• Journal of Pharmacopuncture
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• v.15 no.3
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• pp.45-47
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• 2012

Objectives: The aim of this study is to investigate the correlation between the constitution of Sasang and the bee venom hypersensitive reaction, as well as the hypersensitive reaction occurrence ratio between males and females, for patients treated with sweet bee venom (SBV) and who had undergone an examination of the constitution of the Sasang. Methods: All 81 patients enrolled in the study were treated with SBV and underwent an examination of the constitution of Sasang from January 2010 to July 2012. We divided them into two groups for the hypersensitive reaction and no response and compared the distributions of the Sasang-constitution types for the two groups as well as the hypersensitive reaction occurrence ratio between males and females. Results: No significant differences were found between the hypersensitive-reaction group and the no-response group (p = 0.390), but the hypersensitive-reaction occurrence ratio was statistically higher in females than in males (p = 0.001). Conclusions: Hypersensitive reactions do not seem to be related to the Sasang-constitution types, but the possibility of hypersensitive reactions among females seems to be higher than it is among males.

• The Plant Pathology Journal
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• v.21 no.2
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• pp.99-101
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• 2005

Host cell death occurs during many, but not all, interactions between plants and the pathogens that infect them. This cell death can be associated with disease resistance or susceptibility, depending on the nature of the pathogen. The most well-known cell death response in plants is the hypersensitive response (HR) associated with a resistance response. HR is commonly regulated by direct or indirect interactions between avirulence proteins from pathogen and resistance proteins from plant and it can be the result of multiple signaling pathways. Ion fluxes and the generation of reactive oxygen species commonly precede cell death, but a direct involvement of the latter seems to vary with the plant-pathogen combination. Exciting advances have been made in the identification of cellular protective components and cell death suppressors that might operate in HR. In this review, recent progress in the mechanisms by which plant programmed cell death (PCD) occurs during disease resistance will be discussed.

• Journal of Microbiology and Biotechnology
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• v.20 no.1
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• pp.54-62
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• 2010

A novel harpin-like protein, HpaXm, was described from cotton leaf blight bacteria, Xanthomonas citri subsp. malvacearum. The hpaXm was found to be localized between hrp2 and hrcC. A phylogenetic analysis of the complete amino acid sequence or solely the 13 highly conserved residues $H_2N$-SEKQLDQLLTQLI-COOH in the N-terminal $\alpha$-helix indicates that HpaXm is evolutionarily closer to HpaGXag and HpaXac than to Hpa1Xoo and Hpa1Xoc. A synthesized peptide containing two heptads, 39-LDQLLTQLIMALLQ-52, from the N-terminal a-helical region of HpaXm displayed comparable activity in inducing a hypersensitive response, but two other synthesized derivatives, $HpaXm{\Delta}T44C$ and $HpaXm{\Delta}M48Q$, showed reduced HR-triggering activity. The data from a GST trap test revealed that HpaXm was released into the extracellular medium, hpaXm mutant deficient for the leader peptide (1-MNSLNTQIGANSSFL-15) was unable to be secreted outside cells but still induced HR in tobacco leaves.

• The Plant Pathology Journal
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• v.39 no.6
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• pp.584-591
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• 2023

Active plant immune response involving programmed cell death called the hypersensitive response (HR) is elicited by microbial effectors delivered through the type III secretion system (T3SS). The marine bacterium Hahella chejuensis contains two T3SSs that are similar to those of animal pathogens, but it was able to elicit HR-like cell death in the land plant Nicotiana benthamiana. The cell death was comparable with the transcriptional patterns of H. chejuensis T3SS-1 genes, was mediated by SGT1, a general regulator of plant resistance, and was suppressed by AvrPto1, a type III-secreted effector of a plant pathogen that inhibits HR. Thus, type III-secreted effectors of a marine bacterium are capable of inducing the nonhost HR in a land plant it has never encountered before. This suggests that plants may have evolved to cope with a potential threat posed by alien pathogen effectors. Our work documents an exceptional case of nonhost HR and provides an expanded perspective for studying plant nonhost resistance.

• The Plant Pathology Journal
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• v.22 no.3
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• pp.271-277
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• 2006

The interaction effects of ozone $(O_3)$ and anthracnose (Colletotrichum acutatum) disease were examined in green fruits and seedlings of pepper (Capsicum annuum). Pre-treatment with $(O_3)$ as a factor causing predisposition to the disease prior to infection was investigated in green fruits and stems using an $(O_3)$ concentration of 150 nL/L, which is easily reached in summer in Korea. $(O_3)$ treatment increased antioxidative responses in pepper foliar tissues, and defense against anthracnose was examined in fruits and stems. Anthracnose severity on stems of the $O_3-treated$, ozone-sensitive 'Dabotop' cultivar was always lower than that on untreated plants, but the difference was not always significant (p=0.147). Significantly lower anthracnose severity was found on $O_3-treated$ green 'Dabotop' fruits as compared to untreated green fruits in three of eight replicate experiments. In contrast, hypersensitive responses in 03treated seedlings were significantly accelerated compared to those in untreated seedlings by about 7.8 h (p<0.001). This confirmed previous evidence of increased transcription of plant defense genes with $(O_3)$ treatment. $(O_3)$ treatment significantly decreased chlorophyll concentrations in the leaves in four replicate experiments (p<0.01). $(O_3)$ increased hypersensitive responses in the leaves of pepper seedlings, but this increase did not contribute to the control of anthracnose severity on fruits. Antioxidant reactions to $(O_3)$ were limited to chlorosis and changes in hypersensitive responses in leaves.

