Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

C4b-binding protein is a regulatory factor for both complement and coagulation systems. We found that a human hepatoma cell line, Hep G2, was capable of synthesizing C4b-binding protein and that the secretion of C4b-binding protein was enhanced by interleukin-6 and tumor necrosis factor, which are known to be modulators of acute phase proteins. In addition, the plasma content of C4b-binding protein was found to increase in patients of acute pneumonia. These results suggest that C4b-binding protein is an acute phase protein.
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PMID:Evidence that C4b-binding protein is an acute phase protein. 248 Jan 19

Pneumocystic carinii pneumonia, which is a major cause of death among patients suffering from acquired immunodeficiency syndrome, has often been treated successfully with pentamidine isethionate. This study examines pentamidine effects on cellular and secreted proteins from rat alveolar macrophages by two-dimensional gel electrophoresis and computerized image analysis. Over 100 secreted proteins were detected by fluorography. Fluorography showed pentamidine diminished tumor necrosis factor and interleukin-1 release along with other proteins. Effects of combined bacterial lipopolysaccharide and pentamidine were more pronounced on secreted versus cellular proteins in protein amount and pattern difference. Thus pentamidine exhibited a general repressive effect on cellular and secreted protein expression in resting and activated macrophages.
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PMID:Gel electrophoretic analysis of cellular and secreted proteins from resting and activated rat alveolar macrophages treated with pentamidine isethionate. 758 50

We examined the kinetics of tumor necrosis factor (TNF) production induced by Escherichia coli lipopolysaccharide (LPS) in relation to LPS tolerance and endotoxemic lesions of piglets. The plasma of piglets demonstrated cytotoxicity to TNF-sensitive L929 cells between 0.5 and 4 h after inoculation with 200 micrograms kg-1 of LPS. This cytotoxicity was neutralized by anti-bovine TNF serum. These piglets had disseminated intravascular coagulation (DIC) and meningoencephalitis. However, if piglets were first treated with three doses of 40 micrograms kg-1 of LPS, both TNF production and the occurrence of DIC were inhibited when 200 micrograms kg-1 of LPS was inoculated into these piglets. Repetitive inoculation with increasing doses of LPS induced fibrinoid vasculitis, meningoencephalitis and pneumonitis, while hemorrhage was minimal. A very low amount of TNF activity was detected from most of the samples of a piglet after repeated LPS inoculation. These results suggested that severity of the hemorrhagic and thrombotic lesions might relate to the amount of endogenous TNF activity, and that LPS tolerance might relate to inhibition of TNF production.
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PMID:Endogenous tumor necrosis factor (TNF) production and modification of pathological lesions in experimental Escherichia coli endotoxemia of piglets. 760 37

Critical illness is often associated with gram-negative bacterial colonization of the airways, increasing the risk of nosocomial pneumonia. Cytokines, released in response to endotoxin, might contribute to this phenomenon by causing changes in epithelial cell binding of bacteria. To investigate this possibility, human monocytes and hamster pulmonary macrophages were cultured without or with Escherichia coli endotoxin (10 micrograms/ml) for 4 and 24 h. Hamster and human tracheal epithelial cells were treated with supernates from monocyte cultures for 24 h, and subsequent binding of 14C-labeled Pseudomonas aeruginosa to the epithelial cells was measured (percent adherence). In separate experiments, recombinant human (rh) tumor necrosis factor-alpha (TNF-alpha) (25 to 100 ng/ml) and interleukin-1 beta (IL-1 beta) (2,000 to 8,000 pg/ml) were added to hamster monolayers. Neither monocyte supernates nor purified cytokines were toxic to the epithelial cells for up to 48 h. There was no significant change in P. aeruginosa adherence to either hamster or human tracheal epithelial cells after 24 h of exposure to culture supernates from either endotoxin-stimulated human monocytes or hamster macrophages. Similarly, purified rhTNF and rhIL-1 exposure did not increase bacterial adherence. However, when polymorphonuclear leukocytes were coincubated with the monocyte supernates and epithelial cells, P. aeruginosa adherence was significantly increased. Moreover, this effect was enhanced by an epithelial cell-derived substance. Thus, while inflammatory cytokines may participate in enhancing bacterial colonization of the lung in vivo, they do not do so by a direct action on tracheal epithelial cells but can act via a neutrophil-dependent mechanism.
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PMID:Cytokines affect pseudomonas binding to tracheal cells via a neutrophil-mediated process. 766 5

