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Interleukin lung injury

Nakamura M, Fujishima S, Sawafuji M, Ishizaka A, Oguma T, Soejima K, Matsu-bara H, Tasaka S, Kikuchi K, Kobayashi K, Ikeda E, Sadick M, Hebert CA, Aikawa N, Kanazawa M, Yamaguchi K. Importance of interleukin-8 in the development of reexpansion lung injury in rabbits. Am J Respir Crit Care Med 2000 161 1030-1036. [Pg.111]

Modelska K, Pittet IF, Folkesson HG, Courtney Broaddus V, Matthay MA. Acid-induced lung injury. Protective effect of anti-interleukin-8 pretreatment on alveolar epithelial barrier function in rabbits. Am J Respir Crit Care Med 1999 160 1450-1456. [Pg.111]

Folkesson HG, Matthay MA, Hebert CA, Broaddus VC. Acid aspiration-induced lung injury in rabbits is mediated by interleukin-8-dependent mechanisms. J Clin Invest 1995 96 107-116. [Pg.220]

Antonini JM, Murthy GGK, Brain JD. Responses to welding fumes—lung injury, inflammation, and the release of tumor necrosis factor-alpha and interleukin-1-beta. Exp Lung Res 1997 23 205-227. [Pg.398]

Sekido N, Mukaida N, Harada A, Nakanishi I, Watanabe I, Matsushima K. Prevention of lung perfusion injury in rabbits by a monoclonal antibody against interleukin-8. Nature 1993 365 654-657. [Pg.82]

Many of the manifestations of intraabdominal infections, particularly peritonitis, result from cytokine activity. Inflammatory cytokines, such as tumor necrosis factor a (TNF-a), interleukin 1 (IL-1), IL-6, IL-8, and interferon-y (INF-y), are produced by macrophages and neutrophils in response to bacteria and bacterial products or in response to tissue injury resulting from the surgical incision. These cytokines produce wide-ranging effects on the endothelium of organs, particularly the liver, lungs, kidneys, and heart. With uncontrolled activation of these mediators, sepsis may result (see Chap. 117). [Pg.2057]

Ultrastmctural studies suggest that endothelial and/or epithelial injury precedes inflammation and fibrosis in early SSc-ILD (51). Thereafter, both proliferation of myofibroblasts and the overdevelopment of capillary microvessels seem to be involved in progressive lung fibrosis (66). T lymphocytes may play a fundamental role. T-cell responses to epitopes of DNA topoisomerase I are restricted, both in healthy subjects and in those with SSc (67-69). Thus, the anti-topoisomerase antibody may provoke a pathogenetic immune response in individuals with responsive T-cell clones. Lung tissue of patients with SSc-ILD displays lymphoid follicles with germinal centers and CD4 T cells of both THl and TH2 subsets that express the hallmark profile of cytokines [interleukin-4 (EL-4), EL-5, and y-interferon (INF-y)] in balanced numbers at the mRNA level (10), as well as accumulation of memory type lymphocytes (70). In BAL, patients with SSc-ELD show a predominance of CD8 T cells that produce Th2 cytokines, most notably EL-4, in contrast to those with no ILD (71). [Pg.435]

Arai T, Abe K. Introduction of the interleukin-10 gene into mice inhibited bleomycin-ittdrrcedluttg injury in vivo. Am J Physiol (Lung Cell Mol Physiol) 2000 278 L914-L922. [Pg.452]


See other pages where Interleukin lung injury is mentioned: [Pg.220]    [Pg.297]    [Pg.119]    [Pg.566]    [Pg.3]    [Pg.1117]    [Pg.101]    [Pg.324]    [Pg.432]    [Pg.508]    [Pg.222]    [Pg.229]    [Pg.432]    [Pg.62]    [Pg.317]    [Pg.328]    [Pg.83]    [Pg.121]    [Pg.141]    [Pg.194]    [Pg.465]    [Pg.465]    [Pg.473]   
See also in sourсe #XX -- [ Pg.679 ]




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