UMLS:C0036690 - FACTA Search

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Query: UMLS:C0036690 (sepsis)
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The complement system may be activated by two pathways, the classical and the alternate. To evaluate their respective participation in different forms of glomerulonephritis, the plasma values of C3, C4, C3PA, C1q and properdin were determined in 70 patients. In systemic lupus erythematosus (LED), acute poststreptococcal glomerulonephritis (AGN) and septicemia the classical pathway appears to be mainly involved, whereas the amplification loop and the alternate pathway seem to be of secondary importance. By contrast, in membranoproliferative glomerulonephritis (MPGN) the alternate pathway plays a major role. However, the present data suggest that activation of the classical pathway may often be involved as well. In minimal change glomerulonephritis no signs indicating involvement of the complement system were apparent. Follow-up observation demonstrated a correlation between decreases in plasma complement concentrations and the clinical severity of the primary disease in LED, AGN and septicemia, but not in MPGN.
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PMID:[Activation of the complement system in different forms of glomerulonephritis]. 33 69

Total hemolytic complement (CH50), conversion of C3 by inulin and cobra venom factor (CoVF), and immunochemical levels of Clq, C4, C2, C3, C5, factor B, properdin, C3b inactivator (KAF), and immunoglobulins (Igs) G, A, and M were measured in the sera of ten patients with abdominal trauma and ten medical patients with septicemia without trauma. Reduction in C3 conversion by CoVF and decrease in the levels of properdin and KAF were demonstrated in the trauma sera. CH50 and the level of C5 were also decreased. Conversion of C3 by inulin and levels of factor B, Clq, C4, C2, and C3 were found to be normal in the patients' sera. Complement levels and activities were found to be normal in the sera of the septic non-trauma patients. A decrease in serum IgM was observed in both patient groups; levels of IgG and IgA were normal. These results indicated that abnormalities of immunoglobulin and of the alternative and classical complement pathways were associated with nonburn trauma. Moreover, the data suggested that consumption of the classical complement pathway associated with septicemia in the thermally injured patient resulted from synergism between the trauma and infection rather than from septicemia per se.
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PMID:Host defense against opportunist microorganisms following trauma. II. Changes in complement and immunoglobulins in patients with abdominal trauma and in septic patients without trauma. 66 70

Total hemolytic complement (CH(50)), conversion of C3 by inulin, and immunochemical levels of Clq, C4, C2, C3, C5, factor B, C3b inactivator (KAF), and properdin were measured in the sera of 15 patients with severe thermal injury during nine weeks postburn. Five of the 15 patients had multiple episodes of septicemia as documented by positive blood cultures and clinical findings. Decrease in CH(50), Clq, C4, C2, C3, and C5 occurred prior to and during septic episodes in these patients. Although conversion of C3 by inulin was often reduced during septic episodes, levels of factor B and KAF were generally normal or elevated. In only one patient did consumption of complement occurring during septicemia decrease the opsonic capacity of the patient's sera for the patient's infecting microorganism, an isolate of E. coli; sera from the same patient opsonized her infecting strain of S. aureus normally. The microorganisms isolated from the other septic patients, which were opsonized normally by the patients' sera despite complement consumption, were also with one exception strains of Staphylococci. In the nonseptic burned patients, decrease in properdin and C3 conversion by inulin, and increase in C3, factor B and KAF were demonstrated as we have previously reported. The results indicate that the classical complement pathway was activated during septicemia in burned patients and that activation of this pathway occurred preferentially due to inhibition of the alternative pathway. In addition, the data show that complement consumption may reduce the opsonic capacity of a patient's sera for certain microorganisms and not for others.
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PMID:Host defense against opportunist microorganisms following trauma. I. Studies to determine the association between changes in humoral components of host defense and septicemia in burned patients. 66 83

