Biomaterial Database

Activated complement in the sputum from patients with cystic fibrosis. 1979

P O Schiøtz, and H Sørensen, and M Høiby

14 cystic fibrosis (CF) patients chronically infected with mucoid P. aeruginosa and presenting multiple precipitins in serum against this bacterium (CF + P) and 13 CF patients without P. aeruginosa infection (CF-P) had their plasma and sputum sol phase examined for albumin, Clq. C3/C3c, C4 and C5 by means of electroimmunoassays. Their sputum sol phase was examined also for factor B by rocketimmunoelectrophoresis. C3c was demonstrated in the sputum sol phase but significantly more frequent (p less than 0.01) among the CF + P patients than among the CF-P patients. Factor B was also demonstrated in the sputum sol phase, but no significant difference in frequency could be demonstrated between the CF + P and the CF-P patients. None of the results indicated that a local pulmonary production of complement factors took place. Complement activation was significantly (p less than 0.01) associated with inflammation expressed as increased (formula: see text). The results show the importance of complement mediated inflammation in the pathogenesis of pulmonary tissue damage in patients with CF and support the concept of chronic P. aeruginosa lung infection as an immune complex disease in CF patients.

UI	MeSH Term	Description	Entries
D007123	Immunoelectrophoresis, Two-Dimensional	Immunoelectrophoresis in which a second electrophoretic transport is performed on the initially separated antigen fragments into an antibody-containing medium in a direction perpendicular to the first electrophoresis.	Immunoelectrophoresis, Crossed,Immunoelectrophoresis, 2-D,Immunoelectrophoresis, 2D,2-D Immunoelectrophoresis,2D Immunoelectrophoresis,Crossed Immunoelectrophoresis,Immunoelectrophoresis, 2 D,Immunoelectrophoresis, Two Dimensional,Two-Dimensional Immunoelectrophoresis
D008297	Male		Males
D011014	Pneumonia	Infection of the lung often accompanied by inflammation.	Experimental Lung Inflammation,Lobar Pneumonia,Lung Inflammation,Pneumonia, Lobar,Pneumonitis,Pulmonary Inflammation,Experimental Lung Inflammations,Inflammation, Experimental Lung,Inflammation, Lung,Inflammation, Pulmonary,Inflammations, Lung,Inflammations, Pulmonary,Lobar Pneumonias,Lung Inflammation, Experimental,Lung Inflammations,Lung Inflammations, Experimental,Pneumonias,Pneumonias, Lobar,Pneumonitides,Pulmonary Inflammations
D011552	Pseudomonas Infections	Infections with bacteria of the genus PSEUDOMONAS.	Infections, Pseudomonas,Pseudomonas aeruginosa Infection,Infection, Pseudomonas,Pseudomonas Infection,Pseudomonas aeruginosa Infections
D002648	Child	A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL.	Children
D002908	Chronic Disease	Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).	Chronic Condition,Chronic Illness,Chronically Ill,Chronic Conditions,Chronic Diseases,Chronic Illnesses,Condition, Chronic,Disease, Chronic,Illness, Chronic
D003165	Complement System Proteins	Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).	Complement Proteins,Complement,Complement Protein,Hemolytic Complement,Complement, Hemolytic,Protein, Complement,Proteins, Complement,Proteins, Complement System
D003167	Complement Activation	The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.	Activation, Complement,Activations, Complement,Complement Activations
D003176	Complement C3	A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.	C3 Complement,C3 Precursor,Complement 3,Complement C3 Precursor,Complement Component 3,Precursor-Complement 3,Pro-C3,Pro-Complement 3,C3 Precursor, Complement,C3, Complement,Complement, C3,Component 3, Complement,Precursor Complement 3,Precursor, C3,Precursor, Complement C3,Pro C3,Pro Complement 3
D003181	Complement C4	A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.	C4 Complement,C4 Complement Component,Complement 4,Complement C4, Precursor,Complement Component 4,Pro-C4,Pro-complement 4,C4, Complement,Complement Component, C4,Complement, C4,Component 4, Complement,Component, C4 Complement,Pro C4,Pro complement 4