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)

mRNA from lungs of mice exposed to high-dose oxygen (greater than 95%) for 3 days demonstrated increased expression of the genes for tumor necrosis factor (TNF), interleukin-1, and interleukin-6 compared with mRNA from lungs of mice exposed to room air. Daily treatment of mice exposed to high-dose oxygen with an antibody to TNF improved survival compared with mice receiving a similar dose of control immunoglobulin G. Pretreatment of mice with repetitive sublethal intraperitoneal doses of recombinant human TNF for 3 days or a single intravenous dose followed by exposure to high-dose oxygen afforded a significant survival advantage compared with high-dose oxygen-exposed mice pretreated with vehicle or interleukin-1. The repetitive intraperitoneal TNF pretreatment reduced the development of interstitial pneumonitis, pulmonary edema, and lung weight gain associated with oxygen toxicity and enhanced expression of the gene for the free radical protective enzyme manganous superoxide dismutase in lung tissue, a gene that is augmented as mice are exposed to high-dose oxygen. Furthermore a single intravenous dose of TNF 24 h after oxygen exposure was still protective. The results suggest that the toxicity of oxygen therapy can be partially ameliorated by either treatment with anti-TNF antibody or pretreatment and early treatment with TNF. These findings are consistent with the hypothesis that oxygen exposure induces TNF, which causes part of the toxicity of high-dose oxygen, and that pretreatment or early treatment with TNF induces the gene for an enzyme that recently has been shown to be very effective in protecting mice from the toxicity of oxygen.
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PMID:Role of tumor necrosis factor in oxygen toxicity. 160 98

We measured the serum concentrations of tumor necrosis factor (TNF-alpha), interleukin 1-beta (IL-1-beta), p24 antigen, CD4+/CD8+ cells and immunoglobulins in 35 children at various stages of human immunodeficiency virus infection. Serum TNF-alpha concentrations were significantly higher in children with lymphocytic interstitial pneumonitis and in children with mildly symptomatic illness than in asymptomatic children or children with acquired immunodeficiency syndrome. In addition serum IL-1 concentrations were significantly higher in patients with lymphocytic interstitial pneumonitis than in asymptomatic, mildly symptomatic, or acquired immunodeficiency syndrome patients. Children with lymphocytic interstitial pneumonitis had the highest serum TNF-alpha and IL-1 concentrations. Among symptomatic children serum TNF-alpha concentrations correlated positively with those of IL-1, and both were inversely related to the amount of p24 antigen. TNF-alpha values in excess of 50 pg/ml were observed more frequently among patients with CD4+ cell count greater than 400/mm3 than in those with CD4+ cell count less than 400/mm3. We did not find any association between elevated TNF-alpha concentrations and cachexia, opportunistic infections or progressive encephalopathy.
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PMID:Serum tumor necrosis factor alpha, interleukin 1-beta, p24 antigen concentrations and CD4+ cells at various stages of human immunodeficiency virus 1 infection in children. 167 77

Follow-up studies on the release of tumor necrosis factor-alpha (TNF-alpha) in 114 patients confirm that this cytokine is released early in the course of endothelial complications, acute graft-versus-host disease, and interstitial pneumonitis following allogeneic bone marrow transplantation. Possible sources of systemic TNF-alpha activity are, in particular, tissue macrophages of the recipient type that are stimulated by pretransplant conditioning and endotoxin and subsequently further activated by interferon gamma released by donor lymphocytes. Consideration of these interactions permits the early recognition of high-risk patients, and suggests new strategies for prophylaxis and treatment of complications.
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PMID:[TNF-alpha in allogeneic bone marrow transplantation. Significance for immunologic reconstitution, acute graft versus host disease and risk of complications after bone marrow transplantation]. 185 57

