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)

Differential cell counts and fibronectin levels were recorded in bronchoalveolar lavage fluids (BALF) from patients with lung cancer, idiopathic pulmonary fibrosis (IPF), sarcoidosis, pneumonia, acquired immunodeficiency syndrome (AIDS), and chronic obstructive lung disease (COLD). In all groups fibronectin levels were significantly higher than in the control group; patients with sarcoidosis had a six-fold higher fibronectin level (mean values), AIDS 5.4-fold, pneumonia 4.4-fold, lung cancer, IPF and COLD 2.4-3.0-fold. In control smokers the fibronectin level was significantly higher compared to healthy nonsmokers (p less than 0.002). The increased fibronectin levels could not be explained by contamination of BALF with blood or leakage of plasma proteins. Thus, increased fibronectin levels probably reflect local (e.g. macrophage/fibroblast) synthesis.
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PMID:Distribution of bronchoalveolar cells and fibronectin levels in bronchoalveolar lavage fluids from patients with lung disorders. 224 65

Attachment of pathogens to host cells is a prerequisite for the development of many infections. Pneumocystis carinii (PC) pneumonia is characterized by attachment of PC trophozoites to the alveolar epithelium. The mechanism of this process is unknown. Fibronectin (Fn) is a glycoprotein present in the alveolar space known to mediate cell-cell attachment, including the attachment of certain pathogens to host epithelial cells. In this study the binding of Fn to PC trophozoites has been characterized in vitro using 125I-Fn. Fn binds saturably and specifically to 6.4 x 10(5) binding sites per organism with an apparent binding constant, Kd, of 1.2 x 10(-8) M. Fn binding to PC was inhibited by the addition of Arg-Gly-Asp-Ser (RGDS), a tetrapeptide containing the active site of the cell-binding domain of Fn. PC attachment to an alveolar epithelial cell line was quantified using 51Cr-labeled PC trophozoites. Attachment was decreased from 24 +/- 1.9% to 12.1 +/- 1% (P less than 0.01) by the addition of an anti-Fn antibody, an effect that could be overcome by the addition of excess free Fn. It is concluded that binding of Fn to PC may be an important initial step in the attachment of the organism to alveolar epithelial cells. Furthermore, it appears that PC recognizes and binds to the RGDS cell attachment site of Fn.
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PMID:Role of fibronectin in Pneumocystis carinii attachment to cultured lung cells. 229 9

Idiopathic bronchiolitis obliterans-organizing pneumonia (BOOP) is characterized by air space fibrosis of unknown origin. Clinical resolution under steroid treatment suggests the removal of the fibrotic lesion. Open lung biopsies of four patients with idiopathic BOOP were studied by immunochemistry and electron microscopy. Three distinct cell-matrix patterns of intra-alveolar bud were found to represent the sequential evolution of the fibrotic process: fibrinoid inflammatory cell clusters in which immunoglobulins and procoagulant factors (fibrinogen, factors VII and X) were identified; fibroinflammatory buds in which desmin-containing fibroblasts were observed migrating, proliferating, and secreting matrix proteins; fibrotic buds in which myofibroblasts organized a loose connective matrix predominantly composed of fibronectin and type III collagen. Extending forms of fibrotic buds may join contiguous alveoli. Fibrotic bud remodeling ability is correlated to the nature and organization of the matrix components but the factors permitting intra-alveolar matrix degradation must be characterized.
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PMID:Intra-alveolar fibrosis of idiopathic bronchiolitis obliterans-organizing pneumonia. Cell-matrix patterns. 237 39

Plasma fibronectin (PFN) concentrations were assessed in 21 patients with AIDS, in seven with AIDS-related complex (ARC), in 17 asymptomatic seropositive patients, and in 36 age and sex matched healthy control subjects. A single radial immunodiffusion technique was used to determine PFN concentration. A significant decrease in PFN concentrations was observed in patients with ARC and AIDS (especially in those patients with Pneumocystis carinii pneumonitis). On the other hand, normal PFN concentrations were observed in asymptomatic seropositive patients. The determination of PFN concentration in patients with AIDS and ARC may contribute to the diagnosis of such patients.
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PMID:Plasma fibronectin concentrations in patients with human immunodeficiency virus infection. 238 Apr 4

