Macrophages alveolar, cytokine production

Losa Garcia JE, Mateos RF, Jimenez A, Salgado MJ, et al. 1998. Effect of cyclosporin A on inflammatory cytokine production by human alveolar macrophages. Resp Med. 92 722-728. 

Baldwin GC, Tashkin DP, Buckley DM, Park AN, Dubinett SM, Roth MD (1997) Marijuana and cocaine impair alveolar macrophage function and cytokine production. Am J Respir Crit Care Med 156 1606-161.3... 

Sugiyama, Y, Yanagisawa, K., Tominaga, S.-I., and Kitamura, S. (1999). Effects of long-term administration of erythromycin on cytokine production in rat alveolar macrophages. Eur. Respir. 

Abe, Y., Hashimoto, S., and Horie, T., Curcumin inhibition of inflammatory cytokine production by human peripheral blood monocytes and alveolar macrophages, Pharmacol Res., 39(1), 41 1,1999. 

Exposure of guinea pig alveolar macrophages to 0.4 ppm O3 for 60 min increased the IL-6 activity by 252 60% and TNF activity by 202 35% (Arsa-LANE et al. 1995). The increase of monokine production by human alveolar macrophages was 443 208% for TNFa 484 171% for IL-ip, 383 147 % for IL-6, and 226 45 % for IL-8 after a 60 min exposure to 0.4 ppm O3. Lowest O3 concentrations (0.1 and 0.2 ppm) only increased TNFa secretion. Shorter (30 min) or longer (120 min) exposure duration to 0.4 ppm O3 were also associated with a significant increase in monokine production, suggesting that the effect of ozone on cytokine production did not depend on the exposure duration. The mRNA expression of TNFa, IL-ip, IL-6, and IL-8 was increased in human alveolar macrophages. 

Becker S, Soukup JM, Gilmour IM, Devlin RB. Stimulation of human and rat alveolar macrophages with urban air particulates effects on oxidant radical generation and cytokine production. Toxicol Appl Pharmacol 1996 141 637-648. 

Intratracheal instillation 14d Alveolar macrophages activation production pro-inflammatory cytokines Blood high-levels pro-inflammatory cytokines differentiation of CD4+ T cell to Thl and Th2 cells [108]... 

Airway epithelia and alveolar macrophages constitutively express neurotrophins, and under normal conditions, low levels of neurotrophins are produced. However, in allergic inflammation, these levels rise considerably in atopic patients. After inhalation of an allergen by asthmatic patients, there are high concentrations of NGF, NT-3 and BDNF. The cellular sources of the increased neurotrophins include invading leukocytes and resident lung cells. Inflammatory cytokines, IL-1 and TNF-a stimulate epithelial neurotrophin expression. The increased production of neurotrophins... 

M. tuberculosis bacteria persist in the harsh environment of the host s alveolar macrophages. These bacteria are able to survive by downregulating the host s immune response. Specifically, M. tuberculosis prevents activation of the infected macrophages. Macrophage activation would lead to production of pro-inflammatory cytokines, such as IL-12, IL-18 and tumor necrosis factor a (TNF-a), and to production of interferon-y producing T cells, allowing the host to combat the infection [303]. Both the LAMs and the mycolic acids of M. tuberculosis are able to modulate the host s immune response. 

Bilyk, N. and Holt, P.G. (1994). Cytokines modulate the immunosuppressive phenotype of pulmonary alveolar macrophages via regulation of nitric oxide production (submitted). 

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