Impact of Eurygaster maura (Heteroptera: Scutelleridae) feeding on quality of bread wheat in relation to attack period.

Sunn pest (or cereal bug) (Heteroptera: Pentatomidae and Scutelleridae) infestations of wheat, Triticum aestivum L., in the grain filling stage have the potential to adversely affect the quality of harvested grain for bread making. In the absence of resistant wheat cultivars, producers must rely on chemical control to protect their crop from sunn pest infestations. To implement an efficient environment friendly control strategy, there is a need to pinpoint the relationships between the timing of the bug attack and gluten degradation. Recent outbreaks of Eurygaster maura (L.) in northwestern Italy have increased the local concern toward this problem. A 3-yr study was carried out by caging plants of two bread wheat cultivars, characterized by different seed texture and bread-making quality, and introducing adults of E. maura in four periods corresponding to different grain filling stages: heading, early milk-ripe, milk-ripe, and late milk-ripe. The degree of bread-making quality depletion was assessed by analytical and biochemical methods and related to the attack period. Using analysis of variance, significant differences were found in the quality traits of kernels attacked by E. maura in different grain filling stages, the maximum damage occurring with bug feeding at the late milk-ripe stage. Biochemical investigations on gluten confirmed analytical results; in grain samples infested at the late milk-ripe stage, SDS gel electrophoresis revealed the degradation of some components of the high-molecular-weight glutenins, and high-performance liquid chromatography analyses showed a breakdown of the first peak of the insoluble fraction, mainly containing polymeric proteins highly related to dough strength.

Hypoxia inhibits the expression of the CCR5 chemokine receptor in macrophages.

Hypoxia, a decrease in oxygen tension occurring in pathological tissues, has a profound effect on macrophage functions. Here, we provide the first evidence that hypoxia inhibits CCR5 chemokine receptor expression in mouse macrophages. CCR5 was constitutively expressed in macrophages and upregulated by IFNgamma. Hypoxia downregulated both constitutive and IFNgamma-induced CCR5 mRNA and protein. Reoxygenation of hypoxic cells reverted CCR5 inhibition. CCR5 upregulation by IL-10, LPS, and IL-4 was also antagonized by hypoxia. CCR5 inhibition may be a way to retain/concentrate recruited macrophages at hypoxic sites or a feedback mechanism to control the autocrine activation of macrophages which produce CCR5 ligands.

Macrophage activating properties of the tryptophan catabolite picolinic acid.

Recent studies have suggested a role for aminoacid catabolites as important regulators of macrophage (Mphi) activities. We reported previously that picolinic acid (PA), a tryptophan catabolite produced under inflammatory conditions and a costimulus with IFNgamma of Mphi effector functions, is a selective inducer of the Mphi inflammatory protein-1alpha (MIP-1alpha) and -1beta (MIPs), two CC-chemokines involved in the elicitation of the inflammatory reactions and in the development of the Th1 responses. In this study, we have investigated the effects of IFNgamma on PA-induced MIPs expression and secretion by mouse Mphi as well as the regulation of MIP-1alpha/beta receptor, CCR5, by both stimuli alone or in combination. We demonstrated that IFNgamma inhibited MIPs mRNA stimulation by PA in a dose-and time-dependent fashion, despite its ability to induce other CC- or CXC chemokines. MIPs mRNA down-regulation was associated with decreased intracellular chemokine expression and secretion and was dependent on both mRNA destabilization and gene transcription inhibition. Moreover, IFNgamma inhibitory effects were stimulus-specific because MIPs induction by PA was either unaffected or increased by the anti-inflammatory cytokines, IL-10 and IL-4, or the pro-inflammatory stimulus, LPS, respectively. In contrast, we found that IFNgamma increased CCR5 basal expression, whereas PA down-regulated both constitutive and IFNgamma-induced CCR5 mRNA and protein levels. These results demonstrate that IFNgamma and PA have reciprocal effects on the production of MIPs chemokines and the expression of their receptor. The concerted action of IFNgamma and PA on MIP-1alpha/beta chemokine/receptor system is likely to be of pathophysiological significance and to represent an important regulatory mechanism for leukocyte recruitment and distribution into damaged tissues during inflammatory responses.