RESUMEN

BACKGROUND: The anti-inflammatory peptide, adrenomedullin (AM), and its cognate receptor are expressed in lung tissue, but its pathophysiological significance in airway inflammation is unknown. OBJECTIVES: This study investigated whether allergen-induced airway inflammation involves an impaired local AM response. METHODS: Airway AM expression was measured in acute and chronically sensitized mice following allergen inhalation and in airway epithelial cells of asthmatic and nonasthmatic patients. The effects of AM on experimental allergen-induced airway inflammation and of AM on lung epithelial repair in vitro were investigated. RESULTS: Adrenomedullin mRNA levels were significantly (P < 0.05) reduced in acute ovalbumin (OVA)-sensitized mice after OVA challenge, by over 60% at 24 h and for up to 6 days. Similarly, reduced AM expression was observed in two models of chronic allergen-induced inflammation, OVA- and house dust mite-sensitized mice. The reduced AM expression was restricted to airway epithelial and endothelial cells, while AM expression in alveolar macrophages was unaltered. Intranasal AM completely attenuated the OVA-induced airway hyperresponsiveness and mucosal plasma leakage but had no effect on inflammatory cells or cytokines. The effects of inhaled AM were reversed by pre-inhalation of the putative AM receptor antagonist, AM ((22-52)) . AM mRNA levels were significantly (P < 0.05) lower in human asthmatic airway epithelial samples than in nonasthmatic controls. In vitro, AM dose-dependently (10(-11) -10(-7) M) accelerated experimental wound healing in human and mouse lung epithelial cell monolayers and stimulated epithelial cell migration. CONCLUSION: Adrenomedullin suppression in T(H) 2-related inflammation is of pathophysiological significance and represents loss of a factor that maintains tissue integrity during inflammation.

Asunto(s)

RESUMEN

Molecular markers for resistance of sorghum to the hemi-parasitic weed Striga hermonthica were mapped in two recombinant inbred populations (RIP-1, and -2) of F(3:5) lines developed from the crosses IS9830 x E36-1 (1) and N13 x E36-1 (2). The resistant parental lines were IS9830 and N13; the former is characterized by a low stimulation of striga seed germination, the latter by "mechanical" resistance. The genetic maps of RIP-1 and RIP-2 spanned 1,498 cM and 1,599 cM, respectively, with 137 and 157 markers distributed over 11 linkage groups. To evaluate striga resistance, we divided each RIP into set 1 (116 lines tested in 1997) and set 2 (110 lines evaluated in 1998). Field trials were conducted in five environments per year in Mali and Kenya. Heritability estimates for area under the striga number progress curve (ASNPC) in sets 1 and 2 were respectively 0.66 and 0.74 in RIP-1 0.81 and 0.82 in RIP-2. Across sites, composite interval mapping detected 11 QTL (quantitative trait loci) and nine QTL in sets 1 and 2 of RIP-1, explaining 77% and 80% of the genetic variance for ASNPC, respectively. The most significant RIP-1 QTL corresponded to the major-gene locus lgs (low stimulation of striga seed germination) in linkage group I. In RIP-2, 11 QTL and nine QTL explained 79% and 82% of the genetic variance for ASNPC in sets 1 and 2, respectively. Five QTL were common to both sets of each RIP, wtih the resistance alleles deriving from IS9830 or N13. Since their effects were validated across environments, years and independent RIP samples, these QTL are excellent candidates for marker-assisted selection.

Asunto(s)

RESUMEN

During the 1998-99 season, maize plants showing viruslike symptoms were observed at two locations in the Andhra Pradesh state in Southern India. Several hybrids were evaluated at Hyderabad in a replicated yield trial and most were affected, with disease incidence ranging from 4.4 to 61.8% of the plants among plots. Hybrid 4642 (Proagro 3-way hybrid, late maturity) and the pre-commercial hybrid YLY102 were the most susceptible, whereas the popular hybrid 4640 was among the least susceptible entries. In seed production fields near Eluru, incidence ranged from 10 to 15% among plots, with the female parent of hybrid 4210 (Proagro 3-way hybrid, early maturity) being especially affected. Symptoms observed in hybrids varied, presumably, according to the infection time and included severe plant dwarfing, dark-green leaves, enations on the lower leaf surface, and small malformed ears with few or no kernels. Symptomatic and asymptomatic field plants (root and leaf tissues) were tested by ds-RNA polyacrylamide gel electrophoresis and by double-antibody sandwich enzyme linked immunosorbent assay (DAS-ELISA) with antiserum to Mal de río cuarto virus (MRCV), a Reoviridae-Fijivirus member. MRCV and Maize rough dwarf virus (MRDV) were selected as controls because the symptoms were similar to those caused by these maize viruses (1,2). ds-RNA gels from symptomatic plants showed 10 bands with banding patterns different from those of MRCV or MRDV. DAS-ELISA indicated a distant relationship to MRCV. These results provide evidence of a reovirus infection to maize hybrids in India and suggest that a virus belonging to the family Reoviridae, genus Fijivirus is causing this new disease. The high disease incidence and the severity of symptoms should alert breeders and pathologists in southern Asia about potential yield losses. References: (1) G. Boccardo and R. G. Milne. 1984. Descriptions of Plant Viruses 294. Inst. Hortic. Res., Wellesbourne. (2) C. Marzachi et al. J. Plant Dis. Prot. 106:431-436, 1999.

RESUMEN

Quantitative trait loci (QTLs) for resistance to the fungal pathogen Setosphaeria turcica, the cause of northern corn leaf blight (NCLB), were mapped in a population of 220 F(3) families derived from a cross between two moderately resistant European inbred lines, D32 (dent) and D145 (flint). The population was genotyped with 87 RFLP and 7 SSR markers. Trials were conducted in the field in Switzerland, and in the greenhouse with selected F(3) families in Germany. The F(3) population segregated widely for resistance with transgression of the parents. By composite interval mapping, a total of 13 QTLs were detected with two disease ratings (0 and 3 weeks after flowering). Together these QTLs explained 48% and 62% of the phenotypic variation. Gene action at most QTLs was partially dominant. Eight out of the 13 QTL alleles for resistance were contributed by the more-resistant parent, D145. On chromosomes 3, 5 and 8, QTLs were located in the same chromosomal regions as QTLs in tropical and U.S. Corn Belt germplasm. Some QTLs affected NCLB, head smut and common rust at the same time, with alleles at these loci acting isodirectionally.

RESUMEN

ABSTRACT Northern leaf blight, caused by Setosphaeria turcica, is a serious disease of maize in temperate and tropical environments. To examine the pathogen's population structure, we analyzed 264 isolates from four different continents with 70 random amplified polymorphic DNA markers and determined their mating types. Tropical populations (from Kenya, Mexico, and southern China) had an extremely high genotypic diversity, no or only weak gametic phase disequilibrium, and an even distribution of the two mating types, indicating frequent sexual recombination. Temperate populations (from Europe and northern China) had a much lower genotypic diversity, strong gametic phase disequilibrium, and an uneven distribution of mating types, indicating that sexual recombination has been rare. Populations in different continents were genetically isolated. They shared no haplotypes and carried several "private" alleles. The number of migrants between continents and between regions (between northern and southern China, western and central Kenya, and Europe west and east of the Alps) was estimated to be less than one per generation. Multivariate statistics suggested a greater relatedness of populations from the same continents than from different continents. Within agroecological zones, migration must be extensive. The potential within populations of S. turcica for adaptation should be regarded as very high, especially in tropical climates.