The role of leukocyte chemotaxis in inflammation

Rot, Antal

doi:10.1007/978-94-011-2996-1_14

Cited by 13 publications

(6 citation statements)

References 204 publications

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“…Movement of inflammatory cells from the vascular space to a site of injury is dependent on the co-ordinated expression of adhesion molecules on both the monocytes and endothelium, and on the generation of a chemotactic gradient via the elaboration of specific chemotactic factors [31]. In the present study, the relative potential of various MCF released from A549 cells in response to TNF-a and IL-1a were evaluated.…”

Section: Discussionmentioning

confidence: 97%

Monocyte chemotactic factors released from type II pneumocyte-like cells in response to TNF-alpha and IL-1alpha

Koyama¹,

Sato²,

Nomura³

et al. 1999

Eur Respir J

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It has been reported that tumour necrosis factor (TNF)-a and interleukin (IL)-1 induce the release of monocyte chemotactic factors (MCF), including chemokines, from A549 cells, an alveolar type II cell line. However, the relative contribution of these chemokines to MCF is still uncertain.In the present study, the relative contribution of various chemokines released from A549 cells acting as MCF upon stimulation by TNF-a and IL-1a, was evaluated.TNF-a and IL-1a induced the release of MCF in a dose-and time-dependent manner (p<0.001). The release of MCF was inhibited by cycloheximide and lipoxygenase inhibitors. Molecular sieve column chromatography revealed multiple peaks of MCF (near 60 kDa, 25±22 kDa, 15±13 kDa, 8 kDa, and 400 Da). Leukotriene B 4 (LTB 4 ) receptor-antagonists inhibited MCF by 50% after 24 h and 30% after 72 h. Monocyte chemoattractant protein-1 (MCP-1), transforming growth factor (TGF)-b, "regulated on activation, normal T-cells, expressed and secreted" (RANTES), and granulocyte-macrophage colony-stimulating factor (GM-CSF) were released significantly in response to IL-1a and TNF-a, and antibodies to MCP-1, GM-CSF, and RANTES inhibited MCF activity by 40, 5 and 20% after 24 h, and by 50, 20, and 10% after 72 h, respectively. Each antibody or LTB 4 receptor-antagonist inhibited the corresponding column chromatography-separated molecular weight peak of MCF.These data suggest that A549 cells release monocyte chemoattractant protein-1 as the predominant monocyte chemotactic factor rather than granulocyte-macrophage colony-stimulating factor, RANTES, and transforming growth factor-b, and that leukotriene B 4 is constitutively released as a monocyte chemotactic factor. Eur Respir J 1999; 13: 820±828. The alveolar macrophage, an important phagocyte of the pulmonary airspace and the interstitium, is derived predominantly from differentiated peripheral blood monocytes and to a limited extent from local macrophage replication [1±3]. The recruitment of peripheral blood monocytes to the lung is essential for normal lung immune function but it is also involved in the generation and evolution of an inflammatory response to pulmonary injury. During acute and chronic inflammation, the process of monocyte elicitation is accelerated resulting in a transient or more prolonged increase in alveolar macrophages [4,5]. Although elicited macrophages serve a vital role in the host defence against a number of organisms, the presence of increased numbers of activated macrophages can lead to excessive tissue injury via excessive elaboration of inflammatory cytokines, eicosanoids, proteolytic enzymes, and oxygen radicals [6±8].Alveolar type II (ATII) epithelial cells have been shown to play a significant role in the regulation of the alveolar space. ATII cells synthesize and secrete surfactant, control the volume and composition of the epithelial lining fluid, and proliferate and differentiate into type I alveolar epithelial cells after lung injury in order to maintain the integrity of alveolar wall [9]. Moreove...

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Section: Discussionmentioning

confidence: 97%

Monocyte chemotactic factors released from type II pneumocyte-like cells in response to TNF-alpha and IL-1alpha

