Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As a contribution to knowledge about the etiology of lower respiratory tract infections (LRI) in infants, 235 patients aged one year or less admitted to a children's hospital at northern metropolitan area of Santiago, Chile along years 1987 throughout 1989 with radiologically confirmed diagnosis were studied. Infants were eligible only if their symptoms lasted for not more than five days and their hospital stay was less than two days. Controls consisted on 74 healthy infants. A search for presumptive etiology was done by means of usual bacteriological procedures (pharyngeal swabs and blood cultures), plus latex test for type b Haemophilus influenzae (Hib) and Streptococcus pneumoniae (SP) in concentrated urine specimens; indirect immunofluorescence (IF) for specific Chlamydia trachomatis (CT) IgM; serological tests, isolation and IF in pharyngeal aspirates for syncytial respiratory virus (SRV), influenza, parainfluenzae and adenoviruses were also used. Evidence of viral infection was detected from 135/235 (57.5%) of cases and 21/74 (28.3%) controls, SRV being the most common. From 18/119 and 2/119 studied patients Hib and SP antigens were respectively detected, but urinary antigens were also present in 6/24 controls, raising questions about this test's specificity. IF titers of 1:32 or higher for CT were found in 5/80 patients, all younger than 5 months. It was possible to perform the whole set of available methods in 80 patients, in 70% of which some evidence of a known etiologic agent was found. Serology alone gave etiological clues in only 30% of these cases and usual microbiological cultures of throat swabs and blood from none of them. No combinations of age, fever, respiratory rate, apnea, bronchial obstructive syndrome, white blood cell counts over 15,000 or of band forms over 500 per cu mm, erythrocyte sedimentation rates, reactive C protein and x-ray findings allowed differential diagnosis between presumptive bacterial or viral etiology, except in one case of an infant presenting with pleural effusion and positive antigenuria for Hib.
 ...
PMID:[Etiology of lower respiratory infections in hospitalized infants]. 184 25

Evidence is reviewed that complementary proteins and peptides form complexes with increased antigenicity and/or autoimmunogenicity. Five case studies are highlighted: 1) diphtheria toxin-antitoxin (antibody), which induces immunity to the normally non-antigenic toxin, and autoimmune neuritis; 2) tryptophan peptide of myelin basic protein and muramyl dipeptide ("adjuvant peptide"), which form a complex that induces experimental allergic encephalomyelitis; 3) an insulin and glucagon complex that is far more antigenic than either component individually; 4) various causes of experimental autoimmune myocarditis such as C protein in combination with its antibody, or coxsackie B virus in combination with the coxsackie and adenovirus receptor; 5) influenza A virus haemagglutinin with the outer membrane protein of the Haemophilus influenzae, which increases antigenicity. Several mechanisms cooperate to alter immunogenicity. Complexation alters antigen processing, protecting the components against proteolysis, altering fragmentation and presenting novel antigens to the immune system. Complementary antigens induce complementary adaptive immune responses (complementary antibodies and/or T cell receptors) that produce circulating immune complexes (CIC). CIC stimulate innate immunity. Concurrently, complementary antigens stimulate multiple Toll-like receptors that synergize to over-produce cytokines, which further stimulate adaptive immunity. Thus innate and adaptive immunity form a positive feedback loop. If components of the complex mimic a host protein, then autoimmunity may result. Enhanced antigenicity for production of improved vaccines and/or therapeutic autoimmunity (e.g., against cancer cells) might be achieved by using information from antibody or TCR recognition sites to complement an antigen; by panning for complements in randomized peptide libraries; or using antisense peptide strategies to design complements.
 ...
PMID:How to Make a Non-Antigenic Protein (Auto) Antigenic: Molecular Complementarity Alters Antigen Processing and Activates Adaptive-Innate Immunity Synergy. 2617 68