Статті в журналах: "Host disease resistance"

1

Dixon, G. R. "Interactions of soil nutrient environment, pathogenesis and host resistance." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S87—S94. http://dx.doi.org/10.17221/10326-pps.

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Host plants and soil borne pathogens that attack them exist within an ecological matrix populated by numerous microbial species that may influence the access of pathogenesis. These events are moderated by physical and chemical components of the soil. The impact of inorganic and organic nutrients on pathogenesis and the development of host resistance are discussed in this review using two host – pathogen combinations as examples. Calcium, boron, nitrogen and pH have been demonstrated to affect the processes of resting spore germination, host invasion and colonisation in the Plasmodiophora brassicae-Brassica combination that results in clubroot disease. Organic nutrients that have associated biostimulant properties have been demonstrated to influence the development of Pythium ultimum-Brassica combination that results in damping-off disease. This latter combination is affected by the presence of antagonistic microbial flora as demonstrated by increased ATP, extra-cellular enzyme and siderophore production. In both examples there are indications of the manner by which host resistance to pathogenesis may be enhanced by changes to the nutrient status surrounding host plants. These effects are discussed in relation to the development of integrated control strategies that permit disease control with minimal environmental impact.

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2

Alemu, Gadisa. "Wheat Breeding for Disease Resistance: Review." Open Access Journal of Microbiology & Biotechnology 4, no. 2 (2019): 1–10. http://dx.doi.org/10.23880/oajmb-16000142.

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Breeding for disease resistance is a central focus of plant breeding programs, as any successful variety must have the complete package of high yield, disease resistance, agronomic performance, and end - use quality. Wheat breeding is focused on high yield, pathogen resistance and abiotic stress tolerance. Among diseases of wheat yellow rust, stem rust, and leaf rust are the most damaging diseases of wheat and other small grain cereals . Disease resistance in wheat breeding with one exception, the diseases of wheat that is important because of their effect on yield. Resistance to all diseases together can is important to avoid an unexpected loss in effectiveness of the resistance of a cu ltivar to a major disease. The genetic resistance to stem rust, leaf rust and yellow rust can be characterized as qualitative and quantitative resistances. Vertical resistance is specific to pathogen isolates based on single or very few genes. Race - specifi c is used to describe resistance that interacts differentially with pathogen races. Quantitative resistance is defined as resistance that varies in continuous way between the various phenotypes of the host population, from almost imperceptible to quite str ong. With the need to accelerate the development of improved varieties, genomics - assisted breeding is becoming an important tool in breeding programs. With marker - assisted selection, there has been success in breeding for disease resistance. Generally, bre eding programs have successfully implemented molecular markers to assist in the development of cultivars with stem, leaf and stripe rust resistance genes. When new rust resistance genes are to be deployed in wheat breeding programs, it unfortunately takes several years before the new sources of resistance will become available in commercial wheat cultivars. This is due to the long process involved in the establishment of pure breeding wheat lines. Biotechnology based techniques are available to accelerate t he breeding process via doubled haploid production.

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3

Jacobs, Jonathan M., and Caitilyn Allen. "Disease Resistance Against a Broad-Host-Range Pathogen." Plant Health Progress 14, no. 1 (January 2013): 32. http://dx.doi.org/10.1094/php-2013-1125-03-rs.

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The bacterial wilt pathogen Ralstonia solanacearum causes major agricultural losses on many crop hosts worldwide. Resistance breeding is the best way to control bacterial wilt disease, but the biological basis for bacterial wilt resistance is unknown. We found that R. solanacearum uses an AvrE-family, Type III-secreted effector called PopS to overcome plant defenses and cause disease on tomato. Orthologs of PopS are widely conserved across distinct classes of plant pathogenic bacteria and could provide novel, durable targets for resistance. Accepted for publication 25 September 2013. Published 25 November 2013.

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4

Friedl, Karl E. "RE: Does host energy metabolism moderate disease resistance?" Journal of Infection 76, no. 2 (February 2018): 211–12. http://dx.doi.org/10.1016/j.jinf.2017.09.017.

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5

Sutherland, M. L., L. Mittempergher, and C. M. Brasier. "Control of Dutch elm disease by induced host resistance." Forest Pathology 25, no. 6-7 (November 1995): 307–15. http://dx.doi.org/10.1111/j.1439-0329.1995.tb01346.x.

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6

Kim, Bong-Suk, Elizabeth French, Denise Caldwell, Emily J. Harrington, and Anjali S. Iyer-Pascuzzi. "Bacterial wilt disease: Host resistance and pathogen virulence mechanisms." Physiological and Molecular Plant Pathology 95 (July 2016): 37–43. http://dx.doi.org/10.1016/j.pmpp.2016.02.007.

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7

Pilla-Moffett, Danielle, Matthew F. Barber, Gregory A. Taylor, and Jörn Coers. "Interferon-Inducible GTPases in Host Resistance, Inflammation and Disease." Journal of Molecular Biology 428, no. 17 (August 2016): 3495–513. http://dx.doi.org/10.1016/j.jmb.2016.04.032.

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8

Omara, Reda Ibrahim, Said Mohamed Kamel, Sherif Mohamed El-Ganainy, Ramadan Ahmed Arafa, Yasser Sabry Mostafa, Saad Abdulrahman Alamri, Sulaiman A. Alrumman, Mohamed Hashem, and Mohsen Mohamed Elsharkawy. "Host Resistance to Uromyces appendiculatus in Common Bean Genotypes." Plants 11, no. 5 (February 25, 2022): 628. http://dx.doi.org/10.3390/plants11050628.

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Rust, induced by the fungus Uromyces appendiculatus, is one of the most serious bean diseases. The involved mechanisms in rust resistance were evaluated in 10 common bean genotypes during the 2019/2020 and 2020/2021 growing seasons. The disease parameters such as final rust severity (FRS%), area under the disease progress curve (AUDPC) and disease increase rate (r-value) were lower in the resistant genotypes than in highly susceptible genotypes. Biochemical compounds such as total phenols and the activity of antioxidant enzymes such as catalase, peroxidase and polyphenol oxidase were increased in the resistant genotypes compared to susceptible genotypes. In the resistance genotypes, the levels of oxidative stress markers such as hydrogen peroxide (H2O2) and superoxide (O2•−) increased dramatically after infection. The electrolyte leakage percentage (EL%), was found to be much greater in susceptible genotypes than resistant genotypes. The resistant gene SA14, which was found in genotypes Nebraska and Calypso at 800 bp, had an adequate level of resistance to bean rust with high grain yield potential. After infection, the transcriptions levels of 1,3-D-glucanases and phenylalanine ammonia lyase) were higher in the resistant genotypes than susceptible genotypes. In conclusion, the resistant genotypes successfully displayed desirable agronomic traits and promising expectations in breeding programs for improving management strategies of common bean rust disease. The resistance was mediated by antioxidant enzymes, phenolic compounds, and defense gene expressions, as well as the resistant gene SA14.

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9

de Silva, Kumudika, Douglas Begg, Karren Plain, Auriol Purdie, Satoko Kawaji, Navneet Dhand, and Richard Whittington. "Early biomarkers of resistance and susceptibility to mycobacterial disease (160.1)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 160.1. http://dx.doi.org/10.4049/jimmunol.188.supp.160.1.