A 63-aged woman with cutaneous T cell lymphoma successfully treated with local administration of tumor necrosis factor (TNF) was reported. She was admitted to our hospital because of tumors and subcutaneous nodules on her bilateral inner thigh. A pathological study of her skin of right inner thigh showed mononuclear atypical cells with hyperlobulated nuclei. In peripheral blood the same lymphoid cells were found. Immunohistochemical staining of these cells was positive for OKT-3 and OKT-4, but negative for OKT-8. No lymph node swelling and no visceral involvement were detected by a CT scan and a Echography of the chest and the abdomen. A diagnosis of cutaneous T cell lymphoma was made (stage IIb TNM classification). Although the chemotherapy of VEPA and CHOP was done, about 70% (PR) of the bilateral inner thigh tumors were retracted. Owing to the interstitial pneumonia aroused in the period of bone marrow suppression and cardiomyopathy after chemotherapy, we gave up further systemic chemotherapy. And then the local administration of TNF was done and the disappearance of the bilateral inner thigh tumors was obtained. Our therapy with local administration of TNF for CTCL in the first report.
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PMID:[A case of cutaneous T cell lymphoma improved with local administration of tumor necrosis factor]. 262 96

Rats treated with recombinant human tumor necrosis factor-cachectin, 100 micrograms/kg ip twice daily for 5 consecutive days, had a 56% decrease in food intake, a 54% decrease in nitrogen balance, and a 23-g decrease in body weight gain vs. saline-treated controls. Concurrent neutral protamine hagedorn insulin administration of 2 U/100 g sc twice daily reversed all of these changes to control levels without causing any treatment deaths. The improvement seen with insulin was dose independent. Five days of cachectin treatment caused a severe interstitial pneumonitis, periportal inflammation in the liver, and an increase in wet organ weight in the heart, lungs, kidney, and spleen. Concurrent insulin treatment led to near total reversal of these histopathologic changes. Cachectin treatment did not significantly change blood glucose levels from control values of 130-140 mg/dl, but insulin plus cachectin caused a significant decrease in blood glucose from 1 through 12 h after injection. Administration of high-dose insulin can near totally reverse the nutritional and histopathologic toxicity of sublethal doses of cachectin in rats.
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PMID:Reversal of the toxic effects of cachectin by concurrent insulin administration. 266 May 86

Trehalose dimycolate is a glycolipid component of the cell walls of mycobacteria, nocardia, and corynebacteria. When trehalose dimycolate is injected into certain strains of mice, they develop interstitial pneumonitis that is characterized by mononuclear cell infiltration of the alveolar walls, intra-alveolar hemorrhages, and in some animals, granuloma formation. The disorder is seldom fatal, and in approximately 4 weeks, the lungs are normal. There is strong evidence that T lymphocytes are essential for production of interstitial pneumonitis by trehalose dimycolate, but little is known about the mechanisms of lung injury in this model. The experiments described in this report were conducted to identify the roles of the various cells that accumulate in the lungs of mice with this form of interstitial pneumonitis. We found that Mac3+ macrophages were the first cells to appear in the alveolar walls. Increases in the number of L3T4+ T lymphocytes, Lyt2+ T lymphocytes, and surface-immunoglobulin-positive lymphocytes followed, but significant increases in the number of lymphoid cells were not observed until day 7, when the pulmonary lesions were well developed. Treatment of the mice with cyclophosphamide or anti-T-cell sera significantly reduced the number of lymphoid cells in the alveolar walls but did not affect the number of Mac3+ cells and did not affect development of intra-alveolar hemorrhages. Treatment with poly(I.C) significantly decreased the number of Mac3+ cells in the lungs, and these mice did not develop pulmonary hemorrhages. We conclude that although development of pulmonary lesions in trehalose dimycolate-treated mice is a T-cell-dependent process, macrophages are also essential and are more directly involved in production of the lung injury. We postulate that the lung lesions are the direct effect of macrophage-produced cytokines, such as tumor necrosis factor.
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PMID:Phenotypes of infiltrating cells in trehalose dimycolate-induced interstitial pneumonitis. 273 85