Fibroblasts in healthy adult lung are quiescent, synthesizing little collagen. We studied lung biopsies from 30 patients with pulmonary fibrosis, using immunohistochemistry with monoclonal antibodies against the propeptides of type I collagen to localize fibroblasts actively synthesizing collagen. Adjacent sections were stained with antibodies to type III and IV collagen, fibrin, cytokeratin, plasma fibronectin, or EDIIIa-containing "cellular" fibronectin (cFN). In rapid pulmonary fibrosis, including the proliferative phase of diffuse alveolar damage, organizing pneumonia, and subacute idiopathic fibrosis, collagen-synthesizing cells were numerous in organizing exudate filling airspaces but were also seen in the interstitium of the alveolar walls, interlobular septa, and walls of blood vessels. The new matrix deposited in the airspaces also contained type III collagen and EDIIIa-containing fibronectin. In chronic pulmonary fibrosis, more than half of the biopsies showed foci of collagen synthesis and cFN deposition near the air-tissue interface. The foci were consistently localized outside remnants of basal lamina and therefore within airspaces. The results indicate that (1) fibrosis in chronic idiopathic pulmonary fibrosis results mainly from organization of exudate within airspaces, just as it does after acute lung injury, and (2) during this process, fibroblasts increase their synthesis of collagen and fibronectin coordinately. Foci of active matrix deposition provide evidence for the progressive nature of chronic pulmonary fibrosis.
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PMID:An immunohistochemical study of architectural remodeling and connective tissue synthesis in pulmonary fibrosis. 260 97

Because the pharyngeal flora may be an important determinant of the etiology of pneumonia, the presence of gram-negative bacilli in the oropharynx might be expected to be a prelude to pneumonia due to these organisms. Colonization of the upper respiratory tract by gram-negative bacilli is correlated with adherence of gram-negative bacilli to epithelial cells. Increased adherence is associated with a loss of fibronectin from the surface of oral epithelial cells, which presumably occurs as a result of the action of secretory proteases that denude cells of fibronectin. Thus, fibronectin may be described as a modulator of the composition of the oral flora. It seems more likely that the level of protease activity or the determinants that control the level of protease activity are the true modulators of the composition of the oral flora. The delineation of these determinants should lead to a greater understanding of the pathogenesis of gram-negative bacillary pneumonia.
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PMID:Role of fibronectin in the pathogenesis of gram-negative bacillary pneumonia. 312 81

Host defense mechanisms spaced along the respiratory tree and in the alveolar spaces effectively remove or contend with micro-organisms that enter the airways, so serious lung infections occur rarely in healthy people. Special circumstances, such as virgin exposure to a virulent microbe or a large innoculum of a pathogen, can result in illness, but usually routine surveillance host defenses are protective and suffice to keep colonizing airway flora in check. When pneumonia develops or recurrent sinopulmonary infection exists, however, some element of the normal defense apparatus may have failed or is inadequate. This review highlights several components of the apparatus, that is immunoglobulins IgG and IgA and the interaction of alveolar macrophages and lymphocytes, and examines deficiencies in their function that may result in infection. Along the conducting airways, poor mucociliary clearance and/or deficiencies in certain IgG subclass antibodies or destruction of IgA may predispose to sinopulmonary infections; these may be a manifestation of a hereditary disease. In pneumonia the alveolar macrophage is positioned as the central cell which must respond in several directions. This scavenger phagocyte first intercepts the microbe and either can kill or contain it or must call in some other phagocytic cell or inflammatory mediator(s) for assistance. Opsonic antibodies (IgG) and other nonimmune opsonins (complement and surfactant or fibronectin fragments) facilitate phagocytosis, but an absence of antibody may permit infection to develop with encapsulated bacteria (pneumococcus). Insufficient bone marrow reserves of PMNs or a paucity of chemotactic factors to attract them into the alveoli is a situation that may permit gram-negative bacilli and fungal organisms to flourish. Inability of immune T-lymphocytes to energize macrophages, through soluble cellular mediators that provide cell-mediated immunity and activation, makes containment of certain intracellular microbes impossible for these phagocytes (Legionella or mycobacteria). Likewise, concomitant infection of macrophages with viruses (human immunodeficiency virus, and cytomegalovirus or herpes viruses) plus an excessive T-lymphocyte suppressor cell influence may make P. carinii and common bacterial and fungal organisms difficult to contain in the lungs of AIDS patients. Consideration about what the lung host deficiency might be can make therapy more specific through immunization to develop special antibodies, replacement of certain immunoglobulins (IgG subclasses), or selective administration of cell mediators (gamma-interferon or interleukins).
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PMID:Host defense impairments that may lead to respiratory infections. 331 80

