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D Kreutzer

Publications and source records attributed to D Kreutzer.

24 records · Page 2Linked to original sources
PubMed1982

Evidence of impaired anterior segment fibrinolytic activity in chronic uveitis.

Purified homologous fibrinogen (2.4-9.4 mg) was injected intracamerally in cat eyes at approximate six months intervals for up to 30 months in order to assess, in vivo, the long-term impact of chronic uveitis on anterior segment fibrinolytic capability. Normal and acutely inflamed eyes responded with slow clotting, small clot formation and rapid lysis (2-3 days). Chronically inflamed eyes showed rapid clotting, larger clots and much slower lysis, with BCG-induced uveitis much slower than endotoxin-induced uveitis. Suppression of plasminogen activator levels within aqueous humor of chronically inflamed eyes was indicated, using modified fibrin plate methods. The normal balance between fibrinolysis and fibrinogenesis within tissues bounding the anterior chamber is apparently tilted in favor of the latter function when inflammation is prolonged.

Animals↗
PubMed1981

Meningococcal meningitis in familial deficiency of the fifth component of complement.

Absence of the fifth component of complement (C5) by immunochemical assay and marked deficiency by hemolytic assay (less than 0.1%) was found in a family in which the oldest male child had suffered severe and recurrent meningococcemia at age 15 years, two brothers developed meningococcal meningitis four years later (at ages 18 and 14 years), and a sister had the gonococcal arthritis-dermatitis syndrome. Although group-specific meningococcal antibody was present in the sera from all four siblings, serum bactericidal activity against Neisseria meningitidis could be demonstrated only in the presence of exogenous rabbit complement. Serum total hemolytic complement activity was undetectable in all four, but was restored to normal by the addition of purified C5. Subsequently, a second episode of group Y meningococcal meningitis was experienced by one brother and presumed gonococcal arthritis-dermatitis syndrome recurred in the sister. The family is the largest C5-deficient kindred to be reported and emphasizes the importance of C5 in host susceptibility to invasive Neisseria infections. In contrast to the peak incidence of N meningitidis disease in the general population in the first year of life, age of onset of meningococcal infection in these patients and in the 13 previously reported patients with terminal complement component deficiency has usually been in adolescence and early adulthood.

Adolescent↗
PubMed1980

Interrelationships between serum chemotactic factor inactivator, alpha 1-antitrypsin deficiency, and chronic obstructive lung disease.

Serum chemotactic factor inactivator (CFI) activity was quantitated in 22 subjects with chronic airflow obstruction (CAO); 8 had normal antitrypsin levels (Pi M phenotype), 6 had intermediate antitrypsin deficiency (Pi MZ phenotype), and 8 had severe antitrypsin deficiency (Pi Z phenotype). We studied 19 healthy subjects with normal lung function as controls; 3 had Pi M and 6 had Pi MZ phenotypes. Subjects with CAO, irrespective of the alpha 1-antitrypsin (AAT) phenotype, had significantly lower CFI activity than the normal subjects; the lowest levels were found in those with CAO and Pi Z phenotype. Normal subjects with intermediate AAT deficiency and MZ phenotype had normal levels of CFI. The results suggest that deficiency of serum CFI may be important in the pathogenesis of chronic airflow obstruction, particularly in those with severe AAT deficiency.

Adult↗
PubMed1979

C5 chemotactic fragment induces leukocyte production of tissue factor activity: a link between complement and coagulation.

Complement-activated human plasma causes generation of tissue factor in human leukocytes. This phenomenon appears to be related to the fifth component of complement (C5) as demonstrated by the use of C5 deficient-plasma and suppression of activity with antibody to C5. Isolation of the chemotactic factor from activated serum or trypsinization of purified C5 reproduces the phenomenon. These data provide evidence for a direct link between complement products and activation of the coagulation system. Because chemotactic peptides from C5 can be generated by a variety of enzymes, our findings suggest a relationship between complement, coagulation, and inflammation.

Blood Coagulation↗
PubMedDate not supplied

Interleukin-3 interleukin-5, and granulocyte-macrophage colony-stimulating factor expression in nasal polyps.

PURPOSE: Nasal polyps (NP) are grape-like clusters of chronically inflamed tissue. Little is known about the underlying cells and cytokines involved in nasal polyposis. For the present study, we hypothesize that elevated tissue levels of interleukin-3 (IL-3), interleukin-5 (IL-5), and granulocyte-macrophage colony-stimulation factor (GM-CSF) contribute to eosinophil recruitment and activation in NP. MATERIALS AND METHODS: To begin to test this hypothesis, we evaluated IL-3, IL-5, and GM-CSF levels and distributions in nasal polyp specimens obtained intraoperatively from 13 patients and two normal controls. For these studies, nasal polyp levels were determined by enzyme-linked immunosorbent assay (ELISA), and IL-3, IL-5, and GM-CSF distribution was determined by immunohistochemistry. RESULTS: Immunohistochemical staining of the NP indicated that in all 13 patient samples, IL-3, IL-5, and GM-CSF were associated with infiltrating cells, primarily eosinophils, in the NP. Quantitation of IL-3, IL-5, and GM-CSF in NP tissue homogenates indicated that IL-3, IL-5, and GM-CSF levels were evaluated in the NP tissues when compared with control tissues. Additionally, elevation of individual cytokines correlated with previous polypectomy (IL-3), steroid use (IL-3, IL-5, and GM-CSF), asthma (IL-5), and age (GM-CSF). CONCLUSION: These data support our hypothesis that IL-3, IL-5, and GM-CSF are likely to play a key role in eosinophil recruitment/activation and NP formation and support recently advanced theories that cytokines play a key role in the pathogenesis of this disease.

Adult↗