Koyama¹,

Sato²,

Nomura³

et al. 1999

Eur Respir J

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“…However, mounting evidence suggests that TNF is a critical component of effective antibacterial host defense (7,9,13,16). Specifically, TNF is a potent activator of both PMN and macrophages, leading to enhancement of protease release, stimulation of the respiratory burst, and induction of leukocyte and vascular adhesion molecule expression, which are essential for transmigration of these cells into sites of infection (8,19,26). Moreover, PMN and macrophage microbicidal activity is augmented by endogenous or exogenous TNF (24,28).…”

mentioning

confidence: 99%

Tumor necrosis factor mediates lung antibacterial host defense in murine Klebsiella pneumonia

et al. 1996

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Tumor necrosis factor (TNF) is a proinflammatory cytokine which has recently been shown to have beneficial effects in the setting of acquired host immunity. However, the role of TNF in innate immune responses, as in the setting of bacterial pneumonia, has been incompletely characterized. To determine the role of TNF in gram-negative bacterial pneumonia, CBA/J mice were challenged with 10 2 CFU of Klebsiella pneumoniae intratracheally, resulting in the time-dependent expression of TNF MRNA and protein within the lung. Passive immunization of animals with a soluble TNF receptor-immunoglobulin (Ig) construct (sTNFR:Fc) intraperitoneally 2 h prior to K. pneumoniae inoculation resulted in a significant reduction in bronchoalveolar lavage neutrophils, but not macrophages, at 48 h, as compared with animals receiving control IgG1. Furthermore, treatment with sTNFR:Fc resulted in 19.6-and 13.5-fold increases in K. pneumoniae CFU in lung homogenates and plasma, respectively, as compared with animals receiving control IgG1. Finally, treatment of Klebsiellainfected mice with sTNFR:Fc markedly decreased both short-and long-term survival of these animals. In conclusion, our studies indicate that endogenous TNF is a critical component of antibacterial host defense in murine Klebsiella pneumonia.

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“…Invasion by gram-positive and gram-negative bacterial organisms triggers a rather complex and dynamic host response, which is characterized by the recruitment and activation of inflammatory leukocytes. The elicitation of inflammatory cells to a site of infection is dependent upon the coordinated expression of adhesion molecules on leukocytes and endothelial cells, as well as the establishment of chemotactic gradients via the local generation of chemotactic factors (22). The resident mononuclear phagocytes (M+) are believed to be critically involved in the process of leukocyte recruitment, since these cells are the predominant cellular source of several proinflammatory mediators, including tumor necrosis factor alpha (TNF-a) (30), interleukin-1 (IL-1) (8), and a variety of leukocyte chemotactic factors.…”

mentioning

confidence: 99%

Lipoteichoic acid induces secretion of interleukin-8 from human blood monocytes: a cellular and molecular analysis

et al. 1994

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Invasion by gram-positive and gram-negative bacterial organisms is characterized immunopathologically by the activation of mononuclear phagocytic cells, leading to the elaboration of macrophage-derived regulatory and chemotactic factors, and the resultant influx of inflammatory leukocytes. Little is known regarding the mechanisms by which gram-positive organisms initiate macrophage activation and subsequent inflammation. In this investigation, we postulated that lipoteichoic acid (LTA) purified from two different gram-positive bacterial species was an important signal for the expression of chemotactic cytokines from human peripheral blood monocytes (PBM). In initial experiments, we demonstrated that cell-associated interleukin-8 (IL-8) was expressed by mononuclear phagocytes present in inflamed areas of endocardium in cases of acute Staphylococcus aureus endocarditis. We next demonstrated that LTA purified from either Staphylococcus aureus or Streptococcus pyogenes induced the time-and dose-dependent expression of IL-8 mRNA and protein from human PBM. The expression of IL-8 mRNA from LTAbut not lipopolysaccharide (LPS)-treated PBM was superinduced by concomitant treatment with cycloheximide, indicating that the expression of IL-8 mRNA from LTA-treated PBM was negatively controlled by repressor proteins. Furthermore, mRNA stability studies indicated that IL-8 mRNA was less stable in the presence of LTA than in the presence of LPS. Our findings indicate that LTA can induce the secretion of the polymorphonuclear leukocyte chemotactic factor IL-8 and that LTA may be an important cellular mediator of inflammatory cell recruitment that characterizes immune responses to gram-positive bacterial infections.

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The role of leukocyte chemotaxis in inflammation

Cited by 13 publications

References 204 publications

Monocyte chemotactic factors released from type II pneumocyte-like cells in response to TNF-alpha and IL-1alpha

Monocyte chemotactic factors released from type II pneumocyte-like cells in response to TNF-alpha and IL-1alpha

Tumor necrosis factor mediates lung antibacterial host defense in murine Klebsiella pneumonia

Lipoteichoic acid induces secretion of interleukin-8 from human blood monocytes: a cellular and molecular analysis

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