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Abstract Mycobacterial diseases such as tuberculosis and paratuberculosis continue to be of serious health and economic concern to humans and livestock globally. Lack of knowledge on the nature of the protective immune response as well as immunological markers of disease susceptibility and latency hamper the development of effective vaccines and other therapies. The use of a well-characterised ruminant infection model enabled us to follow the host response to mycobacterial challenge from the time of exposure until manifestation of clinical disease in a natural host. This study (30 controls and 58 challenged in 2 trials) tracked cellular and humoral responses, and quantity of mycobacterial shedding, for up to 30 months post challenge in sheep. Infection was defined as the presence of viable organisms in tissue sections taken at necropsy. The IFNγ response increased after exposure regardless of disease outcome. Parameters measured could distinguish severely diseased animals from those that had been exposed but were uninfected. Infectious or severely diseased animals were more likely to have a lower IFNγ response early (4 months post exposure) compared to exposed uninfected animals. This latter group were also more likely to have an elevated early IL-10 response. These studies demonstrate the complexity of the immune response to pathogenic mycobacteria and illustrate the fact that measurement of a single immunological parameter is insufficient to determine the outcome of disease.

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10

Kayihan, Gögçe C., C. Dana Nelson, Dudley A. Huber, Henry V. Amerson, Timothy L. White, and John M. Davis. "Clonal evaluation for fusiform rust disease resistance: effects of pathogen virulence and disease escape." Canadian Journal of Forest Research 40, no. 6 (June 2010): 1042–50. http://dx.doi.org/10.1139/x10-045.

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We evaluated the precision of phenotypic classification for fusiform rust resistance of Pinus taeda L. in a clonally propagated population segregating for the pathotype-specific resistance gene Fr1. In all marker-defined Fr1/fr1 clones screened with low complexity or ambient inoculum, marker–trait cosegregation was complete with no exceptions. Uncommon exceptions (4 of 30) in which marker-defined Fr1/fr1 clones screened with high complexity inoculum were diseased were probably due to a low frequency of spores virulent to Fr1 resistance. Marker–trait cosegregation for fr1/fr1 clones was less reliable, as all ramets of a few clones (5 of 29, 3 of 25, and 4 of 16) remained disease-free with low complexity, high complexity, or ambient inoculum, respectively. We termed disease-free fr1/fr1 ramets “escapes”, since the genetics of the host–pathogen interaction predicted them to be diseased. For nonmarker-defined materials, we considered escapes to be disease-free ramets within clones that had at least one diseased ramet. Narrow-sense heritability estimates for escape rate were 29% and 23% for the low and high complexity inocula, respectively, suggesting that genetic variation in the host is an important component of this resistance mechanism.

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11

Muller, M., and G. Brem. "Transgenic strategies to increase disease resistance in livestock." Reproduction, Fertility and Development 6, no. 5 (1994): 605. http://dx.doi.org/10.1071/rd9940605.

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Approaches to modify disease resistance or susceptibility by transgenic means will be a major asset to animal welfare as well as to the economics of animal production. Candidates for gene transfer experiments include all genes known to influence non-specific and specific host defence mechanisms against infectious pathogens. Additional strategies such as 'intracellular immunization', 'genetic and congenital immunization', antisense RNA approaches and targeted disruption of disease susceptibility genes promise to gain importance in conferring increased disease resistance. The cytokine network regulates cellular viability, growth and differentiation in physiological and pathophysiological states. Detailed understanding of cytokine signal transduction pathways and transcriptional activators will provide not only new target molecules for modulating the immune response but will also facilitate the elucidation of host-pathogen interactions.

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12

PIRENNE, JACQUES, J. GRAHAM WILLIAMS, JAIME L. MAYORAL, RAOUF E. NAKHLEH, and DAVID L. DUNN. "RESISTANCE TO GRAFT-VERSUS-HOST DISEASE FOLLOWING SMALL BOWEL TRANSPLANTATION." Transplantation 51, no. 1 (January 1991): 51–56. http://dx.doi.org/10.1097/00007890-199101000-00007.

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13

Hamilton, M. G., D. R. Williams, P. A. Tilyard, E. A. Pinkard, T. J. Wardlaw, M. Glen, R. E. Vaillancourt, and B. M. Potts. "A latitudinal cline in disease resistance of a host tree." Heredity 110, no. 4 (December 5, 2012): 372–79. http://dx.doi.org/10.1038/hdy.2012.106.

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14

Carlsson-Granér, U., B. E. Giles, and P. H. Thrall. "Patterns of disease and host resistance in spatially structured systems." European Journal of Plant Pathology 138, no. 3 (October 28, 2013): 499–511. http://dx.doi.org/10.1007/s10658-013-0316-2.

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15

Harp, James A. "Cryptosporidiumand host resistance: historical perspective and some novel approaches." Animal Health Research Reviews 4, no. 1 (June 2003): 53–62. http://dx.doi.org/10.1079/ahrr200352.

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AbstractCryptosporidium parvumis recognized as a major cause of diarrheal disease in neonatal bovine calves. In addition, this protozoan parasite has emerged as an important cause of disease in both immunocompromised and immunocompetent humans. Despite years of research, no consistently effective means of prevention or treatment are readily available for cryptosporidiosis in any species. Infection through ingestion of contaminated water has been widely documented;C. parvumwas reported to be responsible for the largest waterborne outbreak of infectious disease in US history. In addition to its role as a primary disease agent,C. parvumhas potential to initiate or exacerbate other gastrointestinal disorders, such as inflammatory bowel disease. Thus, control ofC. parvuminfection in both animals and humans remains an important objective. Research in our laboratory has focused on understanding mechanisms of resistance toC. parvum. We have demonstrated that acquisition of intestinal flora increases resistance toC. parvum.Substances present in the intestinal mucosa of adult animals can transfer resistance when fed to susceptible infants. Both expression of intestinal enzymes and rate of proliferation of epithelial cells may be altered followingC. parvuminfection. These and other changes may have profound effects on host resistance toC. parvum.

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16

Rodríguez-Salamanca, Lina M., and Mary K. Hausbeck. "Evaluating Host Resistance to Limit Colletotrichum coccodes on Onion." HortScience 53, no. 7 (July 2018): 916–19. http://dx.doi.org/10.21273/hortsci12957-18.

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Leaf and neck anthracnose is incited by Colletotrichum coccodes (Wallr.) Hughes, a new foliar disease of onion (Allium cepa L.) in Michigan that has been observed in the state since 2010. Symptoms include elliptical lesions on the leaves, necks, or both that appear bleached with a pale salmon to dark brown center. To develop an effective integrated disease management strategy, field studies were conducted in 2011 and 2012 to evaluate 16 commercial onion cultivars for their susceptibility to the pathogen. The incidence and severity of anthracnose were evaluated weekly following inoculation. Onion cultivars differed significantly in disease severity and incidence; differences between years were also observed. ‘Hendrix’ had the lowest disease severity, whereas ‘Highlander’ and ‘Candy’ exhibited severe onion leaf and neck anthracnose symptoms. Using less susceptible onion cultivars combined with effective fungicides against C. coccodes may limit crop losses for Michigan growers.

