• ALGAE
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• 제24권4호
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• pp.249-256
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• 2009

The occurrence of Laminarionema elsbetiae (Ectocarpaceae, Phaeophyceae), as epi-endophyte of Rhodymenia pseudopalmata (Rhodymeniales, Rhodophyta), described from Santa Isabel, Rawson, Argentina. L. elsbetiae grows in the host tissues forming epi-endophytic relationship in the epidermal, cortical and medullar layers. Epiphytic thalli of L. elsbetiae were unbranched filaments emerging from hostis surface. Reproductive structures of L. elsbetiae on the host were absent. On the contrary, free cultured individuals formed different reproductive structures. Macrozoosporangia containing a single large motile zoospore originated from vegetative cells, they were conical to cylindrical in shape, 30-50 ${\mu}m$ in length and 18-20 ${\mu}m$ in wide. Uniseriate plurilocular zoosporangia were cylindrical shape, 40 ${\mu}m$ in length and 10-13 ${\mu}m$ in wide. Sexual fusion was not seen. In mixed cultures of L. elsbetiae with R. pseudopalmata fronds, L. elsbetiae infected the host, grew as in natural host and, formed macrosporangia between host subcortical cells. Gametophytes of L. elsbetiae were filaments with diffuse growth, branched with a branch pattern alternate or opposite. Gametangia were plurilocular, uni or biseriate and lateral. When mature they contained 2 to 6 isogametes. The presence L. elsbetiae on R. pseudopalmata could be defined as an epi-endophytic relationship. The percentage of infection of R. pseudopalmata thalli by L. elsbetiae was 34%.A25% of the infected thalli presented a low, non-symptomatic level infection, whereas a 62% and a 13% of them exhibited respectively moderate and high indexes of infection.

• Parasites, Hosts and Diseases
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• 제52권5호
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• pp.459-469
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• 2014

Entamoeba histolytica is a tissue-invasive protozoan parasite causing dysentery in humans. During infection of colonic tissues, amoebic trophozoites are able to kill host cells via apoptosis or necrosis, both of which trigger IL-8-mediated acute inflammatory responses. However, the signaling pathways involved in host cell death induced by E. histolytica have not yet been fully defined. In this study, we examined whether calpain plays a role in the cleavage of pro-survival transcription factors during cell death of colonic epithelial cells, induced by live E. histolytica trophozoites. Incubation with amoebic trophozoites induced activation of m-calpain in a time- and dose-dependent manner. Moreover, incubation with amoebae resulted in marked degradation of STAT proteins (STAT3 and STAT5) and NF-${\kappa}B$ (p65) in Caco-2 cells. However, $I{\kappa}B$, an inhibitor of NF-${\kappa}B$, was not cleaved in Caco-2 cells following adherence of E. histolytica. Entamoeba-induced cleavage of STAT proteins and NF-${\kappa}B$ was partially inhibited by pretreatment of cells with a cell-permeable calpain inhibitor, calpeptin. In contrast, E. histolytica did not induce cleavage of caspase-3 in Caco-2 cells. Furthermore, pretreatment of Caco-2 cells with a calpain inhibitor, calpeptin (but not the pan-caspase inhibitor, z-VAD-fmk) or m-calpain siRNA partially reduced Entamoeba-induced DNA fragmentation in Caco-2 cells. These results suggest that calpain plays an important role in E. histolytica-induced degradation of NF-${\kappa}B$ and STATs in colonic epithelial cells, which ultimately accelerates cell death.

• 대한의생명과학회지
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• 제15권1호
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• pp.55-60
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• 2009

Insect cells such as Spodoptera frugiperda Clone 9 (Sf9) cells are widely chosen as the host for heterologous expression of a mammalian sugar transport protein using the baculovirus expression system. Characterization of the expressed protein is expected to include assay of its function, including its ability to transport sugars and to bind inhibitory ligands such as cytochalasin B. It is therefore very important first to establish the transport characteristics and other properties of the endogenous sugar transport proteins of the host insect cells. However, very little is known of the transport characteristics of Sf9 cells, although their ability to grow on TC-100 medium strongly suggested the presence of endogenous glucose transport system. In order to investigate the substrate and inhibitor recognition properties of the Sf9 cell transporter, the ability of pentoses to inhibit 2-deoxy-D-glucose (2dGlc) transport was investigated by measuring inhibition constants $(K_i)$. To determine the time period over which of sugar into the Sf cells was linear, the uptake of 2dGlc 0.1mM extracellular concentration was measured over periods ranging from 30 seconds to 30 minutes. The uptake was linear for at least 2 minutes at the concentration, implying that uptake made over a 1 minute time course would reflect initial rates of the sugar uptake. The data have also revealed the existence of a saturable transport system for pentose uptake by the insect cells. The transport was inhibited by D-xylose and D-ribose, although not as effective as hexoses. However, L-xylose had a little effect on 2dGlc transport in the Sf9 cells, indicating that the transport is stereoselective. Unlike the human erythrocyte-type glucose transport system, D-ribose had a somewhat greater apparent affinity for the Sf9 cell transporter than D-xylose. It is therefore concluded that Sf9 cells contain an endogenous sugar transport activity that in some aspects resembled the human erythrocyte-type counterpart, although the Sf9 and human transport systems do differ in their affinity for cytochalasin B.

