acute murine cytomegalovirus (MCMV) infection alters the course of graft-vs-host (GVH) disease involving major histocompatibility (MHC) antigens and induces interstitial pneumonitis. F1 (B10 x B10.BR) mice given 20 x 10(6) B10.BR spleen cells and MCMV (1 x 10(5) plaque-forming units [PFU]) develop severe, diffuse pneumonitis not seen with either MCMV or GVH alone. As one index of the host immune processes operating in the lungs during MCMV/GVH pneumonitis, we examined the types of cells recovered from the lung by bronchoalveolar lavage (BAL) during pneumonitis. During MCMV/GVH pneumonitis, the total cells recovered significantly increased, due primarily to an influx of Thy 1.2 lymphocytes. Characterization of cells using multiparameter flow cytometric analysis revealed that greater than 80% of all BAL cells were Thy 1.2-positive lymphocytes of donor origin. In addition, donor Thy 1.2-positive cells were of both the L3T4+ (43% of BAL cells) and Lyt 2+ (38% of BAL cells) phenotype. Thus, MCMV infection during GVH to MHC antigens induces interstitial pneumonitis, characterized by an influx of T lymphocytes (both helper and suppressor/cytotoxic) from the donor. The antigenic specificity of these cells is not known.
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PMID:Interstitial pneumonitis during murine cytomegalovirus infection and graft-versus-host reaction. Characterization of bronchoalveolar lavage cells. 244 6

A 62-year-old male, was admitted on Oct. 7, 1987 because of productive cough and dyspnea. He worked for an iron factory, where pneumoconiosis was regarded as an occupational disease, for 40 years. No abnormal finding had been noted on his mass screening chest roentgenograms. He was well until three years ago when hypertension and Parkinsonism were noted. Since then he was treated with beta blockers, L-DOPA, amantadine and bromocriptine. Two weeks before admission, he suddenly complained of dyspnea and productive cough. His chest roentgenograms showed diffuse reticulonodular infiltration in both lung fields. The partial pressure of oxygen of the arterial blood was 65.9 Torr. The first transbronchial lung biopsy obtained from right B8 on Sept. 29, 1987 (before the admission) revealed some epithelioid granulomas and the second biopsy obtained from right B10 on Oct. 14, 1987 demonstrated bronchiolar edema and infiltration of inflammatory cells. Fibrotic changes associated with carbon dust between airways and vessels were also noted. Lymphocyte stimulation index by bromocriptine was 362%, and that by amantadine, 139%, L-DOPA, 150%, respectively. After ceasing the administration of bromocriptine, productive cough, dyspnea and the reticulonodular shadows diminished gradually. These findings strongly suggest that the interstitial pulmonary lesions are bromocriptine-induced interstitial pneumonitis. His occupational exposure to inorganic dust may be a predisposing factor.
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PMID:[A case of bromocriptine-induced interstitial pneumonitis in an iron factory worker exposed to sand dust]. 261 76

Irradiated (CBA x B10)F1 hybrid mice were injected with parental T lymphocyte-depleted bone marrow cells, (BMC), or with parental BMC together with T lymphocytes in an amount inducing greater than 80% mortality by day 40. Recipients of T cell depleted BMC did not show any mortality or significant pulmonary alterations, whereas recipients of BMC with T lymphocytes showed an alveolitis during the acute phase of the graft-versus-host reaction (GVHR) (day 15 to 25), characterized by: (a) alveolar hemorrhages, (b) increase of the number of alveolar leukocytes, (c) platelet microthrombi, (d) damage of the alveolar endothelial and epithelial cells, (e) increase of the turnover rate of the alveolar cells as shown by 3HTdR labelling, (f) increase in cell number and protein content of the bronchoalveolar lavage. These lesions were severe in the B10 versus F1, but absent in the reciprocal CBA versus F1 GVHR combination. The alveolitis was associated with a marked increase in the level of tumor necrosis factor-alpha mRNA, as shown by Northern gel analysis of lung RNA and was partially prevented by passive immunization with a rabbit anti-mouse tumor necrosis factor-alpha antibody. Mice examined after 25 days of evolution (i.e., chronic GVHR) presented an interstitial pneumonitis characterized by the accumulation of mononucleated cells, resembling large granular lymphocytes, which infiltrated first the intima of the blood vessels, and subsequently the interstice and the bronchi. These data demonstrate that the GVHR alone (in the absence of chemotherapy or overt infection) can induce two types of pneumopathies, an alveolitis and an interstitial pneumonitis.
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PMID:Pneumopathies of the graft-versus-host reaction. Alveolitis associated with an increased level of tumor necrosis factor mRNA and chronic interstitial pneumonitis. 274 16