Influx of inflammatory cells

NiS04 and NiCl2 instilled into rat lungs also produced an inflammatory response (17). However, analysis of bronchoalveolar lavage fluid from rodents exposed to diesel exhaust containing 3.5 mg soot/m3, 7 h/day for 2, 12 or 17 days indicated no influx of inflammatory cells (20). Thus, the diesel soot, at lung burdens of 0.5 mg/g lung, does not produce an acute inflammatory response. 

Therapeutic irradiation is known to have multiple interactions with the vasculature of the irradiated tissue (12). Radiation has direct cytotoxic effects on the vascular endothelium, likely due to induction of oxidative injury. Radiation-induced injury stimulates inflammation and influx of inflammatory cells in addition to creating aprocoagulant state in the vascular space by the transcriptional induction of tissue factor with the subsequent activation of coagulation factors as well as von Willebrand factor and platelets. Experimental evidence suggests that the mechanism by which radiation initiates these responses is in part through the induction of cell-adhesion molecules including ICAM-1, E-selectin, and P-selectin and in part through local cytokine production and release (13). 

Allergic asthma patients have higher blood levels of NGF. The influx of inflammatory cells in lungs is observed as the neurotrophin expression is augmented. Multiple targets may be affected by neurotrophins as they play a role in allergic inflammation, which include recruitment, maintenance and activation of mast cells and eosinophils and facilitation of TH2 response. Whether neurotrophins can alter TH1/TH2 balance in humans has not yet been established. 

Figure 2 Diagram outlining the pathogenesis of liver fibrosis. Damage to parenchymal cells (PC) results in the activation of Kupffer cells (KC) and endothelial cells (EC) and the influx of inflammatory cells (IC). These cells release growth factors, cytokines, and ROS that induce the activation and proliferation of hepatic stellate cells (HSC). HSC gradually transform into a myofibroblasts (MF), the major producers of extracellular matrix proteins (ECM).

Alveolar lining fluid contains higher concentrations of glutathione (GSH) than found in most extracellular fluids (151). The concentration of GSH in BALF from patients with IPF is 23% of normal (152). Depletion of GSH may place the alveolar space at increased risk of additional injury caused by ROS generated by the influx of inflammatory cells during the inflammatory phase of the development... 

Vascular permeability Mucosal permeability Smooth muscle contraction Influx of inflammatory cells Influx of inflammatory cells Vascular permeability Vascular permeability... 

Repeated exposure of sensitized mice to nebulized OVA (OVA mice) without SEB contact induced bronchial inflammation characterized by mainly eosinophils in the BAL fluid and influx of inflammatory cells in bronchial tissue, as illustrated on hematoxylin-and-eosin-stained sections. When SEB was administered onto the nasal mucosa during the development of bronchial allergic inflammation in response to OVA inhalation, bronchial inflammation was clearly aggravated. Compared to nasal application of SEB in OVA mice, bronchial administration of SEB in OVA mice equally aggravated the inflammatory response in the lower airways. Thus, in bronchial tissue of OVA mice, the inflammatory response was aggravated by SEB contact via the nose and the bronchi. 

HETE, and leukotriene in combination with increases in capillary permeability induced by other mediators such as histamine, the leukotrienes, and PAF leads to the influx of inflammatory cells (neutrophils, eosinophils, and macrophages) into the lung. These elicited cells may then be direct contributors to the secondary inflammatory response often associated with an attack of allergic asthma. 

CB2-receptors also exist, in low levels, in cells of the gastrointestinal and cardiovascular system, bone and neuronal cells, liver tissue, and other ceU types [26]. CB2 is up-regulated in inflamed colonic tissue of colitis patients. It is believed that the CB2-receptors are in close interaction with the PPARy-receptor, and both are considered targets for treatment of inflammatory bowel diseases. That was the motivation for Bento et al. [27] to investigate the effect of oral BCP in DSS (dextran sulfate sodium)-induced colitis experimental models. The results showed that BCP inhibited the influx of inflammatory cells. 

Bascom R, Pipkom U, Lichtenstein LM, Naclerio RM. The influx of inflammatory cells into nasal washings during late response to antigen challenge effect of corticosteroid pretreatment. Am Rev Respir Dis 1988 138 406-412. 

Figure 2 Schematic of the transport of metal associated with particles and fibers by the host Mediators can function to protect the host by (1) directing an influx of inflammatory cells that have a capacity to isolate the iron by reducing the Fe " using superoxide and (2) modifying iron metabolism in the host resulting in the sequestration of the catalytically active iron associated with these dusts. Mediator release after exposure to silica and asbestos may represent an attempt of the cell to coordinate the transport and sequestration of catalytically active iron. This response would diminish the oxidative stress associated with the particle and fiber and injury after their exposure.

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