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17

Fernández-Falcón, Marino, Andres A. Borges, and Andres Borges-Pérez. "Induced resistance to Fusarium wilt of banana by exogenous applications of indoleacetic acid." Phytoprotection 84, no. 3 (June 15, 2004): 149–53. http://dx.doi.org/10.7202/008492ar.

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Fusarium wilt of banana (Panama disease), caused by Fusarium oxysporum f.sp. cubense, is a soilborne systemic disease which occludes host vascular system. We report here two experiments on resistance induction with banana plants (cv. Dwarf Cavendish) carried out in glass greenhouse with different indoleacetic acid treatments, which are capable of inducing resistance to Panama disease. The results obtained in these experiments suggest that the exogenous application of indoleacetic acid to banana plants induce resistance to Panama disease and that the resistance induction is more effective when performed using low doses and frequent applications. This work seems to confirm the role played by indoleacetic acid according to Beckman’s models as, one of the major defence factors of the host plant in vascular wilt diseases.

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18

Hasan, Jakir, Swati Megha, and Habibur Rahman. "Clubroot in Brassica: recent advances in genomics, breeding, and disease management." Genome 64, no. 8 (August 2021): 735–60. http://dx.doi.org/10.1139/gen-2020-0089.

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Clubroot disease, caused by Plasmodiophora brassicae, affects Brassica oilseed and vegetable production worldwide. This review is focused on various aspects of clubroot disease and its management, including understanding the pathogen and resistance in the host plants. Advances in genetics, molecular biology techniques, and omics research have helped to identify several major loci, QTL, and genes from the Brassica genomes involved in the control of clubroot resistance. Transcriptomic studies have helped to extend our understanding of the mechanism of infection by the pathogen and the molecular basis of resistance/susceptibility in the host plants. A comprehensive understanding of the clubroot disease and host resistance would allow developing a better strategy by integrating the genetic resistance with cultural practices to manage this disease from a long-term perspective.

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19

Koskella, Britt, Derek M. Lin, Angus Buckling, and John N. Thompson. "The costs of evolving resistance in heterogeneous parasite environments." Proceedings of the Royal Society B: Biological Sciences 279, no. 1735 (December 14, 2011): 1896–903. http://dx.doi.org/10.1098/rspb.2011.2259.

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The evolution of host resistance to parasites, shaped by associated fitness costs, is crucial for epidemiology and maintenance of genetic diversity. Selection imposed by multiple parasites could be a particularly strong constraint, as hosts either accumulate costs of multiple specific resistances or evolve a more costly general resistance mechanism. We used experimental evolution to test how parasite heterogeneity influences the evolution of host resistance. We show that bacterial host populations evolved specific resistance to local bacteriophage parasites, regardless of whether they were in single or multiple-phage environments, and that hosts evolving with multiple phages were no more resistant to novel phages than those evolving with single phages. However, hosts from multiple-phage environments paid a higher cost, in terms of population growth in the absence of phage, for their evolved specific resistances than those from single-phage environments. Given that in nature host populations face selection pressures from multiple parasite strains and species, our results suggest that costs may be even more critical in shaping the evolution of resistance than previously thought. Furthermore, our results highlight that a better understanding of resistance costs under combined control strategies could lead to a more ‘evolution-resistant’ treatment of disease.

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20

Oscarsson, Jan, Rolf Claesson, Mark Lindholm, Carola Höglund Åberg, and Anders Johansson. "Tools of Aggregatibacter actinomycetemcomitans to Evade the Host Response." Journal of Clinical Medicine 8, no. 7 (July 22, 2019): 1079. http://dx.doi.org/10.3390/jcm8071079.

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Periodontitis is an infection-induced inflammatory disease that affects the tooth supporting tissues, i.e., bone and connective tissues. The initiation and progression of this disease depend on dysbiotic ecological changes in the oral microbiome, thereby affecting the severity of disease through multiple immune-inflammatory responses. Aggregatibacter actinomycetemcomitans is a facultative anaerobic Gram-negative bacterium associated with such cellular and molecular mechanisms associated with the pathogenesis of periodontitis. In the present review, we outline virulence mechanisms that help the bacterium to escape the host response. These properties include invasiveness, secretion of exotoxins, serum resistance, and release of outer membrane vesicles. Virulence properties of A. actinomycetemcomitans that can contribute to treatment resistance in the infected individuals and upon translocation to the circulation, also induce pathogenic mechanisms associated with several systemic diseases.

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21

Fernando, Krishni, Priyanka Reddy, German C. Spangenberg, Simone J. Rochfort, and Kathryn M. Guthridge. "Metabolic Potential of Epichloë Endophytes for Host Grass Fungal Disease Resistance." Microorganisms 10, no. 1 (December 29, 2021): 64. http://dx.doi.org/10.3390/microorganisms10010064.

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Asexual species of the genus Epichloë (Clavicipitaceae, Ascomycota) form endosymbiotic associations with Pooidae grasses. This association is important both ecologically and to the pasture and turf industries, as the endophytic fungi confer a multitude of benefits to their host plant that improve competitive ability and performance such as growth promotion, abiotic stress tolerance, pest deterrence and increased host disease resistance. Biotic stress tolerance conferred by the production of bioprotective metabolites has a critical role in an industry context. While the known antimammalian and insecticidal toxins are well characterized due to their impact on livestock welfare, antimicrobial metabolites are less studied. Both pasture and turf grasses are challenged by many phytopathogenic diseases that result in significant economic losses and impact livestock health. Further investigations of Epichloë endophytes as natural biocontrol agents can be conducted on strains that are safe for animals. With the additional benefits of possessing host disease resistance, these strains would increase their commercial importance. Field reports have indicated that pasture grasses associated with Epichloë endophytes are superior in resisting fungal pathogens. However, only a few antifungal compounds have been identified and chemically characterized, and these from sexual (pathogenic) Epichloë species, rather than those utilized to enhance performance in turf and pasture industries. This review provides insight into the various strategies reported in identifying antifungal activity from Epichloë endophytes and, where described, the associated antifungal metabolites responsible for the activity.

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22

Martins, Rui, Ana Rita Carlos, Faouzi Braza, Jessica A. Thompson, Patricia Bastos-Amador, Susana Ramos, and Miguel P. Soares. "Disease Tolerance as an Inherent Component of Immunity." Annual Review of Immunology 37, no. 1 (April 26, 2019): 405–37. http://dx.doi.org/10.1146/annurev-immunol-042718-041739.

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Pathogenic organisms exert a negative impact on host health, revealed by the clinical signs of infectious diseases. Immunity limits the severity of infectious diseases through resistance mechanisms that sense and target pathogens for containment, killing, or expulsion. These resistance mechanisms are viewed as the prevailing function of immunity. Under pathophysiologic conditions, however, immunity arises in response to infections that carry health and fitness costs to the host. Therefore, additional defense mechanisms are required to limit these costs, before immunity becomes operational as well as thereafter to avoid immunopathology. These are tissue damage control mechanisms that adjust the metabolic output of host tissues to different forms of stress and damage associated with infection. Disease tolerance is the term used to define this defense strategy, which does not exert a direct impact on pathogens but is essential to limit the health and fitness costs of infection. Under this argument, we propose that disease tolerance is an inherent component of immunity.