Serum opsonic activity for E. coli 075, conversion of C3 by inulin, total hemolytic complement (CH(50)), levels of native C3, factor B, C3b inactivator (KAF), properdin (P), and immunoglobulins (Ig) were determined in 14 patients with burns involving 13% to 91% body surface during 6 to 8 weeks postburn. In the 12 uninfected patients, levels of IgG and IgA were reduced during the first 10 days postburn, and decreased concentrations of P and IgM were demonstrated from three to 6 weeks postburn. C3 conversion was reduced from 10 days to 6 weeks postburn. Levels of C3, factor B, and KAF were normal or elevated for the entire study period. No difference in the occurrence of humoral abnormalities was noted in patients with burns caused by flame, immersion scald, or acid contact. Reduction in C3 conversion and P concentration were the only abnormalities which correlated with increasing burn size. Bacteremia and/or fungemia was documented in the other two patients. In one of these patients, reduction in CH(50) occurred during septicemia due to S. aureus, and in the other, reduction in all measurements of complement was associated with candidemia and Pseudomonas septicemia and occurred prior to the development of shock. Serum opsonic activity was only reduced significantly during sepsis, suggesting that this abnormality occurred as a result rather than a cause of infection. These results indicate that consumption of components of the classical and/or alternative pathways of complement activation may be an important mechanism by which infection is perpetuated in the burn patient. They also emphasize the importance of the clinical management of the burn patient in preventing the development of septic complications.
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PMID:Changes in humoral components of host defense following burn trauma. 87 73

Persistent pulmonary hypertension of the newborn (PPHN), initially described by Gersony et al as persistent foetal circulation (PFC syndrome), results from a flawed transition from foetal to extrauterine pulmonary circulation. It is characterised by the maintenance of a high pulmonary vascular resistance and right-to-left shunting through the ductus arteriosus and foramen ovale. Infants with a wide variety of underlying clinical conditions develop PPHN. According to Rudolph three main anatomic types of PPHN can be identified: normal pulmonary vascular development increased pulmonary vascular smooth muscle development decreased cross-sectional area of pulmonary vascular bed. It is important to realize that several pathophysiologic mechanisms may coexist and interact. Besides metabolic and respiratory acidosis, hypercapnia and hypoxaemia some other factors induce pulmonary vasoconstriction. Thromboxane, leukotrienes and prostaglandins play a decisive role. Since PPHN can be associated with a broad spectrum of clinical conditions, a specific clinical picture is lacking. The baby is usually term or post-term, cyanotic immediately after birth or some hours later. Birth asphyxia, hyperviscosity, sepsis and aspiration of meconium have been recognized as predisposing factors. The diagnosis can be confirmed by echocardiography. Contrast echo will indicate right-to-left shunting with normal anatomy. Currently hyperventilation, tolazolin, chlorpromazin and dopamine/dobutamine have been advocated as central foci for clinical therapy. Recently prostacyclin was introduced as a specific pulmonary vasodilatator.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Persistent pulmonary hypertension of newborn. The PFC syndrome]. 229 36

Rabbits immunized intravenously(iv) with sheep erythrocytes(SRBC) (primary response) pass through a period which begins at about Day 35 postprimary immunization and extends to about Day 120 during which time all detectable spontaneous AFC (immediate PFC) and memory AFC(cells which generate PFC in culture) are detected only in the spleen. Prior to Day 30 postprimary iv immunization, large numbers of immediate PFC are detected in the circulation and the bone marrow as well as in the spleen. By Day 120 postprimary iv immunization, memory cells can be detected in significant numbers in the thymus and the popliteal lymph nodes (PLN) as well as in the spleen. The number of memory cells in the PLN and thymus increases over the course of the following 6 months. Rabbits splenectomized on Day 40 postprimary iv immunization and subjected to reimmunization iv with 10(9) SRBC 1, 5, or 8 months later were unable to give significant secondary immune responses. Only the thymus and PLN cells, cultured in vitro with the antigen(SRBC), 1, 5, or 8 months postprimary immunization, generated secondary immune(PFC) responses and these responses were feeble at best. The failure of the immunized rabbit to give a significant secondary immune response to SRBC if splenectomy was first carried out at a time postprimary iv immunization when all memory cells to the original antigen are sequestered only in the spleen (i.e., days 40 to 100) constitutes an animal model which provides a credible immunological explanation for the postsplenectomy syndrome which affects a minority of splenectomized individuals. These individuals, like the rabbits splenectomized on Day 40 postprimary immunization, lack the capacity to evoke a strong secondary immune response to particular infectious microorganisms and succumb in a few days with fulminant septicemia unless aggressive chemotherapy is instituted upon initial sign of infection.
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PMID:Cells involved in the immune response. XXXII. Surgical extirpation of the spleen in the early memory period following primary i.v. immunization of the outbred rabbit results in a marked impairment of a subsequent immune response to the specific antigen: an immunological explanation for the overwhelming postsplenectomy syndrome. 369 43

