PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Complement Pathway, Alternative”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1984

Mechanisms of acute allergic reactions.

Acute allergic reactions range from mild conditions of local tissue swelling and pruritus to severe multisystem syndromes including asthma, urticaria and/or angioedema, gastrointestinal distress, and vascular collapse. Such reactions share a common pathophysiology characterized by vasodilation and postcapillary permeability, resulting in increased extravasation of fluid within minutes after exposure to an eliciting substance. Smooth muscle contraction of the respiratory or gastrointestinal tracts may also be involved. Most of these changes can be explained by the release of chemical mediators from circulating basophilic leukocytes and tissue mast cells. Human basophils and mast cells can be activated to release chemical mediators by several known pathways: crosslinking by allergens of specific immunoglobulin E antibodies attached to basophils and mast cells; anaphylatoxin formation following immune complex activation of the classical complement pathway; anaphylatoxin formed from direct activation of the alternative complement pathway by negatively charged surfaces; non-complement-, non-antibody-mediated direct histamine release; and idiosyncratic mechanisms involving physical exercise, psychological stress, or aspirin intolerance. Any or all of these mechanisms could be operative in patients experiencing acute allergic reactions at the commencement of hemodialysis.

Anaphylaxis↗
PubMed1983

Immune complexes and complement profile in essential mixed cryoglobulinemia before and after plasma exchange.

Five patients affected by essential mixed cryoglobulinemia (EMC) with renal involvement unresponsive to high doses of corticosteroids, have been treated with 16 plasma exchanges (PE). The plasma removed at each apheresis was 1652 +/- 416 ml. The following data were evaluated before and after PE: levels of immune complexes as detected by cryocrit and C1q binding assay; total complement activity (CH50) and alternative pathway complement activity (APCH 50); concentrations of 9 complement components (C1q, C1s, C4, C3, C5, C6, B, I and H) and of the C3 split product C3d. By definition all serum samples had detectable cryoprecipitates and 4 out 5 had C1q binding activity higher than the upper limit of 2 SD. The effect of the PE was the decrease of cryocrit and of C1q binding activity approximately to one half their initial values. The basal complement profile suggested and excessive activation of complement through the classical pathway. Indeed we found low levels of the early complement components (C1q, C1s and C4), reduced CH50, normal levels of C3 and an increase of C3 split product C3d concentrations. APCH50 as well as C5, C6, B, I and H concentrations were found within the normal range. After each PE a significant decrease of the previously normal components was observed. The decrease was independent of the replacement fluid used (5% albumin solution or fresh plasma or cryoglobulin-depleted autologous plasma) and had a short duration. Indeed all these components after the drop following the PE increased rapidly reaching the basal level over a period of 24-48 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigen-Antibody Complex↗
PubMed1977

Alternative pathway of complement: nonenzymatic, reversible transition of precursor to active properdin.

A method for the purification of properdin in precursor state (pre-P) has been elaborated. Precursor properdin, in contrast to activated properdin (P), does not initiate the formation of a C3 convertase when added to properdin-depleted serum, rather it requires the presence of an activating substance such as zymosan for expression of its activity. Comparing the activities of pre-P and P it was found that some P preparations contained significant amounts of pre-P because they were fully active only in the presence of zymosan. This observation indicated that P can partly revert to pre-P. Comparison by immunoelectrophoresis and sodium dodecyl sulfate polyacrylamide gel electrophoresis revealed no charge or size differences between pre-P and P. Radiolabeled pre-P, when analyzed after its participation in the reactions of the pathway, displayed an unchanged subunit m.w. of 50,000. Taken together, these results strongly suggest that the transition of pre-P to P is due to a partly reversible change in the conformation of the protein rather than the result of proteolytic cleavage.

Complement System Proteins↗
PubMed2002

Bacteriolytic activity of rainbow trout (Oncorhynchus mykiss) complement.

The total bacteriolytic activity comprising of the classical, alternative and possible lectine pathways as well as the bacteriolytic activity of the alternative pathway (AP) of rainbow trout (Oncorhynchus mykiss) complement was assessed in temperatures ranging from 0 to 35 degrees C against a recombinant strain Escherichia coli containing two reporter genes gfp and lucFF. At 35 degrees C there was no difference between the total (TC) activity and the activity of the AP, but at 10 degrees C the TC was notably higher than the AP. Total activity peaked at 30 degrees C and gradually grew smaller towards 0 degrees C. The activity of the AP was similarly temperature-dependent, but CB50 value was found to be beyond measurable range at temperatures below 10 degrees C. When compared to human serum complement, the peak human TC activity at 37 degrees C was four times higher than the TC of rainbow trout at 30 degrees C. Human TC activity was 10.1-fold lower at 25 degrees C when compared to the activity at 37 degrees C. At 37 degrees C the human AP bacteriolytic activity was 4.5-fold less effective than human TC, but at 25 degrees C there was no difference between human TC and AP. In contrast to previous reports where AP activity of fish was assayed as hemolytic activity our study showed that the bacteriolytic activity of AP was lower than that of TC and very low at temperatures below 10 degrees C suggesting that the earlier proposed particular importance of AP in fish should be reconsidered.

Animals↗
PubMed1983

Inherited disorders of complement.

Isolated complement component deficiencies are uncommon. Deficiencies of all eleven components and two inhibitors of the classical pathway have been described. Complete absence of the components of the alternative pathway has not been described. The consequences of a single defect in complement are often predictable from an understanding of the biologic activities associated with activation of the complement system. Deficiency of C1 esterase inhibitor gives rise to the disease, hereditary angioedema; deficiency of the early components of the classical pathway are associated with lupus erythematosus; C3 and C3 inactivator deficiencies with pyogenic infections; C5 dysfunction with Leiner's disease; deficiencies of the terminal components with recurrent Neisseria bacteremia; and C9 deficiency with normal health. The complement system and its associated biologic activities are reviewed. The present knowledge of the inherited complement deficiencies and associated diseases, with particular emphasis on the dermatologic manifestations, genetics, and diagnosis, is summarized.

Angioedema↗
PubMed1981

Sendai virus infected cells are readily cytolysed by guinea-pig complement without antibody.

HeLa cells infected with Sendai virus (SV) acquired the ability to activate the alternative pathway (AP) of guinea-pig complement without antibody reaction. For induction of complement activating ability (CAA), at least 2 hr incubation of the infected cells was required. However, ultraviolet (UV)-irradiation (8400 erg/mm2) of SV did not impair the inducibility of CAA and 51Cr-labelled HeLa cells infected with UV-irradiated SV (UV-SV) became readily cytolysed by C4-deficient guinea-pig complement without antigen-antibody reaction. This phenomenon may represent a primary in vivo defence mechanism against SV infection by eliminating the virus-infected cells via activation of complement on the cell surface. Although SV-infected HeLa cells activated the AP of guinea-pig complement, they did not activate the AP of human or mouse complement. The species restriction in the CAA induced by SV infection may result in different pathological manifestations in virus-infected animals and may affect their susceptibility to this type of infection.

Animals↗