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23

Vinijsanun, T., DF Cameron, JAG Irwin, and A. Barnes. "Phenotypic variation for disease resistance and virulence within naturalized populations of Stylosanthes humilis and Colletotrichum gloeosporioides." Australian Journal of Agricultural Research 38, no. 4 (1987): 717. http://dx.doi.org/10.1071/ar9870717.

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The extent of variation for host disease reaction and pathogen virulence was studied in naturalized populations of Stylosanthes hurnilis and Colletotrichurn gloeosporioides, the causal fungus of an anthracnose disease of Stylosanthes spp. Diseased plants (S0) were collected from the field at three sites (Townsville, Wrotham Park and Niall) in North Queensland, and first generation selfed (S1) progenies (host-lines) and single spore fungal cultures were grown for each of the collections made. Within a site, all host-lines were inoculated with each fungal isolate from that site, and a fourth experiment was conducted with representative host-pathogen combinations from each site. Sufficient seed was obtained to allow testing of 12, 10 and 8 collections from Niall, Wrotham Park and Townsville respectively. Significant variation (P < 0.01) between disease severity values for host-line means, fungal isolate means and host-line/fungal isolate interactions was found in all four experiments. Differences between fungal isolate means were the main source of variation in three of the four experiments. Both the differences in virulence within the pathogen population and the differences in resistance of the hostlines appeared to be quantitatively inherited. One host-line from Wrotham Park was significantly more resistant than the susceptible check, cv. Paterson, in two replicated experiments indicating that selection for some improvement in resistance within the naturalized populations should be possible. However, none of the host-lines from the Townsville and Niall sites were significantly more resistant than Paterson, suggesting that little natural selection for resistance has occurred within the naturalized host populations over the 10 years following the first outbreak of the disease in northern Australia.

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Wolowicka, Laura, Hanna Bartkowiak, and Ryszard Gorny. "Host Resistance in Patients after Resuscitation." Prehospital and Disaster Medicine 1, no. 3 (1985): 219–23. http://dx.doi.org/10.1017/s1049023x00065687.

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There has recently been a steady increase in the number of patients treated in intensive care units (ICUs) and requiring resuscitation. This number has risen from 1 to 3% in patients after cardiac arrest (19) and from 7 to 13% in those with severe injuries (18). The immune system investigations, introduced more and more widely in intensive care medicine for prophylactic, therapeutic and prognostic reasons, did not, in principle, concern the cases of post-resuscitation disease after cardiac arrest. Only a few reports have been published on this subject (11).The aims of our investigations were the analysis of selected humoral and cellular factors in patients after cardiac arrest in comparison to those with multiple injuries, evaluation of the host resisctance against infection and of prognostic values of some immunological indices.Examinations were carried out in 50 patients, treated in an ICU of 15 beds, from 1981 to 1982, and in 20 healthy volunteers. The patients were divided into two main groups (Fig. 1): The first group consisted of 25 patients after cardiac arrest, age 47±12. The second group consisted of 25 patients after severe multiple injuries, age 42±18 y; they corresponded to an abbreviated injury scale (AIS) of 4–6 (8). 56% of the patients with cardiac arrest could not be resuscitated. In 64% of the trauma patients treatment was unsuccessful. Infection complications, influencing recovery were observed in 10 (40%) after cardiac arrest and in 12 (48%) after trauma. The cardiopulmonary-cerebral resuscitation methods used were standard (16).

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25

McCallum, Hamish. "Disease and the dynamics of extinction." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1604 (October 19, 2012): 2828–39. http://dx.doi.org/10.1098/rstb.2012.0224.

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Invading infectious diseases can, in theory, lead to the extinction of host populations, particularly if reservoir species are present or if disease transmission is frequency-dependent. The number of historic or prehistoric extinctions that can unequivocally be attributed to infectious disease is relatively small, but gathering firm evidence in retrospect is extremely difficult. Amphibian chytridiomycosis and Tasmanian devil facial tumour disease (DFTD) are two very different infectious diseases that are currently threatening to cause extinctions in Australia. These provide an unusual opportunity to investigate the processes of disease-induced extinction and possible management strategies. Both diseases are apparently recent in origin. Tasmanian DFTD is entirely host-specific but potentially able to cause extinction because transmission depends weakly, if at all, on host density. Amphibian chytridiomycosis has a broad host range but is highly pathogenic only to some populations of some species. At present, both diseases can only be managed by attempting to isolate individuals or populations from disease. Management options to accelerate the process of evolution of host resistance or tolerance are being investigated in both cases. Anthropogenic changes including movement of diseases and hosts, habitat destruction and fragmentation and climate change are likely to increase emerging disease threats to biodiversity and it is critical to further develop strategies to manage these threats.

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26

Wang, Qi, Nadia Shakoor, Adam Boyher, Kira M. Veley, Jeffrey C. Berry, Todd C. Mockler, and Rebecca S. Bart. "Escalation in the host-pathogen arms race: A host resistance response corresponds to a heightened bacterial virulence response." PLOS Pathogens 17, no. 1 (January 11, 2021): e1009175. http://dx.doi.org/10.1371/journal.ppat.1009175.

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The zig-zag model of host-pathogen interaction describes the relative strength of defense response across a spectrum of pathogen-induced plant phenotypes. A stronger defense response results in increased resistance. Here, we investigate the strength of pathogen virulence during disease and place these findings in the context of the zig-zag model. Xanthomonas vasicola pv. holcicola (Xvh) causes sorghum bacterial leaf streak. Despite being widespread, this disease has not been described in detail at the molecular level. We divided diverse sorghum genotypes into three groups based on disease symptoms: water-soaked lesions, red lesions, and resistance. Bacterial growth assays confirmed that these three phenotypes represent a range of resistance and susceptibility. To simultaneously reveal defense and virulence responses across the spectrum of disease phenotypes, we performed dual RNA-seq on Xvh-infected sorghum. Consistent with the zig-zag model, the expression of plant defense-related genes was strongest in the resistance interaction. Surprisingly, bacterial virulence genes related to the type III secretion system (T3SS) and type III effectors (T3Es) were also most highly expressed in the resistance interaction. This expression pattern was observed at multiple time points within the sorghum-Xvh pathosystem. Further, a similar expression pattern was observed in Arabidopsis infected with Pseudomonas syringae for effector-triggered immunity via AvrRps4 but not AvrRpt2. Specific metabolites were able to repress the Xvh virulence response in vitro and in planta suggesting a possible signaling mechanism. Taken together, these findings reveal multiple permutations of the continually evolving host-pathogen arms race from the perspective of host defense and pathogen virulence responses.

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27

Reeves, Gregory, Ariadna Monroy-Barbosa, and Paul W. Bosland. "A Novel Capsicum Gene Inhibits Host-Specific Disease Resistance to Phytophthora capsici." Phytopathology® 103, no. 5 (May 2013): 472–78. http://dx.doi.org/10.1094/phyto-09-12-0242-r.