Splenectomy continues to be the most commonly chosen method of management of traumatic injury to the spleen. However, patients of all age groups who have undergone splenectomy have significant impairment of immune functions as demonstrated by decreased production of IGM, tufsin, and properdin. This immune deficiency has been clinically manifested by an increased incidence of postsplenectomy pneumonia and sepsis which is reduced but not eliminated by the use of pneumococcal vaccine and/or prophylactic antibiotics. This paper presents the results of a study of the feasibility of repair and replantation of injured spleens using microsurgical techniques. Twenty cats had their spleens removed, finger-fractured, and debrided. The cats were then assigned to one of four groups. Group I had the entire spleen replanted but only 75% of the parenchyma revascularized. Group II had 75% of the parenchyma revascularized and replanted. Group III had 50% revascularized and replanted, and Group IV 25% revascularized and replanted. Patency of the anastomoses was assessed by postoperative arteriography. Restoration of reticuloendothelial (filter) function was assessed by the use of technetium sulphur colloid scans which showed preservation of reticuloendothelial function of the revascularized segments but absence of function in nonrevascularized segments which had been replanted. Histologic examination of replanted spleens harvested at 8 weeks showed normal architecture of red and white pulp in all areas that had been revascularized. However, in those spleens where the entire spleen had been replanted but only partially revascularized, the nonrevascularized segments were degenerated and atrophic.
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PMID:Debridement and replantation of the spleen with microsurgical restoration of blood flow. 402 93

We have developed a new, specific, and highly sensitive enzyme-linked immunosorbent assay (ELISA) which quantitates activation of the alternative pathway in human serum, plasma, or on the surface of activators. The ELISA detects the third component of complement (C3b), proteolytic fragment of complement Factor B (Bb), and properdin (P) complex or its derivative product, C3b,P. In the method, activator-plasma mixtures, plasma containing an activated alternative pathway, or other samples are added to the wells of microtitration plates precoated with antibody to P. C3b, Bb,P or C3b,P complexes which become bound are quantitated by subsequently added, enzyme-labeled, anti-C3. The resulting hydrolysis of the chromogenic substrate is expressed as nanograms of C3b by reference to a C3 standard curve. In addition to absolute specificity for activation of the pathway because of the nature of the complex detected by the assay, the ELISA is highly sensitive and able to reproducibly detect 10-20 ng/ml of C3b,P complexes in serum. This value corresponds to 0.0015% of the C3 in serum. In a series of studies to validate the parameters of the ELISA, reactivity was found to be dependent on the presence of alternative pathway proteins, the functional integrity of the pathway, and on the presence of magnesium. Sheep erythrocytes were converted to activators by treatment with neuraminidase. By using a variety of activators, the kinetics of activation and the numbers of bound C3b molecules quantitated by the ELISA were very similar to those measured by C3b deposition. The ELISA also detected identical activation kinetics when MgEGTA-serum and a mixture of the purified alternative pathway proteins were used as sources of the pathway. ELISA reaction kinetics also correlated with the restriction index, a measure of alternative pathway-activating ability. These studies cumulatively validate the ELISA as a direct and quantitative assay for alternative pathway activation. The sensitivity of the ELISA has permitted its use to detect direct alternative pathway activation by several viruses. The ELISA has also shown that certain classical pathway activators trigger the amplification loop of the alternative pathway while others do not. In addition, stable ELISA reactive complexes appeared in the supernatant of mixtures of serum with certain, but not other activators. The ability of the ELISA to detect activation which has already occurred and the stability of the reactive complexes permits studies of clinical sera. Normal human sera (20) contained low levels (5-20 ng/ml) of ELISA-reactive complexes. A proportion of sera from individuals with the adult respiratory distress syndrome (9-10), typhoid fever (8-10), malaria (3-5), gram-negative sepsis (9 of 47), acute trauma and shock (6 f 25), and systemic lupus erythematosus (3 of 29) showed elevated levels of complexes reactive in the alternative pathway ELISA. In contrast, nine sera from patients with circulating C3 nephritic factor were not reactive in the ELISA.
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PMID:Development and application of an enzyme-linked immunosorbent assay for the quantitation of alternative complement pathway activation in human serum. 641 67

