Macrophages Respiratory activity

Reynaud, S. et al., The effects of 3-methylcholanthrene on macrophage respiratory burst and biotransformation activities in the common carp (Cyprinus carpio L.), Fish Shellfish Immunol., 12, 17, 2002. 

In the early 90 s, a clinical trial on Feibao syrup , which contains H. diffusa together with Radix astragali and other medicinal plant extracts, was reported. In this study, Feibao syrup was used to treat reversal respiratory tract infection in children. The clinical research proved that after taking the medicine, the general condition was improved and if the disease occurred, the symptoms were mild and the disease course was short. The efficacy of the medicine was 92.5%. Furthermore, experiment on mice indicated that the medicine could enhance the macrophage phagocytic activity and lymphocyte transformation rate [41]. 

Alveolar macrophage Respiratory bursts, superoxide generation Antibacterial activity... 

Arthur, M.J.P., Kowalski-Saunders, P. and Wright, R. (1986a). C. /Mm -elicited hepatic macrophages demonstrate enhanced respiratory burst activity compared with resident Kupffer ceUs in the rat. Gastroenterology 91, 174-181. 

Mahida, Y.R., Wu, K.C. and Jewell, D.P. (1989). Respiratory burst activity of intestinal macrophages in normal and inflammatory bowel disease. Gut 30, 1362-1370. 

Inflammatory cell phenomenon are also contributors to lipid peroxidation. Activated neutrophils may adhere to damaged endothelium and amplify traumatic, ischaemic or ischaemia-reperfiision injury. Many cyclooxygenase products of the metabolism of atachidonic acid modulate the inflammatory responses of cells. Macrophages, neutrophils and microglia are important sources of reactive oxygen at the injury site. When activated, they produce a respiratory burst that is traced to activated nicotinamide adenine dinucleotide (NADPH/NADH) oxidase. 

Respiratory allergies and infections are the most common form of illness in the United States and Europe and account for more missed school and work days than any other disease [1], A substantial body of experimental work has clearly shown that airborne toxicants such as tobacco smoke, ozone, and other air pollutants can alter many aspects of the host defense network to either decrease resistance to infection, or exacerbate respiratory allergies and asthma [2], Exposure to air toxicants can suppress a number of key host defenses including mucociliary clearance in the airways, pulmonary macrophage function, and development of specific immune responses such as IgG antibody production and cell mediated immunity. In contrast, immune stimulation in the form of increased T cell activity and IgE antibody formation has also has been shown to occur under some circumstances, resulting in increased incidence or severity of allergic lung disease. 

Haeberle, H.A., et al., Respiratory syncytial virus-induced activation of nuclear factor-kappaB in the lung involves alveolar macrophages and toll-like receptor 4-dependent pathways, J. Infect. Dis. 186, 9, 1199, 2002. 

Numerous studies in animals have investigated the respiratory effects of nickel exposure. Intermittent exposure (6 hours/day, 5 days/week) of rats and mice for 16 days or 13 weeks resulted in chronic active inflammation in the lungs, fibrosis, macrophage hyperplasia, interstitial infiltrates, and increased lung weight following exposure to 0.06 mg nickel/m as nickel sulfate, 0.11 mg nickelM as nickel subsulfide, and 0.4 mg nickel/m as nickel oxide (Benson et al. 1987, 1988, 1989 Durmick et al. 

Body weights of female rats were 6-9% lower than controls during the second year. Hematology examinations completed at a 15 month interim sacrifice showed no effects. The only treatment-related changes noted were in the respiratory tract. Minimal to mild chronic active inflammation was observed at all concentrations at the 7 month interim sacrifice, but only at the two higher concentrations at two years. The inflammation was described as multifocal, minimal to mild accumulations of macrophages, neutrophils and cell debris within alveolar spaces. Fibrosis was observed in 2/54, 6/53, 35/53 and 43/53 male rats, and 8/52, 7/53, 45/53, and 49/53 female rats at 0, 0.03, 0.06, and 0.11 mg/m, respectively. Hyperplasia of the bronchial lymph nodes and atrophy of the olfactory epithelium were observed at the high dose. 

IFN-y also induces the costimulatory molecules on the macrophages, which increases cell-mediated immunity. As a consequence, there is activation and increase in the tumoricidal and antimicrobial activity of mononuclear phagocytes, granulocytes and NK cells. The activation of neutrophils by IFN-y includes an increase in their respiratory burst. IFN-y stimulates the cytolytic activity of NK cells. It is an activator of vascular endothelial cells, promoting CD4+ T lymphocyte adhesion and morphological alterations, which facilitates lymphocyte extravasation. IFN-y promotes opsonization by stimulating the production of IgG subclasses that activate the complement pathway. A summary of the characteristics of selected cytokines is shown in Table 2.3. 

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