Recruitment of neutrophils from blood vessels to sites of infection represents one of the most important elements of innate immunity. Movement of neutrophils across blood vessel walls to the site of infection first requires that the migrating cells firmly attach to the endothelial wall. Generally, neutrophil extravasation is mediated at least in part by two classes of adhesion molecules, β2 integrins and selectins. However, in the case of streptococcal pneumonia, recent studies have revealed that a significant proportion of neutrophil diapedesis is not mediated by the β2 integrin/selectin paradigm. Galectin-3 is a β-galactoside-binding lectin implicated in inflammatory responses as well as in cell adhesion. Using an in vivo streptococcal pneumonia mouse model, we found that accumulation of galectin-3 in the alveolar space of streptococcus-infected lungs correlates closely with the onset of neutrophil extravasation. Furthermore, immunohistological analysis of infected lung tissue revealed the presence of galectin-3 in the lung tissue areas composed of epithelial and endothelial cell layers as well as of interstitial spaces. In vitro, galectin-3 was able to promote neutrophil adhesion to endothelial cells. Promotion of neutrophil adhesion by galectin-3 appeared to result from direct cross-linking of neutrophils to the endothelium and was dependent on galectin-3 oligomerization. Together, these results suggest that galectin-3 acts as an adhesion molecule that can mediate neutrophil adhesion to endothelial cells. However, accumulation of galectin-3 in lung was not observed during neutrophil emigration into alveoli induced by Escherichia coli infection, where the majority of neutrophil emigration is known to be β2 integrin dependent. Thus, based on our results, we propose that galectin-3 plays a role in β2 integrin-independent neutrophil extravasation, which occurs during alveolar infection with Streptococcus pneumoniae.

This study examined the moderating effects of child temperament on the association between maternal socialization and 4–6-year-old children’s dynamic respiratory sinus arrhythmia (RSA) change in response to anger-themed emotional materials (N = 180). We used latent growth curve modeling to explore adaptive patterns of dynamic RSA change in response to anger. Greater change in RSA during anger-induction, characterized by more initial RSA suppression and a subsequent return to baseline, was related to children’s better regulation of aggression. For anger-themed materials, low levels of authoritarian parenting predicted more RSA suppression and recovery for more anger-prone children, whereas more authoritative parenting predicted more RSA suppression and recovery for less anger-prone children. These findings suggest that children’s adaptive patterns of dynamic RSA change can be characterized by latent growth curve modeling, and that these patterns may be differentially shaped by parent socialization experiences as a function of child temperament.

During gel (gum) formation in angiosperm trees, fibrillar material accumulated in protective layers of xylem parenchyma cells before being secreted across half-bordered pit membranes into vessel elements. Immunogold labeling demonstrated that this fibrillar material was mainly composed of partially esterified pectic polysaccharides. The primary wall of expanding tyloses, an extension of the parenchyma protective layer, secreted similar pectic substances to completely block vessel elements. In most studies, these occluding structures were reported to be formed in response to causative factors such as aging processes, injuries, or infections. Current observations support the view that partial to complete embolism, which almost always accompanies these factors, might be the main cause triggering the formation of vessel occlusions. Whereas pectin seems to be the basic component of gels (gums) and of the external layer of tyloses, other substances, such as phenols, were also detected either as a part of these plugs or as accumulations beside them in vessels. Finally, it is proposed that the term 'gel' instead of 'gum' be used in future studies to describe the occluding material secreted by ray and paratracheal parenchyma cells.

Pneumococcal pneumonia still is associated with a high mortality rate, despite appropriate antimicrobial therapy. Many gaps remain in the understanding of the pathogenesis of this deadly infection. The microbial and inflammatory events that characterize survival or death after intranasal inoculation of mice with an LD(50) inoculum of Streptococcus pneumoniae were investigated. Survival was associated with rapid bacterial clearance and low inflammation (surfactant and red blood cells in alveoli), but no neutrophil recruitment or lung tissue injury was noted. By contrast, death was preceded by strong bacterial growth that peaked 48 h after the infection and was associated with gradual increases in pulmonary levels of interleukin-6, macrophage inflammatory protein (MIP)-1alpha, MIP-2, monocyte chemoattractant protein-1, KC, and neutrophil recruitment. The injection of tumor necrosis factor-alpha or the addition of lipopolysaccharide or heat-killed S. pneumoniae to the inoculum enhanced early host response and survival. These observations may help develop appropriate markers of evolution of pneumonia, as well as new therapeutic strategies.