In order to elucidate the role played by alveolar cytokines in the pathogenesis of HIV-related lung damage, levels of interleukin (IL) 1 beta, IL-2, IL-6, tumor necrosis factor (TNF)-alpha, and interferon (Ifn) were assessed on supernatant of bronchoalveolar lavage fluid from 30 consecutive HIV-1 seropositive (HIVAb+) patients with clinical and radiologic evidence of pneumonia, from 20 HIV- seronegative (HIVAb-) patients with pulmonary sarcoidosis, and from 10 HIVAb- healthy control subjects. Cytokine levels were expressed as picogram (IL-1, TNF), nanogram (IL-6), and international unit (IL-2, Ifn) per milligram of albumin per deciliter. Total and differential cell counts, cytofluorimetric enumeration of CD3+, CD3+/DR+, CD4+, CD8+, and CD8+/CD16+ cells, as well as microbiologic investigations for opportunistic agents were performed on lavage pellets. HIV-related pneumonia was characterized by higher mean alveolar level of IL-2 (12 +/- 5 IU), and by more elevated mean counts of T cells (109 +/- 16), activated T cells (60 +/- 12), and CD8+ cells (90 +/- 13)/microliters if compared with both active sarcoidosis and control subjects, where respective values of 0.2 +/- 0.1 and 0.3 +/- 0.2 IU IL-2/mgAlb/dl, of 52 +/- 11 and 7 +/- 2 T cells, of 20 +/- 5 and 1.2 +/- 0.3 activated T cells, and of 11 +/- 2 and 3 +/- 0.6 CD8+ cells per microliter were found. HIV-infected patients with opportunistic lung infections (OIs) showed the highest mean IL-2 level (21 +/- 4 IU), and higher counts of both CD8+ (117 +/- 20) and CD8+/CD16+ (36 +/- 7) cells per microliter if compared with patients without evidence of OIs (respectively, 62 +/- 13 CD8+ and 18 +/- 3 CD8+/CD16+ cells per microliter). By contrast, extremely high IL-1 levels (1,463 +/- 760 pg), and IL-2 levels similar to control subjects (3.4 +/- 1.2 IU), were found in the absence of OIs. Different mechanisms depending respectively on IL-2-mediated cytotoxic cell recruitment and activation, or IL-1-mediated tissue injury may account for HIV-related lung damage, depending on the presence or absence of opportunistic agents.
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PMID:Alveolar immune mediators in HIV-related pneumonia. Different role of IL-2 and IL-1 in inducing lung damage. 767 46

Corynebacterium pseudotuberculosis infection is a common cause of pyogranulomas in ovine lungs and often occurs as a dual infection with lentiviruses. This coinfection usually leads to the development of chronic pneumonia and cachexia that is similar to the clinical syndrome seen in human beings with AIDS-related pneumonias. Recent in vitro studies indicate that monokines such as tumor necrosis factor-alpha (TNF alpha) are induced by C. pseudotuberculosis, suggesting that TNF alpha is involved in the pathogenesis of corynebacterial lesions in vivo. To substantiate in vitro observations concerning bacterial induction of TNF alpha in ovine pulmonary macrophages, immunohistochemical labeling techniques were used in combination with in situ hybridization to identify TNF-producing cells in corynebacterial lesion sites in vivo. TNF alpha message and translation product were found in macrophages comprising pyogranulomas that were induced by naturally acquired and experimental pulmonary C. pseudotuberculosis infections.
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PMID:Local production of tumor necrosis factor-alpha in corynebacterial pulmonary lesions in sheep. 772 1

Alcohol exerts potent suppressive effects on the immune system that significantly increase host susceptibility to a variety of infections, particularly pneumonia. Historically, tuberculosis has been strongly associated with alcohol abuse. Although the relationship between alcohol abuse and tuberculosis is widely appreciated, the basic mechanisms by which alcohol immunosuppresses the host remain to be clarified. A major obstacle in furthering our understanding of this association has been the difficulty in distinguishing between the effects of alcohol per se and the other frequent sequelae of alcoholism such as nutritional deficiencies, liver disease, cigarette smoking, hygienic factors, and lifestyle. This article focuses on the role of tumor necrosis factor-alpha (TNF) in host defense and how alcohol modulates the activity of this important cytokine. While TNF's role in mediating the lethal consequences of infection has been the subject of much conjecture, this review focuses on the emerging evidence that TNF is an essential factor in the normal immune response to numerous infections, including tuberculosis.
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PMID:Alcohol, tumor necrosis factor, and tuberculosis. 777 45