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A novel disease resistance inhibitor gene (inhibitor of P. capsici resistance [Ipcr]), found in the chile pepper (Capsicum annuum) variety ‘New Mexico Capsicum Accession 10399’ (NMCA10399), inhibits resistance to Phytophthora capsici but not to other species of Phytophthora. When a highly P. capsici-resistant variety was hybridized with NMCA10399, the resultant F1 populations, when screened, were completely susceptible to P. capsici for root rot and foliar blight disease syndromes, despite the dominance inheritance of P. capsici resistance in chile pepper. The F2 population displayed a 3:13 resistant-to-susceptible (R:S) ratio. The testcross population displayed a 1:1 R:S ratio, and a backcross population to NMCA10399 displayed complete susceptibility. These results demonstrate the presence of a single dominant inhibitor gene affecting P. capsici resistance in chile pepper. Moreover, when lines carrying the Ipcr gene were challenged against six Phytophthora spp., the nonhost resistance was not overcome. Therefore, the Ipcr gene is interfering with host-specific resistance but not the pathogen- or microbe-associated molecular pattern nonhost responses.

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Mekapogu, Manjulatha, Jae-A. Jung, Oh-Keun Kwon, Myung-Suk Ahn, Hyun-Young Song, and Seonghoe Jang. "Recent Progress in Enhancing Fungal Disease Resistance in Ornamental Plants." International Journal of Molecular Sciences 22, no. 15 (July 26, 2021): 7956. http://dx.doi.org/10.3390/ijms22157956.

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Fungal diseases pose a major threat to ornamental plants, with an increasing percentage of pathogen-driven host losses. In ornamental plants, management of the majority of fungal diseases primarily depends upon chemical control methods that are often non-specific. Host basal resistance, which is deficient in many ornamental plants, plays a key role in combating diseases. Despite their economic importance, conventional and molecular breeding approaches in ornamental plants to facilitate disease resistance are lagging, and this is predominantly due to their complex genomes, limited availability of gene pools, and degree of heterozygosity. Although genetic engineering in ornamental plants offers feasible methods to overcome the intrinsic barriers of classical breeding, achievements have mainly been reported only in regard to the modification of floral attributes in ornamentals. The unavailability of transformation protocols and candidate gene resources for several ornamental crops presents an obstacle for tackling the functional studies on disease resistance. Recently, multiomics technologies, in combination with genome editing tools, have provided shortcuts to examine the molecular and genetic regulatory mechanisms underlying fungal disease resistance, ultimately leading to the subsequent advances in the development of novel cultivars with desired fungal disease-resistant traits, in ornamental crops. Although fungal diseases constitute the majority of ornamental plant diseases, a comprehensive overview of this highly important fungal disease resistance seems to be insufficient in the field of ornamental horticulture. Hence, in this review, we highlight the representative mechanisms of the fungal infection-related resistance to pathogens in plants, with a focus on ornamental crops. Recent progress in molecular breeding, genetic engineering strategies, and RNAi technologies, such as HIGS and SIGS for the enhancement of fungal disease resistance in various important ornamental crops, is also described.

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29

Xia, Chao, Nana Li, Yawen Zhang, Chunjie Li, Xingxu Zhang, and Zhibiao Nan. "Role of Epichloë Endophytes in Defense Responses of Cool-Season Grasses to Pathogens: A Review." Plant Disease 102, no. 11 (November 2018): 2061–73. http://dx.doi.org/10.1094/pdis-05-18-0762-fe.

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Various cool-season grasses are infected by Epichloë endophyte, and this symbiotic relationship is always of benefit to the host grass due to an increased resistance to abiotic and biotic stresses. Fungal diseases adversely affect the yield, quality, and economic benefits of rangelands, which affects the production of animal husbandry. Therefore, it is imperative to breed resistant cultivars and to better understand the role of fungal endophytes in order to protect grasses against pathogens. The present review introduces research regarding how these endophytes affect the growth of pathogens in vitro and how they change the resistance of host plants to plant diseases. From the perspective of physical defense, changes in physiological indexes, and secretion of chemical compounds, we summarize the potential mechanisms by which endophytes are able to enhance the disease resistance of a host grass. Through these, we aim to establish a solid theoretical foundation for plant disease control and disease resistance breeding by application of fungal endophytes. A broader understanding of fungal endophyte effects on hosts could create a new opportunity for managing or introducing fungal symbioses in both agronomic or non-agronomic ecosystems.

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30

Garrett, K. A., and C. C. Mundt. "Epidemiology in Mixed Host Populations." Phytopathology® 89, no. 11 (November 1999): 984–90. http://dx.doi.org/10.1094/phyto.1999.89.11.984.

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Although plant disease epidemiology has focused on populations in which all host plants have the same genotype, mixtures of host genotypes are more typical of natural populations and offer promising options for deployment of resistance genes in agriculture. In this review, we discuss Leonard's classic model of the effects of host genotype diversity on disease and its predictions of disease level based on the proportion of susceptible host tissue. As a refinement to Leonard's model, the spatial structure of host and pathogen population can be taken into account by considering factors such as autoinfection, interaction between host size and pathogen dispersal gradients, lesion expansion, and host carrying capacity for disease. The genetic composition of the host population also can be taken into account by considering differences in race-specific resistance among host genotypes, compensation, plant competition, and competitive interactions among pathogen genotypes. The magnitude of host-diversity effects for particular host-pathogen systems can be predicted by considering how the inherent characteristics of a system causes it to differ from the assumptions of the classic model. Because of the limited number of studies comparing host-diversity effects in different systems, it is difficult at this point to make more than qualitative predictions. Environmental conditions and management decisions also influence host-diversity effects on disease through their effect on factors such as host density and epidemic length and intensity.

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Hoy, J. W., M. C. Avellaneda, and J. Bombecini. "Variability in Puccinia melanocephala Pathogenicity and Resistance in Sugarcane Cultivars." Plant Disease 98, no. 12 (December 2014): 1728–32. http://dx.doi.org/10.1094/pdis-01-14-0074-re.

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Brown rust, caused by Puccinia melanocephala, is an important disease of sugarcane worldwide, controlled primarily with host plant resistance. Disease response shifts from resistant to susceptible have been repeatedly observed for cultivars. However, information is limited concerning pathogen variability related to host reactions. To evaluate variability in the pathogen population and characterize resistance responses in different host genotypes, seven cultivars were inoculated with four urediniospore collections from three cultivars. Greenhouse-grown plants were inoculated under controlled conditions favorable for infection and disease development. Severity assessed as leaf area occupied by lesions, lesion density, and lesion size was determined and compared. Three cultivars that shifted from resistance to high susceptibility while under cultivation exhibited differential disease severity when inoculated with spore collections from two of the respective cultivars. Two cultivars exhibited consistent moderate to high levels of quantitative resistance against all spore collections and two cultivars, including one with the Bru1 resistance gene, were highly resistant to all collections. Differential reactions were best revealed by assessing percent leaf area. Pathogenic variability related to host genotype was confirmed, and quantitative resistance was detected that could be useful to improve breeding and selection for effective, durable resistance to brown rust.

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32

Al-Lami, Hebba F. D., Ming Pei You, and Martin J. Barbetti. "Relative host resistance to Alternaria leaf spot in canola and mustard varieties is defined by Alternaria species." Crop and Pasture Science 71, no. 7 (2020): 689. http://dx.doi.org/10.1071/cp20024.

