Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interferon (IFN)-gamma was subcutaneously administered to four patients with chronic granulomatous disease (CGD) in order to evaluate its effects in controlling infection. Patients 1 to 3 were all males, while patient 4 was female. In patients 2 and 4, the length of infection-associated hospitalization during the year of IFN therapy was significantly shorter than that during the whole observed period prior to IFN therapy. In patients 1 and 2, the length of hospitalization during a year of IFN therapy was shorter than that during 1 year prior to the therapy. Patient 3 exhibited no reduction in terms of the length of infectious disease during IFN therapy, because he suffered from a liver abscess before and during the therapy. As soon as the IFN therapy was stopped, patient 2 developed pneumonia and lymphadenitis, which were promptly relieved by readministering the agent. During 1 year of IFN therapy, patients 1, 2 and 4 showed no significant changes in either the nitroblue tetrazolium test, O2- production or the expression of NADPH oxidase components in neutrophils. On the other hand, the O2- generating ability of neutrophils from patient 3 slightly increased. Our limited observations suggest that IFN-gamma may be variably beneficial for infection control in CGD-patients, irrespective of the in vitro phagocyte functions. A longer follow-up time is needed to confirm the IFN response in CGD-patients.
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PMID:Interferon-gamma therapy for infection control in chronic granulomatous disease. 764 79

Entamoeba histolytica is the parasite responsible for human amoebiasis. The analysis of the natural resistance mechanisms of some rodents to amoebic liver abscess (ALA) may reveal alternative pathogenicity mechanisms to those previously discovered in the experimental model of ALA in hamsters. In this work the natural resistance of BALB/c mice to ALA was explored by performing: (i) in vivo chemotaxis analysis with a specifically designed chamber; (ii) in vitro amoebic survival in fresh and decomplemented serum; (iii) histological temporal course analysis of ALA development in mice with different treatments (hypocomplementemic, hyperimmune and treated with iNOS and NADPH oxidase inhibitors) and (iv) mouse liver amoebic infection by both in situ implantation of ALA from hamsters and inoculation of parasites into the peritoneal cavity. The results show that E. histolytica clearance from the mouse liver is related to a low chemotactic activity of complement, which results in poor inflammatory response and parasite inability to cause tissue damage. Also, the absence of amoebic tropism for the mouse liver is correlated with resistance to experimental liver amoebiasis.
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PMID:Mechanisms of natural resistance of Balb/c mice to experimental liver amoebiasis. 3097 31