The efficacy of treatment with interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF alpha) on Pseudomonas aeruginosa pneumonia was evaluated in a granulocytopenic mouse model. Combined intravenous administration of 2000 U IL-1 beta plus 2000 U TNF alpha significantly diminished mortality from aerosol challenge with P. aeruginosa. Mice treated with IL-1 beta, TNF alpha, or both also exhibited a significant enhancement in pulmonary clearance of P. aeruginosa. Combined cytokine administration induced an increase in the pulmonary content of myeloperoxidase activity. Mature leukocytes were not detected in either circulation or bronchoalveolar lavage fluid from granulocytopenic, cytokine-treated mice. In conclusion, IL-1 beta and TNF alpha treatment exhibited a synergistic protective effect from pulmonary P. aeruginosa challenge in granulocytopenic hosts, probably due to enhancement of nonspecific antibacterial mechanisms.
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PMID:The effect of treatment with interleukin-1 and tumor necrosis factor on Pseudomonas aeruginosa lung infection in a granulocytopenic mouse model. 792 33

Two types of tumor necrosis factor membrane receptors (TNF-R) have been identified, namely 55 and 75 kDa TNF-R. Soluble forms of these receptors are present in the human serum. Recent findings on the role of these two TNF-R in biological cell signaling and the clinical significance of the serum levels of soluble TNF-R (sTNF-R) were reviewed. It is not the uptake of TNF molecules into cells but rather the molecular capping of TNF-R on the cell membrane that initiates the biological activity of TNF. The 55 kDa TNF-R mediates major bioactivities of TNF, while the significance of 75 kDa TNF-R remains unclear. We herein suggest a new concept of the role of these two TNF-R: The 75 kDa TNF-R signal appeared to enhance that of 55 kDa TNF-R in the induction of ICAM-1 expression on HL-60 human promyelocytic leukemic cells. High serum levels of sTNF-R are reported in patients with malignancy, endotoxin shock, pneumonia, and autoimmune diseases. However, the source of elevated serum sTNF-R remains unclear. Studies on the clinical usefulness of serum sTNF-R levels as cancer and inflammation markers are now being carried out.
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PMID:The role of tumor necrosis factor receptors in cell signaling and the significance of soluble form levels in the serum. 800 60

Two distinct types of tumor necrosis factor receptors (TNF-R) have been identified (TNF-R55 and TNF-R75). Both TNF-R also exist in soluble forms (TNF-sR), resulting from the release of the extracellular domains (TNF-sR55 and TNF-sR75). TNF-sR may play an important role in vivo as they can bind to TNF alpha and prevent ligand binding to the cellular TNF-R, thus acting as naturally occurring inhibitors of TNF alpha. Sera from lung allograft recipients with cytomegalovirus (CMV) pneumonitis (12 patients) were assayed for TNF-sR55 and TNF-sR75. The concentrations were compared with those from either control lung recipients displaying neither rejection nor infection (12 patients), or lung recipients with allograft rejection (12 patients). Serum TNF-sR55 and TNF-sR75 concentrations were measured by enzyme-linked immunologic binding assay. Serum TNF-sR55 and TNF-sR75 concentrations were significantly higher during CMV pneumonitis (mean +/- SEM: 13.7 +/- 4.7 ng/ml, and 11.7 +/- 2.7 ng/ml, respectively) than during allograft rejection (3.7 +/- 0.3 ng/ml, p < 0.001, and 2.6 +/- 0.6 ng/ml, p < 0.001, respectively). They were also higher than in control subjects (3.6 +/- 0.3 ng/ml, p < 0.001, and 1.9 +/- 0.5 ng/ml, p < 0.001, respectively). Serum TNF alpha concentration was low in case of rejection or in control subjects (< 20 pg/ml). Conversely increased levels of TNF alpha were detected in the serum of six out of the 12 patients with CMV pneumonitis (p < 0.03 versus rejection and control subjects). Ganciclovir treatment of CMV pneumonitis led to a dramatic decrease of TNF alpha, TNF-sR55, and TNF-sR75 serum levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Soluble TNF receptors (TNF-sR55 and TNF-sR75) in lung allograft recipients displaying cytomegalovirus pneumonitis. 800 30


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