Cytokines alveolar macrophages

Jordana, M., Richards, C., Irving, L.B. and Gauldie, J. (1988). Spontaneous in vitro release of alveolar macrophage cytokines after the intratracheal instillation of bleomycininrats. Am. Rev. Resp. Dis. 137, 1135-1140. 

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]... 

Matsunaga, K. et al., Involvement of nicotinic acetylcholine receptors in suppression of antimicrobial activity and cytokine responses of alveolar macrophages to Legionella pneumophila infection by nicotine, J. Immunol.. 167, 6518, 2001. 

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. 

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... 

Rolls, J. K., Lei, D., Nelson, S., Summer, W. R. and Shellito, J. E. (1997). Pulmonary cytokine gene therapy. Adenoviral-mediated murine interferon gene transfer compartmentally activates alveolar macrophages and enhances bacterial clearance. Chest 111, 104S. 

Blockade of a2, Pi and p2-adrenoreceptors on LPS-stimulated alveolar macrophages reduces the release of interleukin (IL)-ip, IL-6 and cytokine-induced neutrophil chemoattractant-1. In this same condition, TNFa release is also strongly reduced by a2 and p2-adrenoreceptors antagonists. However, the blockade of a2-adrenoreceptors reached the most consistent suppression of the investigated cytokines (Flierl et al., 2007). 

After binding and phagocytosis, alveolar macrophages and monocytes release pro-inflammatory cytokines, e.g. lL-1, interferon-y and tumor necrosis factor-a (fig. 1). These cytokines activate resident cells (epithelial cells, fibroblasts) to produce chemokines such as lL-8, granulocyte-monocyte-colony-stimulating factor, RANTES (regulated on activation normal T cell expressed and secreted) that will result in a second wave of cell recruitment (mononuclear and polymorphonuclear cells). 

Drumm K, Buhl R, Kienast K. 1999. Additional N02 exposure induces a decrease in cytokine specific mRNA expression and cytokine release of particle and fibre exposed human alveolar macrophages. Eur J Med Res 4 59-66. 

Geist EJ, Powers ES, Monick MM, et al. 2000. Asbestos stimulation triggers differential cytokine release from human monocytes and alveolar macrophages. Exp Fung Res 26 41-56. 

Mongan LC, Jones T, Patrick G. 2000. Cytokine and free radical responses of alveolar macrophages in vitro to asbestos fibres. Cytokine 12(8) 1243-1247. 

Perkins RC, Scheule RK, Hamilton R, et al. 1993. Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposure. Exp Lung Res 19(l) 55-65. 

Culpitt SV, Rogers DF, Shah P, de Matos C, Russell RE, Donnelly LE, Barnes PJ. Impaired inhibition by dexamethasone of cytokine release by alveolar macrophages from patients with chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 44. 2003 167 24-31. 

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). 

---