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)

In BALB/c mice, murine cytomegalovirus (MCMV) in conjunction with a single dose of cyclophosphamide (CP) induces a diffuse interstitial pneumonitis not seen with either virus or CP alone. To gain insight into the host immune mechanisms operating in the lung during interstitial pneumonitis, we examined the cells recovered in bronchoalveolar lavage (BAL) fluids of mice with MCMV with and without CP. During MCMV interstitial pneumonitis, there was a significant increase in the total BAL cells recovered, primarily because of an influx of lymphocytes bearing the Thy 1.2 marker. Although the number of cells with Lyt 1 and Lyt 2 markers increased, the most significant increase was in the proportion of lymphocytes with surface asialo-GM1. Delineating the roles of these various cell populations may provide insight into the pathogenetic mechanisms leading to CMV interstitial pneumonitis.
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PMID:Alteration of bronchoalveolar cells during murine cytomegalovirus interstitial pneumonitis. 299 Feb 72

Mice bearing the 'auto-immune' lpr gene develop a lympho-proliferative disease associated with the production of various antibodies. Lethally irradiated recipients were grafted with bone marrow cells (BMC) from syngeneic mice with or without the lpr gene. After 6 months, the survivors were 0/24 and 16/20 for the recipients of lpr and normal BMC respectively. The mortality rate was independent of the presence of T lymphocytes among the BMC. Histological evaluation showed that hepatitis, interstitial pneumonitis, and sclerosis of lymphohaemopoietic organs were the major causes of death for the recipients of lpr BMC. Hepatitis was associated with an increase in the number of liver interstitial cells (LIC) from about 2 X 10(6) up to about 10(7) cells per liver. The LIC associated with the hepatitis were composed of polymorphonuclear leucocytes and large mononuclear leucocytes, showing phenotypic (i.e. Thy.1+, asialo GM1, presence of cytoplasmic granules) and functional (i.e. non-phagocytic and cytolytic) properties of NK cells. The disease can be distinguished both from the spontaneous disease of the lpr mice (by the absence of 'lpr cells' and of anti-DNA antibodies) and from graft versus host disease by the absence of cutaneous and intestinal lesions. It may represent a model of tissue injury mediated by large granular leucocytes.
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PMID:Interstitial pneumonitis and hepatitis after transfer of bone marrow cells bearing the lpr gene to irradiated recipients: a disease due to large granular leucocytes? 332 8

This paper deals with two patients with acetaminophen-induced pneumonitis. A 64-year-old woman suffered from mastitis while being treated by corticosteroid therapy for phemphigoid. She was administered antibiotics and acetaminophen. However, her fever continued and she subsequently developed dyspnea and interstitial pneumonia. The other patient, a 70-year-old woman, was treated with corticosteroid for lower motor neuron disease. Anti-GM1-IgM antibodies were positive in her serum. She developed wet cough and mild fever. During treatment with antibiotics and acetaminophen, her illness was complicated by dyspnea and interstital pneumonia. As a result of histological findings of transbronchial lung biopsy specimens showing interstitial infiltration of mononuclear cells, as well as clinical courses in which cessation of acetaminophen directly lead to the improvement of interstitial pneumonia, both patients were diagnosed to have acetaminophen-induced pneumonitis. The peumonitis responded well to steroid therapy. In vitro culture of peripheral lymphocytes showed stimulated proliferation by acetaminophen in both patients. These findings suggest that allergic mechanism was involved in the pathogenesis of the pneumonitis. Underlying immunological disorders may have enhanced the occurrence. Although acetaminophen is one of the most popular drugs because of a very low incidence of side effects, this drug should be applied carefully, especially with patients who have such immunological disorders.
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PMID:[Two cases of acetaminophen-induced pneumonitis]. 939 56

Interleukin 18 (IL-18) was discovered as an interferon-gamma (IFN-gamma)-inducing factor and plays important roles in natural killer (NK) cell activation. IL-18 also induces proinflammatory cytokines; chemokines; helper T-cell 2 (T(H)2) cytokines (eg, IL-4, IL-13); and immunoglobulin E (Ig-E) and IgG1 production. The combination of IL-18 plus IL-2 or IL-12 up-regulates IFN-gamma gene expression and NK cytotoxicity and has synergistic antitumor activity in vivo and in vitro. Here it is reported that daily administration of IL-18 with IL-2, but not of IL-18 or IL-2 alone, induces lethal lung injury in normal mice, but not in IL-18 receptor alpha (IL-1 receptor-related protein)-deficient (IL-18 receptor alpha(-/-)) mice. Marked interstitial infiltration of lymphocytes, composed mainly of NK cells, was found in the lungs of IL-18/IL-2-treated mice. Increased cytokine and chemokine levels were observed in the sera and lungs of IL-18/IL-2-treated mice. Administration of IL-18/IL-2 was also lethal to mice treated with a metalloproteinase inhibitor, which inhibited tumor necrosis factor-alpha and Fas-ligand release. While IFN-gamma(-/-) mice were partially resistant to the treatment, IL-4(-/-), IL-13(-/-), IL-4/IL-13(-/-), and Stat6(-/-) mice were sensitive to IL-18/IL-2, indicating that these genes were not involved in the host response. The lethal effect by IL-18/IL-2 was completely eliminated in severe combined immunodeficient mice pretreated with antiasialo-GM1 antibody and normal mice pretreated with anti-NK1.1 but not with anti-CD4 or anti-CD8, monoclonal antibody. These results suggest that specific cytokines, chemokines, and NK cells are involved in the pathogenesis of interstitial pneumonia. These results suggest that the clinical use of this interleukin may result in unexpected physiological consequences.
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PMID:Interleukin 18 (IL-18) in synergy with IL-2 induces lethal lung injury in mice: a potential role for cytokines, chemokines, and natural killer cells in the pathogenesis of interstitial pneumonia. 1183 Apr 78