• Journal of Pharmacopuncture
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• v.18 no.4
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• pp.59-62
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• 2015

Objectives: A previous study showed that bee venom (BV) could cause anaphylaxis or other hypersensitivity reactions. Although hypersensitivity reactions due to sweet bee venom (SBV) have been reported, SBV has been reported to be associated with significantly reduced sensitization compared to BV. Although no systemic immediate hypersensitive response accompanied by abnormal vital signs has been reported with respect to SBV, we report a systemic immediate hypersensitive response that we experienced while trying to use SBV clinically. Methods: The patient had undergone BV treatment several times at other Oriental medicine clinics and had experienced no adverse reactions. She came to acupuncture & moxibustion department at Semyung university hospital of Oriental medicine (Je-cheon, Korea) complaining of facial hypoesthesia and was treated using SBV injections, her first SBV treatment. SBV, 0.05 cc, was injected at each of 8 acupoints, for a total of 0.40 cc: Jichang (ST4), Daeyeong (ST5), Hyeopgeo (ST6), Hagwan (ST7), Yepung (TE17), Imun (TE21), Cheonghoe (GB2), and Gwallyeo (SI18). Results: The patient showed systemic immediate hypersensitive reactions. The main symptoms were abdominal pain, nausea and perspiration, but common symptoms associated with hypersensitivity, such as edema, were mild. Abdominal pain was the most long-lasting symptom and was accompanied by nausea. Her body temperature decreased due to sweating. Her diastolic blood pressure could not be measured on three occasions. She remained alert, though the symptoms persisted. The following treatments were conducted in sequence; intramuscular epinephrine, 1 mg/mL, injection, intramuscular dexamethasone, 5 mg/mL, injection, intramuscular buscopan, 20 mg/mL, injection, oxygen ($O_2$) inhalation therapy, 1 L/minutes, via a nasal prong, and intravascular injection of normal saline, 1 L. After 12 hours of treatment, the symptoms had completely disappeared. Conclusion: This case shows that the use of SBV does not completely eliminate the possibility of hypersensitivity and that patients who received BV treatment before may also be sensitized to SBV. Thus, a skin test should be given prior to using SBV.

• The Plant Pathology Journal
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• v.32 no.4
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• pp.347-356
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• 2016

Plants protect themselves from pathogen attacks via several mechanisms, including hypersensitive cell death. Recognition of pathogen attack by the plant resistance gene triggers expression of carboxylesterase genes associated with hypersensitive response. We identified six transcripts of carboxylesterase genes, Vitis flexuosa carboxylesterase 5585 (VfCXE5585), Vf-CXE12827, VfCXE13132, VfCXE17159, VfCXE18231, and VfCXE47674, which showed different expression patterns upon transcriptome analysis of V. flexuosa inoculated with Elsinoe ampelina. The lengths of genes ranged from 1,098 to 1,629 bp, and their encoded proteins consisted of 309 to 335 amino acids. The predicted amino acid sequences showed hydrolase like domains in all six transcripts and contained two conserved motifs, GXSXG of serine hydrolase characteristics and HGGGF related to the carboxylesterase family. The deduced amino acid sequence also contained a potential catalytic triad consisted of serine, aspartic acid and histidine. Of the six transcripts, Vf-CXE12827 showed upregulated expression against E. ampelina at all time points. Three genes (VfCXE5585, VfCXE12827, and VfCXE13132) showed upregulation, while others (VfCXE17159, VfCXE18231, and VfCXE47674) were down regulated in grapevines infected with Botrytis cinerea. All transcripts showed upregulated expression against Rhizobium vitis at early and later time points except VfCXE12827, and were downregulated for up to 48 hours post inoculation (hpi) after upregulation at 1 hpi in response to R. vitis infection. All tested genes showed high and differential expression in response to pathogens, indicating that they all may play a role in defense pathways during pathogen infection in grapevines.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.68.1-68
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• 2003

When plants are infected by plant pathogens, typical disease symptom termed lesion, appears in compatible interaction. Whereas, in incompatible interactions, only small speck of lesions are visible on the leaf surfaces. Hypersensitive response (HR) of plant which is the result of infection by incompatible pathogens, is a well known defense response inducing rapid cell death resulting in complete resistance. However, some rice mutants show spontaneous disease symptoms during the growth stages without interaction with pathogens. We investigated the spontaneous cell death mutant called Blast Lesion Mimic(BLM) generated by EMS mutation, on the relationship with the hypersensitive response as well as resistant characteristics. Accumulation of phenolic compounds were detected around the lesions as lesions develop on leaf surface. Activation of PR gene was detected before the lesion appeared, and that result indicates the defense-related response are started earlier than lesion formation. The BLM mutant showed resistant response to inoculation of Magnaporthe grisea KJ201 with which the wild type Hwacheong is totally susceptible. Informations on the formation of spontaneous lesions and detail analysis of lesion mimic mutants and related genes are very limited to date. It is really important to understand the phenomenon of the defense-related lesion formation for developing resistant cultivar for rice blast pathogens

• Korean Journal Plant Pathology
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• v.14 no.6
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• pp.563-566
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• 1998

Two soybean cultivars, Kwanggyo and Hwanggeum (soybean mosaic potyvirus (SMV)-resistant cultivars), that had been inoculated with a virulent strain (G-5H, 4) of soybean mosaic potyvirus produced necrotic lesions on inoculated leaves as well as on upper trifoliate leaves. Cells in the lesion area contained sparse numbers of virus particles and very few characteristic pinwheel inclusions. Although a hypersensitive-like cellular response occurred in the two resistant cultivars, this response did not prevent the virus from spreading systemically in these resistant hosts, indicating a different mechanism from the general hypersensitive reaction in relation to host resistance.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 1997.06a
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• pp.27-41
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• 1997