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

Cord factors are mycoloyl glycolipids in cell walls of bacteria belonging to Actinomycetales, such as Mycobacterium, Nocardia and Rhodococcus. They induce granuloma formation in the lung and interstitial pneumonitis, associated with production of macrophage-derived cytokines. We studied how cord factors induce biological activities in the cells. Cord factors isolated from M. tuberculosis, trehalose 6-monomycolate (mTMM) and trehalose 6,6'-dimycolate (mTDM), enhanced protein kinase C (PKC) activation in the presence of phosphatidylserine (PtdSer), diacylglycerol and Ca2+, and mTMM activated PKC alpha more strongly than PKC beta or gamma under the same assay conditions. Kinetic studies of mTMM in response to PKC activation revealed that mTMM increased the apparent affinity of PKC to Ca2+ in the presence of both PtdSer and diolein. Although this is similar to observations with unsaturated fatty acids, such as arachidonic acid, mTMM was synergistic with PtdSer for PKC activation, but arachidonic acid was not. mTMM was also different as regards PKC activation, as phorbol ester was. A single i.p. administration of mTMM to mouse induced tumor necrosis factor-alpha (TNF-alpha) in serum and in the lung, which is a unique target tissue of cord factors. Based on our recent finding that TNF-alpha is an endogenous tumor promoter, the correlation between lung cancer and pulmonary tuberculosis is discussed.
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PMID:Activation of protein kinase C by mycobacterial cord factor, trehalose 6-monomycolate, resulting in tumor necrosis factor-alpha release in mouse lung tissues. 755 98

We retrospectively analyzed the clinical presentation of non-insulin-dependent diabetes mellitus (NIDDM) in patients with idiopathic interstitial pneumonia (IIP). Between 1977 to 1993, 75 patients with IIP were admitted to our hospital. None had previously received corticosteroids. To compare the incidence of NIDDM with other pulmonary diseases and the degree of obesity, we randomly selected 200 patients without IIP who were admitted to our hospital in 1992 and 160 healthy subjects. We analyzed weight indices using two methods, body mass index and weight as a percentage of ideal body weight. Eighteen patients (24.0%) with IIP and 9 patients (4.5%) in the disease control group had NIDDM (p < 0.001). As the incidence of NIDDM is approximately 10% in Japan, it was suggested that these IIP patients showed a high prevalence of accompanying NIDDM. Among females, patients with IIP showed a strong tendency toward obesity compared with the healthy control subjects (p < 0.001), but this was not noted among males. Female patients with NIDDM showed a strong tendency toward obesity compared to those without NIDDM, but this was not noted among males. Although the correlation between IIP and NIDDM is unclear, we noted recent reports that advanced glycation and products can stimulate macrophages to secrete tumor necrosis factor and interleukin-1 in vitro, and can stimulate free radical generation by early glycation products in vitro. These cytokines and oxygen radicals may play a role in the pathogenesis or induction of IIP.
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PMID:[Clinical study of patients with idiopathic interstitial pneumonia accompanied by diabetes mellitus]. 785 68

A mouse model of spotted fever group rickettsiosis, in which disease results from disseminated rickettsial infection of endothelial cells and vascular damage, was developed by intravenous inoculation of 6- to 8-week-old, male, Balb/c mice with Rickettsia australis. Animals developed progressively severe vasculitis, interstitial pneumonia, and multifocal hepatic necrosis. These lesions correlated with early disseminated infection of endothelial cells followed by growth and invasion of rickettsiae into perivascular cells. The dose of 2 x 10(6) organisms was uniformly lethal. Serum interleukin- (IL) 1, IL-6, and interferon (IFN) increased by day 3 and tumor necrosis factor (TNF) on day 5. TNF, IL-6, and IFN declined on day 7. Spleen cells responded to Rickettsia australis antigen by producing IFN, TNF, IL-1, and IL-6 on day 5, followed by lower quantities of these cytokines on day 7. Despite the production of antibodies, IFN, TNF, IL-1, and IL-6, a lethal outcome occurred frequently. A decreased ability to secrete IL-2 suggests an element of infection-associated immunosuppression.
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PMID:Rickettsia australis infection: a murine model of a highly invasive vasculopathic rickettsiosis. 849 48


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