PMN influx

Induction of oral tolerance was prevented by the administration of anti-MCP-1. These results indicate that CKs play an important role in the induction of oral tolerance. There is evidence that both CXC and CC CKs are integral components of antibacterial host defense. Specifically, in vitro studies indicate that CXC CKs (lL-8 and MIP-2) and the CC CK MIP-la augment the ability of PMNs and alveolar macrophages, respectively, to phagocytose and kill E. coli. In addition, the intratracheal instillation of Klebsiella pneumoniae in mice results in time-dependent production of MIP-2 and MIP-la. Inhibition of MIP-2 bioactivity in vivo results in decreases in lung PMN influx, impaired bacterial clearance, and early mortality. ... 

Tissue injury induces a rapid mobilization of PMN out of the general circulation and into the tissues. The life span of the tissue-infiltrating PMN is considerably prolonged. Twenty-four hours after the onset of the inflammatory reaction, a large number of PMN are still present at the inflammatory site despite the cessation of PMN influx after 1-4 h [6]. Stimulation with GM-CSF, G-CSF, IFN-7, IL-ip, IL-2, IL-4, lL-6 and IL-15 can rescue PMN from preprogrammed apoptosis [7]. The specific genes required for PMN apoptosis... 

CXCR2 K. pneumoniae, P. aerugi- Impaired lung PMN influx. 

L pneumophila Decreased limg PMN influx, impaired T-1 cytokine expression, decreased bacterial clearance and survival... 

A. fumigatus Impaired lung PMN influx, fungal clearance, and the development of fatal invasive disease... 

Figure 5. Pulmonary inflammatory response to chronic diesel exhaust exposure as measured in bronchoalveolar lavage fluid. The total amount or activity of material removed from the lung has been normalized to the weight of control lungs. Inflammatory response is indicated by influx of neutrophils (PMN). Cytotoxicity is indicated by extracellular lactate dehydrogenase (LDH). (Continued on next page.)...

Prevalence of byssinosis correlates better with airborne endotoxin concentration than with total dust (65). Also, gramnegative bacteria levels in the mill correlate well with disease (66). It has been hypothesized that endotoxins elicit symptoms of byssinosis by activation of both the classical and the alternative pathway of complement with subsequent release of anaphylatoxins, which lead to airway narrowing, and chemotaxins, which cause the influx of PMNs followed by release of lysosomal enzymes and, ultimately, tissue damage. In experiments with guinea pigs using bract, cotton, and gin mill trash extracts, there is a strong correlation between number of PMNs recruited to airways and level of endotoxin (67). 

However, the effects of Ca are not seen with all stimuli the production of Of in response to phorbol myristate acetate was unaffected in medium lacking Ca, Lanthanum, which can act as a competitive inhibitor of Ca, reduced the effect of Ca in suspensions of PMNs stimulated with FMLP , That Ca acted by entering the cell was suggested because calcium ions did not affect the binding of FMLP. However, verapamil which blocks the channel for Ca in cell membranes, produced dose-dependent inhibition of the formation of Of and of the influx of Ca. This inhibition could be overcome by increasing the concentration of Ca in the medium . The reasons for the requirement of Ca for activation by some stimuli but not by others might be related to the site at which the stimulus in question acts. PMA, for example, might act at a site beyond the point at which Ca is required. 

Contrary to this anticipated effect is the effect of products of the burst on chemotactic factors. Clark and Klebanoff showed that both chemotaxins, Cja and FMLP, lost chemotactic activity in the myeloperoxidase system. The anticipated consequence of this action of myeloperoxidase would be to terminate the influx of PMNs into an inflamed site. 

For the case of T. gondii, we found that intraperitoneal tachyzoite injection induces a rapid influx of IL-12-positive PMN (fig. 2). However, although neutrophils are only a minor population in control animals injected with endotoxin-free PBS, approximately 75% of these PMN are IL-12-positive [62]. A similar result was found in noninjected animals, ruling out the possibility that injection alone provides a stimulus for PMN IL-12 induction. Furthermore, approximately 40% of the neutrophils in peripheral blood from noninfected mice are lL-12-positive, arguing against exit from the peripheral blood as a stimulus for lL-12 synthesis [62]. 

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