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Both Alternaria japonica and A. brassicae cause severe Alternaria leaf spot on canola (Brassica napus) and mustard (B. juncea). We tested 103 Brassicaceae varieties including 93 Australian canola, nine Indian mustard, and a single variety of Ethiopian mustard (B. carinata) under greenhouse conditions to identify host resistance to Alternaria leaf spot caused by A. japonica and A. brassicae in terms of disease incidence (percentage leaf disease incidence, %LDI), disease severity (percentage leaf area diseased, %LAD) and defoliation (percentage leaf collapse index, %LCI). Against A. japonica, across the three parameters, B. napus Surpass 404 CL was the most resistant (%LDI 7.5, %LAD 5.0, %LCI 0). Varieties Hyola 635 CC, Oscar, AG-Outback and Rottnest, with %LDI 15.6–19.4 and %LAD 12.5–15.6, also showed strong resistance, and with %LCI 10. Varieties 47C02, ATR-Signal and Clancy of B. napus showed a moderate level of resistance across %LDI (21.2–25.6) and %LAD (15.0–20.6), along with a low level of defoliation (%LCI 10). Varieties 46C03, 46C72, ATR-Cobbler and Granite TT of B. napus also showed a moderate level of resistance, with %LDI 23.1–28.7, %LAD 18.1–20.6 and %LCI 11.2–14.4. The significance of this resistance against A. japonica is highlighted by the severe disease on B. napus Thunder TT (%LDI 78.8, %LAD 72.5, %LCI 47.5). Against A. brassicae, all varieties showed susceptibility; however, B. napus ATR-Grace was the least susceptible in relation to disease incidence (%LDI 41.2) and severity (%LAD 36.2), and B. napus Hyola 450 TT the most susceptible (%LDI 90.0, %LAD 82.5). Variety Hurricane of B. napus was the least susceptible in terms of consequent defoliation (%LCI 11.2) and B. napus CBTM Tribune the most susceptible (%LCI 81.2). The B. carinata variety BCA 1 (ATC 95065) and all test B. juncea varieties showed susceptibility to both pathogens. These findings demonstrate high levels of resistance across Australian canola varieties against A. japonica that can be directly deployed where A. japonica is important and can be utilised by breeders for improving resistance in future varieties. By contrast, susceptibility across Australian canola and mustard varieties to A. brassicae is concerning, highlighting a need to locate suitable resistances and, until effective host resistance can be located, to develop and deploy cultural and chemical options.

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Anes, E., and L. Jordao. "Trick-or-Treat: Dietary Lipids and Host Resistance to Infectious Disease." Mini-Reviews in Medicinal Chemistry 8, no. 14 (December 1, 2008): 1452–58. http://dx.doi.org/10.2174/138955708786786525.

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34

Venisse, J. S., J. P. Paulin, and M. N. Brisset. "MECHANISMS UNDERLYING DISEASE AND RESISTANCE IN HOST PLANTS OF FIRE BLIGHT." Acta Horticulturae, no. 590 (November 2002): 467–68. http://dx.doi.org/10.17660/actahortic.2002.590.72.

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35

Rosshart, Stephan P., Brian G. Vassallo, Davide Angeletti, Diane S. Hutchinson, Andrew P. Morgan, Kazuyo Takeda, Heather D. Hickman, et al. "Wild Mouse Gut Microbiota Promotes Host Fitness and Improves Disease Resistance." Cell 171, no. 5 (November 2017): 1015–28. http://dx.doi.org/10.1016/j.cell.2017.09.016.

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36

Elderd, Bret D., Jonathan Dushoff, and Greg Dwyer. "Host‐Pathogen Interactions, Insect Outbreaks, and Natural Selection for Disease Resistance." American Naturalist 172, no. 6 (December 2008): 829–42. http://dx.doi.org/10.1086/592403.

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37

Sciuto, Simona, Licia Colli, Andrea Fabris, Paolo Pastorino, Nadia Stoppani, Giovanna Esposito, Marino Prearo, et al. "What Can Genetics Do for the Control of Infectious Diseases in Aquaculture?" Animals 12, no. 17 (August 25, 2022): 2176. http://dx.doi.org/10.3390/ani12172176.

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Infectious diseases place an economic burden on aquaculture and a limitation to its growth. An innovative approach to mitigate their impact on production is breeding for disease resistance: selection for domestication, family-based selection, marker-assisted selection, and more recently, genomic selection. Advances in genetics and genomics approaches to the control of infectious diseases are key to increasing aquaculture efficiency, profitability, and sustainability and to reducing its environmental footprint. Interaction and co-evolution between a host and pathogen can, however, turn breeding to boost infectious disease resistance into a potential driver of pathogenic change. Parallel molecular characterization of the pathogen and its virulence and antimicrobial resistance genes is therefore essential to understand pathogen evolution over time in response to host immunity, and to apply appropriate mitigation strategies.

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38

Cohen, Yigal, Kyle M. Van den Langenberg, Todd C. Wehner, Peter S. Ojiambo, Mary Hausbeck, Lina M. Quesada-Ocampo, Aleš Lebeda, Helge Sierotzki, and Ulrich Gisi. "Resurgence of Pseudoperonospora cubensis: The Causal Agent of Cucurbit Downy Mildew." Phytopathology® 105, no. 7 (July 2015): 998–1012. http://dx.doi.org/10.1094/phyto-11-14-0334-fi.

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The downy mildew pathogen, Pseudoperonospora cubensis, which infects plant species in the family Cucurbitaceae, has undergone major changes during the last decade. Disease severity and epidemics are far more destructive than previously reported, and new genotypes, races, pathotypes, and mating types of the pathogen have been discovered in populations from around the globe as a result of the resurgence of the disease. Consequently, disease control through host plant resistance and fungicide applications has become more complex. This resurgence of P. cubensis offers challenges to scientists in many research areas including pathogen biology, epidemiology and dispersal, population structure and population genetics, host preference, host−pathogen interactions and gene expression, genetic host plant resistance, inheritance of host and fungicide resistance, and chemical disease control. This review serves to summarize the current status of this major pathogen and to guide future management and research efforts within this pathosystem.

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39

Wu, Fan, Yao Zhou, Yingying Shen, Zhengxi Sun, Lei Li, and Tao Li. "Linking Multi-Omics to Wheat Resistance Types to Fusarium Head Blight to Reveal the Underlying Mechanisms." International Journal of Molecular Sciences 23, no. 4 (February 18, 2022): 2280. http://dx.doi.org/10.3390/ijms23042280.

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Fusarium head blight (FHB) caused by Fusarium graminearum is a worldwide disease which has destructive effects on wheat production, resulting in severe yield reduction and quality deterioration, while FHB-infected wheat grains are toxic to people and animals due to accumulation of fungal toxins. Although impressive progress towards understanding host resistance has been achieved, our knowledge of the mechanism underlying host resistance is still quite limited due to the complexity of wheat–pathogen interactions. In recent years, disease epidemics, the resistance germplasms and components, the genetic mechanism of FHB, and disease management and control, etc., have been well reviewed. However, the resistance mechanism of FHB is quite complex with Type I, II to V resistances. In this review, we focus on the potential resistance mechanisms by linking different resistance types to multi-omics and emphasize the pathways or genes that may play significant roles in the different types of resistance. Deciphering the complicated mechanism of FHB resistance types in wheat at the integral levels based on multi-omics may help discover the genes or pathways that are critical for different FHB resistance, which could then be utilized and manipulated to improve FHB resistance in wheat breeding programs by using transgenic approaches, gene editing, or marker assisted selection strategies.

