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At least 271 records · Page 15Linked to original sources
PubMed2000

Mechanism underlying acute resident leukocyte disappearance induced by immunological and non-immunological stimuli in rats: evidence for a role for the coagulation system.

OBJECTIVE: To investigate the involvement of the fibrinogen-fibrin system in the acute reduction of the resident leukocyte population following pleural inflammation. METHODS: Sensitized and naive rats were injected intrapleurally (i.pl.) with antigen (ovalbumin) and platelet-activating factor (PAF) or bradykinin, respectively. Heparin (0.25 U/cavity), EDTA (80 microg/cavity) and hirudin (1 U/cavity) were injected locally 5 min before challenge, whereas fucoidin was injected intraperitoneally 30 min before stimulation. RESULTS: Antigen challenge led to a rapid reduction in the number of resident leukocytes 30 min post-challenge (from 7.7 +/- 0.4 x 10(6) cells/cavity to 2.3 +/- 0.2 x 106 cells/cavity, n = 6, p < 0.001). The pleural stimulation of naive rats with either PAF or bradykinin also led to a significant decrease in the pleural leukocyte population, which occurred in parallel with the formation of a fibrin meshwork containing captured cells, as attested by electron microscopy. Heparin prevented the drop in the total leukocyte numbers, without modifying either plasma leakage or histamine release at 30 min or the subsequent neutrophil and eosinophil infiltration noted 4 and 24 h post-challenge, respectively. Similarly, hirudin and EDTA prevented the antigen-induced leukocyte disappearance reaction. Heparin also impaired the drop in the pleural leukocyte numbers evoked by PAF and bradykinin. CONCLUSION: Our data show that the pleural resident cell disappearance phenomenon noted early after inflammatory provocation depends on the activation of the fibrinogen-fibrin system, and is not required for the subsequent leukocyte recruitment.

Animals↗
PubMed1981

Immunological and non-immunological synthesis and release of prostaglandins and thromboxanes from isolated guinea pig trachea.

Specific radioimmunoassays were used to demonstrate the synthesis by the guinea pig trachea of 6-keto PGF1 alpha, TxB2, and PGF2 alpha in addition to PGE2. The rank order of both spontaneous and stimulated release was PGE2 greater than PGF2 alpha greater than 6-keto PGF1 alpha = TxB2. Ovalbumin-induced prostanoid release from sensitized tissue was antigen-specific. The release was unlikely to be secondary consequence of tracheal contraction since incubations with calcium ionophore A23187, at a concentration which produces an equivalent magnitude of contraction of sensitized trachea, did not induce a significant PG or Tx production. In contrast, significantly higher prostanoid synthesis was induced by A23187 in unsensitized than sensitized trachea. Thus sensitization altered the profile of arachidonic acid metabolism evoked by the ionophore.

Animals↗
PubMed1986

Stimulus-related difference in the formation of leukotrienes and PGD2 after immunological and non-immunological challenge of human lung parenchyma "in vitro".

The stimulation of human lung parenchymal fragments with A-23187 induces formation of leukotrienes as well as of PGD2: LTE4 is the compound found in larger amount and independently of the intensity of the stimulus the % of metabolized precursor which is converted to leukotrienes or PGD2 is remarkably similar. However, under conditions of IgE-Anti IgE challenge the predominant conversion of arachidonic acid occurs to PGD2, LTB4 is almost negligible and LTD4 and E4 together represent less than 30% of the oxidative products of arachidonic acid. Whether PGD2 and leukotrienes derive from the same or different subset of cells is unresolved.

Antibodies↗
PubMed2006

Validation of current joint American Academy of Allergy, Asthma & Immunology and American College of Allergy, Asthma and Immunology guidelines for antibody response to the 23-valent pneumococcal vaccine using a population of HIV-infected children.

BACKGROUND: Measuring antibody responses to 23-valent pneumococcal polysaccharide vaccines (PPV) is crucial to evaluation of humoral immune function. However, data are limited comparing responses in immunodeficient subjects. OBJECTIVE: A case-controlled study comparing changes in PPV antibody titer in immunocompetent and immunodeficient children was performed to validate current guidelines. METHODS: A cohort of 95 immunocompetent children and 22 HIV-infected children, ages 2 to 15 years, was vaccinated with PPV, and before and after vaccination, IgG titers against capsular polysaccharides for 12 pneumococcal serotypes were measured. Results were used to calculate the receiver operator characteristic curve, sensitivity, and specificity of various interpretation criteria for their accuracy in detecting suboptimal responders. RESULTS: Immunodeficient subjects had lower CD4%, antidiphtheria, antitetanus titers, and mean post-PPV titers (2.5 +/- 1.7 vs 4.5 +/- 2.1 mug/mL; P < .001) compared with immunocompetent subjects. The interpretation, using individual post-PPV titer of > or =4-fold increase over prevaccination as a positive response, yielded the highest accuracy as measured by area under the curve value (receiver operator characteristic curve = .755). For this criterion, the numbers of serotypes with positive responses of < or =5 of 12 serotypes measured yielded 72.7% sensitivity and 56.8% specificity in detecting antibody-deficient subjects. CONCLUSION: Current guidelines using > or =4-fold increase in post-PPV titers has sufficient sensitivity and specificity to identify antibody deficiency. The minimal positive responses should be at least 50% of serotypes tested. CLINICAL IMPLICATIONS: Measurement of PPV antibody response based on the current guidelines accurately identify children with humoral immunodeficiency.

Acquired Immunodeficiency Syndrome↗
PubMed2004

Mechanical immunology: every mechanical crushing of a cell in living organisms results in an immunological reaction.

Throughout a living organism, the cells are constantly exposed to mechanical stresses. Because of these stresses, cells are continually broken down into various organs and structures. Thus, internal components of the cell that do not appear in the serum or extracellular space under stress-free conditions are released. These components, according to the ideas described here, can lead to an immune reaction and a subsequent inflammatory reaction. For these reasons the organism attempts to prevent the destruction of cells and employs a variety of mechanisms to try and achieve this aim. Apoptosis, i.e. suicide by the damaged cell, is one such mechanism as is the work of phagocytes that appear in the most varied organs. Further protection for the cell consists in the separation of the spaces in which the destruction of cells takes place by means of membranes and basal membranes. A further conclusion, which follows from this concept, is the separation of the CD4 and CD8 T-cell receptor spectra. Whereas CD4 T receptors recognise extracellular antigens the CD8 T-cell receptors recognise intracellular antigens. Conversely, the body's own extracellular structures do not lead to a reaction via the CD4 cells, the corresponding T-cell populations are eliminated and the body's own intracytoplasmic structures do not lead to a reaction via the CD8 cells. Each of the reverse combinations between structures and cell populations should lead, however, to an immune system reaction.

Animals↗