The bactericidal activities of human complement and human antibody directed against specific Haemophilus influenzae type b cell surface determinants were investigated. Strain Eagan, a laboratory isolate, and strain Kn, a clinical isolate, were used as the test organisms and gave qualitatively similar results. In the absence of antibody, both isolates were resistant to killing by 60% agammaglobulinemic serum (AGS) containing normal complement levels. The addition of affinity-purified immunoglobulin G anticapsular antibody was bactericidal with 15% AGS as the complement source. Bactericidal activity was also demonstrated with this antibody when the complement source was AGS-Mg-EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N-tetraacetic acid], C2-deficient human serum (alternative complement pathway), or AGS in which factor D and properdin had been selectively inactivated (classical pathway). Immunoglobulin G fractions from a human serum pool or from serum from an adult who had recovered from H. influenzae type b (Kn) sepsis were absorbed to remove anticapsular antibody. The absorbed fractions containing noncapsular antibodies also activated complement-dependent bactericidal activity. But, in contrast to the results with anticapsular antibody, noncapsular antibodies did not elicit alternative pathway bactericidal activity. Incubation of cells of H. influenzae type b in C2-deficient serum or AGS-Mg-EGTA did not cause complement consumption (total hemolytic complement and C3). The addition of immunoglobulin G anticapsular antibody (but not noncapsular antibody) increased consumption of total complement and C3, paralleling the results of the bactericidal assays. These studies demonstrated an absolute requirement for anticapsular antibody in alternative pathway activation and killing of H. influenzae type b.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antibody-dependent alternative pathway killing of Haemophilus influenzae type b. 660 28

Studies were performed to evaluate complement, opsonins, and the immune response to bacterial infection in burned patients. Concentrations and functional acitivities of components of the classical and alternative complement pathways were measured in the sera of four septic, two bacteremic, and four nonseptic burned patients. In addition, heat-labile and heat-stable opsonic activity and agglutinin titers directed against the infecting bacterial strains were measured in the sera of the four septic patients and in an additional group of 11 septic burned patients with abnormal complement profiles. Functional activity of the alternative complement pathway and the concentration of properdin were shown to be persistently decreased during eight weeks postburn in the septic, bacteremic, and nonseptic burned patients; reduced classical pathway activity was demonstrated during the initial postburn period only in the septic patients. Two of the 15 septic patients had decreased heat-labile serum opsonic activity for their infecting bacterial strains, which occurred only during the initial postburn period. Heat-stable opsonins and agglutinin titers in the patients' sera directed against the infecting bacterial strains were equivalent to those in normal human sera, except for the agglutinin titers to Streptococcus faecalis which were increased in the patients' sera in comparison to the normal sera. These results indicate that the multiple complement abnormalities which occur in septic burned patients do not predispose these patients to bacterial infection by decreasing serum opsonic activity. Moreover, heat-stable immune IgG antibodies are not produced during septicemia which facilitate opsonization of the infecting bacterial strains in the absence of an intact complement system.
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PMID:Complement, opsonins, and the immune response to bacterial infection in burned patients. 676 53

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