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40

Fischer, A. C., M. K. Laulis, L. Horwitz, W. E. Beschorner, and A. Hess. "Host resistance to cyclosporine induced syngeneic graft-versus-host disease. Requirement for two distinct lymphocyte subsets." Journal of Immunology 143, no. 3 (August 1, 1989): 827–32. http://dx.doi.org/10.4049/jimmunol.143.3.827.

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Abstract Cyclosporine is crucial for the prevention of organ allograft rejection and allogeneic graft-vs-host disease (GVHD). Despite its potent immunosuppressive activity, cyclosporine elicits a T cell-mediated autoimmune syndrome after autologous or syngeneic bone marrow transplantation, which has been termed syngeneic GVHD (SGVHD). Recent studies have shown that for disease manifestation, a cytoxan and radiation-sensitive T cell dependent host resistance mechanism must be eliminated, allowing the clonal expansion of autoreactive cells. This report characterizes the autoregulatory lymphocyte population, present in normal animals, capable of inhibiting the adoptive transfer of SGVHD. First, twice the number of unfractionated splenocytes from normal animals to those from autoimmune donors ensured complete inhibition of the adoptive transfer of immune reactivity. Second, the phenotype of this host resistance mechanism in normal splenocytes involves dual regulatory T cell subsets. A helper/inducer subset (W3/25+) must be cotransferred with a cytotoxic/suppressor subset (OX8+) in a ratio that approximates the normal ratio in normal unfractionated splenocytes in order to affect inhibition of the transfer of SGVHD. Moreover the specific inducer regulatory activity resides in the OX22-, W3/25+ subset of Th cells.

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41

Mehraj, Hasan, Ayasha Akter, Naomi Miyaji, Junji Miyazaki, Daniel J. Shea, Ryo Fujimoto, and Md Asad-ud Doullah. "Genetics of Clubroot and Fusarium Wilt Disease Resistance in Brassica Vegetables: The Application of Marker Assisted Breeding for Disease Resistance." Plants 9, no. 6 (June 9, 2020): 726. http://dx.doi.org/10.3390/plants9060726.

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The genus Brassica contains important vegetable crops, which serve as a source of oil seed, condiments, and forages. However, their production is hampered by various diseases such as clubroot and Fusarium wilt, especially in Brassica vegetables. Soil-borne diseases are difficult to manage by traditional methods. Host resistance is an important tool for minimizing disease and many types of resistance (R) genes have been identified. More than 20 major clubroot (CR) disease-related loci have been identified in Brassica vegetables and several CR-resistant genes have been isolated by map-based cloning. Fusarium wilt resistant genes in Brassica vegetables have also been isolated. These isolated R genes encode the toll-interleukin-1 receptor/nucleotide-binding site/leucine-rice-repeat (TIR-NBS-LRR) protein. DNA markers that are linked with disease resistance allele have been successfully applied to improve disease resistance through marker-assisted selection (MAS). In this review, we focused on the recent status of identifying clubroot and Fusarium wilt R genes and the feasibility of using MAS for developing disease resistance cultivars in Brassica vegetables.

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Bell, Richard L., and Tom van der Zwet. "Host Resistance in Pyrus to Fabraea Leaf Spot." HortScience 40, no. 1 (February 2005): 21–23. http://dx.doi.org/10.21273/hortsci.40.1.21.

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Pear leaf spot, caused by the fungus Fabraea maculata Atk. (anamorph: Entomosporium mespili (DC.) Sacc.) occurs in most areas of the world where pears are grown. Most major cultivars of the european pear, P. communis L., for which data are available are susceptible. Ratings appearing in the literature are sometimes contradictory. This study evaluated resistance/susceptibility within a diverse collection of Pyrus cultivars and other germplasm in a randomized and replicated nursery plot using quantitative measures of disease incidence and severity. The least susceptible genotypes were the P. communis cultivars `Beurre Fouqueray' and `Bartlett', the P. pyrifolia cultivars `Imamura Aki', and the P. communis × P. ussuriensis hybrid NJ 477643275.

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Takeuchi, Yuko, Natsumi Kanzaki, and Kazuyoshi Futai. "How different is induced host resistance against the pine wood nematode, Bursaphelenchus xylophilus, by two avirulent microbes?" Nematology 8, no. 3 (2006): 435–42. http://dx.doi.org/10.1163/156854106778493510.

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AbstractPine wilt disease, caused by the pine wood nematode (PWN), Bursaphelenchus xylophilus, has been devastating pine forests in Japan for a century but an effective method for controlling the disease is still needed. Pre-inoculation of the host plant with an avirulent pathogen can induce resistance against subsequent infection with virulent pathogens; this is called 'induced resistance'. Host pine trees have this type of resistance against pine wilt disease but the detailed mechanism is unknown. In this study, 1-year-old potted seedlings of the susceptible Japanese black pine, Pinus thunbergii, were pre-inoculated with an avirulent isolate of PWN (C14-5), as well as an avirulent fungus, Botrytis cinerea, to induce host resistance against PWN. One, 2, 3, 4 and 5 weeks after inoculation, the seedlings were challenged with a virulent isolate of PWN (S10), and the survival of these seedlings was estimated by their external symptoms. Pre-inoculation with either C14-5 or Botrytis delayed the symptom development caused by subsequent inoculation with S10, suggesting that pre-inoculation induced host resistance against PWN. The resistance induced by pre-inoculation with C14-5 lasted for at least 5 weeks, while that induced by Botrytis weakened with time. It has been reported that the PWN survives inside the host seedlings for a long period without causing any symptoms under certain conditions, but Botrytis survives only for a while in the seedlings. Thus, the duration of host resistance induced by pre-inoculation may vary with the viability of the inoculum used for pre-inoculation. In order to obtain durable induced resistance, it may be necessary to repeat inoculations of avirulent microbes to be able to control pine wilt disease.

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Romero, A. M., and D. F. Ritchie. "Systemic Acquired Resistance Delays Race Shifts to Major Resistance Genes in Bell Pepper." Phytopathology® 94, no. 12 (December 2004): 1376–82. http://dx.doi.org/10.1094/phyto.2004.94.12.1376.

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The lack of durability of host plant disease resistance is a major problem in disease control. Genotype-specific resistance that involves major resistance (R) genes is especially prone to failure. The compatible (i.e., disease) host-pathogen interaction with systemic acquired resistance (SAR) has been studied extensively, but the incompatible (i.e., resistant) interaction less so. Using the pepper-bacterial spot (causal agent, Xanthomonas axonopodis pv. vesicatoria) pathosystem, we examined the effect of SAR in reducing the occurrence of race-change mutants that defeat R genes in laboratory, greenhouse, and field experiments. Pepper plants carrying one or more R genes were sprayed with the plant defense activator acibenzolar-S-methyl (ASM) and challenged with incompatible strains of the pathogen. In the greenhouse, disease lesions first were observed 3 weeks after inoculation. ASM-treated plants carrying a major R gene had significantly fewer lesions caused by both the incompatible (i.e., hypersensitive) and compatible (i.e., disease) responses than occurred on nonsprayed plants. Bacteria isolated from the disease lesions were confirmed to be race-change mutants. In field experiments, there was a delay in the detection of race-change mutants and a reduction in disease severity. Decreased disease severity was associated with a reduction in the number of race-change mutants and the suppression of disease caused by the race-change mutants. This suggests a possible mechanism related to a decrease in the pathogen population size, which subsequently reduces the number of race-change mutants for the selection pressure of R genes. Thus, inducers of SAR are potentially useful for increasing the durability of genotype-specific resistance conferred by major R genes.

