Alter Disease Severity Research Articles

Loci controlling partial resistance to rice blast do not show marked QTL × environment interaction when plant nitrogen status alters disease severity

Plant disease susceptibility is often increased by nitrogen (N) application. Therefore, it is important to know if resistance loci are effective in different plant N environments. One-hundred lines of the Bala x Azucena rice (Oryza sativa) mapping population were grown in two N treatments and tested for partial resistance to blast (Magnaporthe grisea) isolate CD100. Disease severity (DS), the number and size of lesions and plant N and C concentrations were measured and the results subject to quantitative trait loci (QTL) and QTL x environment analysis. There was a 66% higher plant N concentration in the high N treatment and DS increased significantly, mostly as a result of increased numbers of lesions. Nine regions contained QTL for disease traits but only one showed evidence of statistically significant QTL x treatment interaction. This was a large effect quantitative trait locus at marker R1933 on chromosome 12 which was less effective at high N. Apparently, blast disease is increased by higher plant N, but the efficacy of partial resistance genes is not greatly affected by N application.

Gender-specific exacerbation of murine lupus by gonadotropin-releasing hormone: potential role of G alpha(q/11).

We have previously demonstrated that GnRH and its analogues modulate the severity of murine systemic lupus erythematosus. In the present study, we demonstrate that GnRH alters disease severity in a sexually dimorphic fashion, even in gonadectomized mice. GnRH administration leads to an exacerbation of lupus in ovariectomized females, whereas it exerts no effect in castrated males. We initially hypothesized that gender differences in lymphocytic expression of GnRH receptor might explain these observations. Using competitive RT-PCR and binding studies to quantitate GnRH receptor expression in lymphoid organs, we found that GnRH administration led to decreased expression of GnRH receptor messenger RNA (mRNA) and GnRH binding, compared with vehicle, in spleens of ovariectomized females after 2 weeks of treatment. These decreases occurred concurrently with increased expression of interleukin-2 receptor mRNA and protein in females. GnRH administration did not alter GnRH receptor or interleukin-2 receptor mRNA or protein in castrated males. GnRH exerts actions on the pituitary through G protein signal transduction, specifically through G alpha(q/11). Competitive RT-PCR revealed that GnRH administration was associated with increases in the expression of G alpha(q/11) mRNA, compared with vehicle, in spleens in ovariectomized females but not in castrated males. Immunoblot analysis revealed a similar pattern. We conclude that gender differences in expression of G alpha(q/11) may contribute to gender differences in immunity and/or autoimmune disease.

Synergy between antibody and P 2-reactive T cells in experimental allergic neuritis

Studies were conducted in experimental allergic neuritis (EAN) to evaluate the possible interaction of cellular and humoral immune mechanisms in the demyelinating process. EAN was induced in Lewis rats by passive transfer of T cells reactive to P 2 myelin protein or by active immunisation with whole myelin. Animals were then given systemic antimyelin antibody or control serum and assessed clinically, electrophysiologically and with semiquantitative histological studies. Animals given intraperitoneal (i.p.) P 2-reactive T cells and systemic antimyelin antibody developed much more severe disease than those given i.p. T cells alone ( P < 0.001). In actively immunised animals, the addition of systemic antimyelin antibody did not significantly alter disease severity. We believe the more severe disease in animals receiving T cells and antimyelin antibody reflects synergy between cellular and humoral immune mechanisms whereby neural antigen-specific T cells breach the blood-nerve barrier, allowing demyelinating antibody access to the endoneurium. In EAN induced by active immunisation with whole myelin it is likely that both B and T cell activation occurs and that the more severe demyelination characteristic of this disease reflects the involvement of both humoral and cellular immunity.