Macrophage chemotactic factor

A macrophage chemotactic factor (MAC) which causes an aeeumulation of mononuclear phagoeytes at the site of the antigen-mediated lymphokine release. 

The mechanism of migration of macrophages to the interstitial lung tissue is not clear. However, it is possible that the increase in vascular permeability after the paraquat exposure iji vivo (12) results in the production of a macrophage chemotactic factor from plasma proteins (13,14) at the interstitial lung tissue. 

TH2 helper cells Pro-Inflammatory Activation of macrophages Produces lnterleukln-2 (IL-2), interferon-y (IFN-y), IL-3, TNF-a, granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage chemotactic factor (MCF), migration inhibitor factor (MIF) Induce lgG2a CD4+... 

Of four guinea pig C3 fragments, C3a, C3b, C3c, and C3d, made with trypsin, only C3b is capable of stimulating spleen cells to elaborate a macrophage chemotactic factor which is similar in molecular size to the chemotactic factor generated after stimulation by lipopolysaccharides (Koopman et al., 1976). 

IkB inhibitory protein kappa B lCAM-1 intercellular adhesion molecule 1 lL-1 interleukin-1 LDL low density lipoprotein MAPKs mitogen activated protein kinases MCP-1 macrophage chemotactic protein 1 M-CSF macrophage colony stimulating factor mmLDL minimally modified LDL NAC A-acetylcysteine NF-kB nuclear factor-kappa B oxLDL oxidised LDL PKC protein kinase C PMA phobol myristate acetate ROS reactive oxygen species TNF-a tumour necrosis factor alpha AM-1 vascular cell adhesion molecule 1... 

Alveolar macrophages release a number of inflammatory mediators, including PAF and leukotrienes B4, C4, and D4. Production of neutrophil chemotactic factor and eosinophil chemotactic factor furthers the inflammatory process. 

Figure 4.8. Hypothesis for the local generation of mast-cell-stimulating peptides by the action of neutrophil-derived enzymes on albumin. Initial stimulation of the mast cell by any of a variety of agents causes the release of preformed histamine (H) neutrophil and eosinophil chemotactic factors (NCF, ECF) and enzymes and the de novo synthesis of prostaglandins (PG) and leukotrienes (LT). These agents increase vascular permeability and vessel diameter. As a result, albumin and later neutrophils (PMN) enter the tissue space where the latter undergo phagocytosis and the secretion of proteolytic enzymes to the extracellular space where they act on albumin to generate NRP (neurotensin-related peptide) and HRP (histamine-releasing peptide). These newly formed peptides then act as a second stimulus to the mast cell. In addition NRP and HRP may affect other immunocompetent celt such as monocytes, macrophages or eosinophils.

One approach to examining inflammation is the assay reported by Elgebaly et al. (1987) for the release of chemotactic factors. Earlier work has elegantly shown that neutrophil or macrophage infiltration from either the endothelial or epithelial surface... 

An immediate response to dust inhalation is the migration of polymorphonuclear leukocytes (PMNs) across epithelial—endothelial junctions to the alveolar space (see Fig. 3.6). Macrophages release a chemotactic factor that mobilizes and attracts PMNs from the pulmonary blood. However, the initial PMN accumulation clears rapidly. 

Macrophage release of chemotactic factors also attracts fibroblasts, an effect that has been studied in animals and humans. The factors are sufficiently strong and specific that fibroblasts migrate up a concentration gradient (tested in artificial chambers) and can induce replication (in vivo experiments). Thus, fibroblasts—the primary source of structural proteins, notably collagen— can be mobilized by AM to the inflammatory sites and can also markedly increase in number in response to secretion of activated AMs. These factors, in addition to the other activities and secretions of the AM, are being characterized (Gee, 1984). 

Levamisole (Ergamisol) was originally developed as an antihelminthic drug (see Chapter 54). It potentiates the stimulatory effects of antigens, mitogens, lymphokines, and chemotactic factors on lymphocytes, granulocytes, and macrophages. It has been shown to increase T cell-mediated immunity. 

Gold alters the morphology and functional capabilities of human macrophages—possibly its major mode of action. As a result, monocyte chemotactic factor-1, interleukin-8, interleukin-IB production, and vascular endothelial growth factor are all inhibited. Intramuscular gold compounds also alter lysosomal enzyme activity, reduce histamine release from mast cells, inactivate the first component of complement, and suppress the phagocytic activities of polymorphonuclear leukocytes. Auranofin also inhibits release of prostaglandin E2 and leukotriene B4. 

Inflammation is a common component associated with sepsis, meningitis, as well as respiratory tract, urinary tract, viral, and bacterial infections (Table 1). Bik is elevated during bacterial or viral infection. The presence of urinary Bik correlates well with standard urinalysis tests for urinary tract infections [20]. Endotoxins released from infectious pathogens induce inflammation and immune cell activation. Macrophages release interleukins and cytokines (IL-1, IL-6, IL-12, IL-15, IL-18, TNF-a) on exposure to lipo-polysaccharide (LPS) and lipoteichoic acid (LTA) endotoxins. These cytokines act as a chemotactic factors causing immune cell migration to the site of the infection followed by activation and release of proteases. Cytokines also induce increased vascular permeability in the endothelial. Bik suppresses further cytokine release by protease and intern additional migration and activation of immune cells. Additionally, a stabilization of the immune cell membrane prevents further release of proteases [4]. 

Hayes AA, Venaille TJ, Rose AH, et al. 1990. Asbestos-induced release of a human alveolar macrophage-derived neutrophil chemotactic factor. Exp Lung Res 16 121-130. 

Wariieit DB, Hill LH, George G, et al. 1986. Time course of chemotactic factor generation and the corresponding macrophage response to asbestos inhalation. Am Rev Respir Dis 134 128-133. 

Macrophage Migration Inhibitory factor (MAP), macrophage activating factor, macrophage aggregating factor, chemotactic factor, AG-dependent MIF... 

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