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Miura, Tomisato, Daisuke Mizuki, Sanae Sasaki, Suguru Hasegawa, Hiroshi Sashinami, and Akio Nakane. "Host Resistance to Listeria monocytogenes Infection Is Enhanced but Resistance to Staphylococcus aureus Infection Is Reduced in Acute Graft-versus-Host Disease in Mice." Infection and Immunity 68, no. 7 (July 1, 2000): 4340–43. http://dx.doi.org/10.1128/iai.68.7.4340-4343.2000.

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ABSTRACT Acute graft-versus-host disease (GVHD) is characterized by the production of high levels of T helper 1 (Th1)-type cytokines. Bone marrow transplantation from allogeneic C57BL/6 cells to CBF1 mice produced acute GVHD. Host resistance to Th1-driven Listeria monocytogenes was enhanced, whereas host resistance to Th2-driven Staphylococcus aureus was reduced during acute GVHD. These results suggest that opposite host responses are observed between Th1-driven and Th2-driven bacterial infections in acute GVHD.

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46

McCorkle, Kestrel L., Katherine Drake-Stowe, Ramsey S. Lewis, and David Shew. "Characterization of Phytophthora nicotianae Resistance Conferred by the Introgressed Nicotiana rustica Region, Wz, in Flue-Cured Tobacco." Plant Disease 102, no. 2 (February 2018): 309–17. http://dx.doi.org/10.1094/pdis-03-17-0339-re.

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Black shank, caused by Phytophthora nicotianae, is one of the most important diseases affecting tobacco worldwide and is primarily managed through use of host resistance. An additional source of resistance to P. nicotianae, designated as Wz, has been introgressed into Nicotiana tabacum from N. rustica. The Wz gene region confers high levels of resistance to all races, but has not been characterized. Our study found Wz-mediated resistance is most highly expressed in the roots, with only a slight reduction in stem-lesion size in Wz genotypes compared with susceptible controls. No substantial relationships were observed between initial inoculum levels and disease development on Wz genotypes, which is generally consistent with qualitative or complete resistance. Isolates of P. nicotianae adapted for five host generations on plants with the Wz gene caused higher disease severity than isolates adapted on Wz plants for only one host generation. Wz-adapted isolates did not exhibit increased aggressiveness on genotypes with other sources of partial resistance, suggesting pathogen adaptation was specific to the Wz gene. To reduce potential for pathogen population shifts with virulence on Wz genotypes, Wz should be combined with other resistance sources and rotation of varying black shank resistance mechanisms is also recommended.

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47

Vila, Taissa, Ahmed S. Sultan, Daniel Montelongo-Jauregui, and Mary Ann Jabra-Rizk. "Oral Candidiasis: A Disease of Opportunity." Journal of Fungi 6, no. 1 (January 16, 2020): 15. http://dx.doi.org/10.3390/jof6010015.

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Oral candidiasis, commonly referred to as “thrush,” is an opportunistic fungal infection that commonly affects the oral mucosa. The main causative agent, Candida albicans, is a highly versatile commensal organism that is well adapted to its human host; however, changes in the host microenvironment can promote the transition from one of commensalism to pathogen. This transition is heavily reliant on an impressive repertoire of virulence factors, most notably cell surface adhesins, proteolytic enzymes, morphologic switching, and the development of drug resistance. In the oral cavity, the co-adhesion of C. albicans with bacteria is crucial for its persistence, and a wide range of synergistic interactions with various oral species were described to enhance colonization in the host. As a frequent colonizer of the oral mucosa, the host immune response in the oral cavity is oriented toward a more tolerogenic state and, therefore, local innate immune defenses play a central role in maintaining Candida in its commensal state. Specifically, in addition to preventing Candida adherence to epithelial cells, saliva is enriched with anti-candidal peptides, considered to be part of the host innate immunity. The T helper 17 (Th17)-type adaptive immune response is mainly involved in mucosal host defenses, controlling initial growth of Candida and inhibiting subsequent tissue invasion. Animal models, most notably the mouse model of oropharyngeal candidiasis and the rat model of denture stomatitis, are instrumental in our understanding of Candida virulence factors and the factors leading to host susceptibility to infections. Given the continuing rise in development of resistance to the limited number of traditional antifungal agents, novel therapeutic strategies are directed toward identifying bioactive compounds that target pathogenic mechanisms to prevent C. albicans transition from harmless commensal to pathogen.

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Kousik, C. S. "The 12th I. E. Melhus Graduate Student Symposium: Host Plant Resistance and Disease Management, Current Status, and Future Outlook." Plant Health Progress 14, no. 1 (January 2013): 28. http://dx.doi.org/10.1094/php-2013-1125-01-ps.

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The 12th I. E. Melhus Graduate Student Symposium was held at the 2012 annual meeting of the American Phytopathological Society in Providence, RI. Its theme was “Host Plant Resistance and Disease Management: Current Status and Future Outlook.” The symposium featured four graduate student presentations highlighting research that leads to a better understanding of host plant resistance, resistance breeding, and disease management. Accepted for publication 6 November 2013. Published 25 November 2013.

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Wohor, Osman Z., Nicolas Rispail, Chris O. Ojiewo, and Diego Rubiales. "Pea Breeding for Resistance to Rhizospheric Pathogens." Plants 11, no. 19 (October 10, 2022): 2664. http://dx.doi.org/10.3390/plants11192664.

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Pea (Pisum sativum L.) is a grain legume widely cultivated in temperate climates. It is important in the race for food security owing to its multipurpose low-input requirement and environmental promoting traits. Pea is key in nitrogen fixation, biodiversity preservation, and nutritional functions as food and feed. Unfortunately, like most crops, pea production is constrained by several pests and diseases, of which rhizosphere disease dwellers are the most critical due to their long-term persistence in the soil and difficulty to manage. Understanding the rhizosphere environment can improve host plant root microbial association to increase yield stability and facilitate improved crop performance through breeding. Thus, the use of various germplasm and genomic resources combined with scientific collaborative efforts has contributed to improving pea resistance/cultivation against rhizospheric diseases. This improvement has been achieved through robust phenotyping, genotyping, agronomic practices, and resistance breeding. Nonetheless, resistance to rhizospheric diseases is still limited, while biological and chemical-based control strategies are unrealistic and unfavourable to the environment, respectively. Hence, there is a need to consistently scout for host plant resistance to resolve these bottlenecks. Herein, in view of these challenges, we reflect on pea breeding for resistance to diseases caused by rhizospheric pathogens, including fusarium wilt, root rots, nematode complex, and parasitic broomrape. Here, we will attempt to appraise and harmonise historical and contemporary knowledge that contributes to pea resistance breeding for soilborne disease management and discuss the way forward.

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Daniels, C. H., B. Fristensky, W. Wagoner, and L. A. Hadwiger. "Pea genes associated with non-host disease resistance to Fusarium are also active in race-specific disease resistance to Pseudomonas." Plant Molecular Biology 8, no. 4 (1987): 309–16. http://dx.doi.org/10.1007/bf00021310.

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