[Relationship between phagocytosis and sensitization to bacterial allergens in patients with chronic bronchitis].
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Phagocytic cells, the first host defence against microbial attack, are remarkably mobile; they can move very rapidly to the infectious or inflammatory site. They migrate toward a chemotactic factor: C5a, lymphokines, bacterial products, leukotriene B4, etc. The binding of the chemotactic factor to its specific receptor on the cell leads to an activation of the phagocytic cell: the electric potential of the membrane changes, ionic fluxes and free calcium rate increase, arachidonic acid metabolites are produced, cyclic nucleotides are activated. This produces a change in shape, a polarization of the cell and, after cytoskeleton reorganization, migration of the cell towards the chemotactic factor. A constitutional or acquired abnormality of one of these steps induces a defect of chemotaxis for the phagocytic cells and severe infections.
The initiation of both the normal and pathologic responses of human neutrophils to surface stimulation and the ensuing biochemical and physiologic events are elucidated. This knowledge has contributed to an understanding of the controlling mechanisms that may account for impaired phagocytic function in several clinical disorders associated with recurrent bacterial infections.
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Patients with the hyperimmunoglobulin E-recurrent infection (Job's) syndrome, which is characterized by an elevated immunoglobulin E level, recurrent staphylococcal infections, and an abnormality of neutrophil chemotaxis, have been reported to have visceral Candida infections in addition to their more frequent pyogenic infections. We report a patient with Job's syndrome who presented with massive hematemesis secondary to esophageal cryptococcosis. A thorough evaluation for an occult neoplasm or extraesophageal cryptococcosis was negative. The patient received a 6-wk course of amphotericin B (970 mg) and 5-fluorocytosine with complete radiographic and endoscopic resolution of the lesion. He is doing well 18 mo after therapy. The patient was not anergic, and his response to T-cell mitogens, helper-to-suppressor T-cell ratio, total number of T cells, and immunoglobulin-producing capability were all normal. This case is unusual in that it is the first documentation of a cryptococcoma of the esophagus and underscores the importance of culturing abnormal specimens for unsuspected pathogens in unusual clinical circumstances.
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Human anti-actin antibodies (from patients with chronic aggressive hepatitis) were used with a second fluorescent anti-serum to study the distribution of actin in granulocytes from ten normal subjects and nine patients with "lazy phagocyte syndromes." Normal cells showed organization of actin at the periphery of the cell within 60 sec of adhering to glass, and this pattern was clearly abnormal in lazy phagocytes. This is a simpler test to confirm abnormal organization of actin in cells from affected patients.
Peculiarities of interaction between the polynuclear leucocyte (PNL) system and bacterial agents are considered within the framework of four typical clinico-biological situations: interaction of a primarily genetically deficient PNL system with a bacterial agent; interaction of a secondarily affected by various diseases and traumas PNL system with a bacterial agent; interaction of an unaltered PNL system with a bacterial agent of an extreme intensity; interaction of an unaltered PNL system with an ordinary bacterial agent. In the first three situations characterized by a purulent inflammatory-infectious process, current methods of investigation detect some disturbances of PNL function reflecting their functional insufficiency. In the fourth situation the functional sufficiency (but not inactivity) of the PNL system determines the state of clinical health. Obviously, regardless of the functional insufficiency, whether absolute or relative, it results in an inflammatory-infectious process.
In France, because of routine vaccination, BCG infection is the rule and not the exception. It may thus incidentally reveal a latent immunodeficiency. Eleven cases (10 fatal) of generalized BCG infection observed from 1967 to 1981 at the Hôpital des Enfants-Malades (Paris) are reviewed. The clinico-pathologic analysis of these 11 cases showed that the underlying immunodeficient states were of various natures. They could be grouped under 3 different headings: (1) Cellular immunodeficiency, as part of a severe combined immunodeficiency (5 cases) and Di George's syndrome (1 case); (2) Deficiency in the bactericidal activity of the macrophages, either isolated (2 cases) or associated with fatal granulomatous disease (1 case); (3) unclassified conditions, probably original, associated with chronic Salmonella infection. The heterogeneity of theses cases emphasizes the complexity and diversity of the mechanisms which lead to the elimination of the intracellular agents. Because they provide useful insight into the poorly understood mechanisms of bactericidal activity of macrophages, further investigations of infantile disseminated BCG infection are necessary.
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