Plasma fibronectin (FNp) concentrations were measured in 63 patients with acute respiratory failure and 28 patients with circulatory failure, using Laurell's electroimmunoassay method. Measurements were made in the acute phase and repeated in the course of the disease. The mean FNp concentration in 20 controls was 262 +/- 59 mg/l. FNp values were normal in the acute phase of chronic obstructive pulmonary disease and in cardiogenic pulmonary oedema. In contrast, they were significantly decreased in adult respiratory distress syndrome and in acute pneumonia, as well as in acute circulatory failure, notably from septic shock. FNp values were also considerably reduced in patients with severe disseminated intravascular coagulation syndrome. Clinical improvement was accompanied by a return to normal of FNp concentrations. The mortality rate was greater in patients with low FNp values than in those with normal values.
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PMID:[Acute respiratory and circulatory failure. Prognostic value of plasma fibronectin levels]. 622 Mar 70

Serious illness is accompanied by markedly increased susceptibility to colonization of the respiratory tract by gram-negative bacilli and an increase in the number of such organisms which adhere to regional epithelial cells during incubation in vitro. Trypsinization of cells from normal subjects causes a similar increase in bacillary adherence. We studied bacillary adherence to buccal cells in vitro, protease activity of upper respiratory secretions with a fibrin plate technique, and the amount of fibronectin on the surface of buccal cells with a direct radioimmunobinding assay. Among 10 patients seriously ill with acute respiratory failure bacillary adherence to buccal cells and protease activity in secretions were increased compared with controls and cell-surface fibronectin was decreased; all patients were colonized in vivo with gram-negative bacilli. These changes were persistent and 80% of the patients died. Serial determinations were made in eight patients undergoing coronary artery bypass surgery. Following surgery, protease activity and bacillary adherence increased and cell-surface fibronectin decreased; 38% of coronary artery bypass patients became colonized. In these uncomplicated patients the changes observed were transient, largely returning to normal by the third postoperative day. Increased protease activity of secretions and alterations in epithelial cell surfaces as reflected by loss of buccal cell-surface fibronectin occur swiftly after major illness and appear to underlie enhanced cell adherence of bacilli and colonization of the upper respiratory tract. These findings suggest new approaches to the prevention of nosocomial pneumonia.
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PMID:Role of salivary protease activity in adherence of gram-negative bacilli to mammalian buccal epithelial cells in vivo. 679 70

Pneumocystis carinii (PC) is an exclusively extracellular pathogen which causes pneumonia in immunocompromised individuals. Histologic studies have demonstrated that PC organisms attach preferentially to type I alveolar epithelial cells and rarely bind to type II cells. Previous reports have demonstrated that cultured type II cells develop a type I cell-like phenotype and express type I cell surface antigens. The current study examines the attachment of PC organisms to isolated rat type II alveolar epithelial cells as a function of time in culture. PC attachment to isolated type II cells increased as the type II cells differentiated in culture from 2.3 +/- 1.2% on Day 2 to 18.4 +/- 2.7% by Day 8. Previous studies have indicated a role for fibronectin (Fn) and Fn receptors as mediators of PC attachment. Addition of anti-Fn antibodies decreased attachment of PC to Day 8 type II cells from 19.4 +/- 2.5% to 9.4 +/- 1.9% (P < 0.01). Addition of antibodies to the alpha v and alpha 5 integrin subunits resulted in significant decreases in PC attachment to Day 8 type II cells. Examination of expression of alpha v and alpha 5 integrins on Day 2 and Day 8 type II cells demonstrated increased expression of both alpha v and alpha 5 integrin subunits on Day 8 type II cells. Overall these data indicate that attachment of PC to isolated rat type II cells increases as the cells differentiate into a type I cell-like phenotype in vitro and correlates with increased expression of Fn-binding integrins on the cell surface of the cultured type II cells.
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PMID:Attachment of Pneumocystis carinii to primary cultures of rat alveolar epithelial cells. 749 34


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