• IMMUNE NETWORK
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• 제20권6호
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• pp.49.1-49.15
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• 2020

C-C chemokine receptor type 5 (CCR5) regulates the trafficking of various immune cells to sites of infection. In this study, we showed that expression of CCR5 and its ligands was rapidly increased in the kidney after systemic Candida albicans infection, and infected CCR5^-/- mice exhibited increased mortality and morbidity, indicating that CCR5 contributes to an effective defense mechanism against systemic C. albicans infection. The susceptibility of CCR5^-/- mice to C. albicans infection was due to impaired fungal clearance, which in turn resulted in exacerbated renal inflammation and damage. CCR5-mediated recruitment of NK cells to the kidney in response to C. albicans infection was necessary for the anti-microbial activity of neutrophils, the main fungicidal effector cells. Mechanistically, C. albicans induced expression of IL-23 by CD11c⁺ dendritic cells (DCs). IL-23 in turn augmented the fungicidal activity of neutrophils through GM-CSF production by NK cells. As GM-CSF potentiated production of IL-23 in response to C. albicans, a positive feedback loop formed between NK cells and DCs seemed to function as an amplification point for host defense. Taken together, our results suggest that CCR5-mediated recruitment of NK cells to the site of fungal infection is an important step that underlies innate resistance to systemic C. albicans infection.

• IMMUNE NETWORK
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• 제15권3호
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• pp.125-134
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• 2015

Acute graft-versus-host-disease (GVHD) is characterized by selective damage to the liver, the skin, and the gastrointestinal tract. Following allogeneic hematopoietic stem cell transplantation, donor bone marrow (BM) cells repopulate the immune system of the recipient. We previously demonstrated that the acute intestinal GVHD (iGVHD) mortality rate was higher in MyD88-deficient BM recipients than that in the control BM recipients. In the present study, the role of MyD88 (expressed by donor BM) in the pathophysiology of hepatic GVHD (hGVHD) was examined. Unlike iGVHD, transplantation with MyD88-deficient T-cell depleted (TCD) BM attenuated hGVHD severity and was associated with low infiltration of T cells into the liver of the recipients. Moreover, GVHD hosts, transplanted with MyD88-deficient TCD BM, exhibited markedly reduced expansion of $CD11b^+Gr-1^+$ myeloidderived suppressor cells (MDSC) in the liver. Adoptive injection of the MDSC from wild type mice, but not MyD88-deficient mice, enhanced hepatic T cell infiltration in the MyD88-deficient TCD BM recipients. Pre-treatment of BM donors with LPS increased MDSC levels in the liver of allogeneic wild type BM recipients. In conclusion, hGVHD and iGVHD may occur through various mechanisms based on the presence of MyD88 in the non-T cell compartment of the allograft.

• IMMUNE NETWORK
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• 제14권3호
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• pp.128-137
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• 2014

Respiratory viruses can induce acute respiratory disease. Clinical symptoms and manifestations are dependent on interactions between the virus and host immune system. Dendritic cells (DCs), along with alveolar macrophages, constitute the first line of sentinel cells in the innate immune response against respiratory viral infection. DCs play an essential role in regulating the immune response by bridging innate and adaptive immunity. In the steady state, lung DCs can be subdivided into $CD103^+$ conventional DCs (cDCs), $CD11b^+$ cDCs, and plasmacytoid DCs (pDCs). In the inflammatory state, like a respiratory viral infection, monocyte-derived DCs (moDCs) are recruited to the lung. In inflammatory lung, discrimination between moDCs and $CD11b^+$ DCs in the inflamed lung has been a critical challenge in understanding their role in the antiviral response. In particular, $CD103^+$ cDCs migrate from the intraepithelial base to the draining mediastinal lymph nodes to primarily induce the $CD8^+$ T cell response against the invading virus. Lymphoid $CD8{\alpha}^+$ cDCs, which have a developmental relationship with $CD103^+$ cDCs, also play an important role in viral antigen presentation. Moreover, pDCs have been reported to promote an antiviral response by inducing type I interferon production rather than adaptive immunity. However, the role of these cells in respiratory infections remains unclear. These different DC subsets have functional specialization against respiratory viral infection. Under certain viral infection, contextually controlling the balance of these specialized DC subsets is important for an effective immune response and maintenance of homeostasis.

• Parasites, Hosts and Diseases
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• 제59권6호
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• pp.573-583
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• 2021

Toxoplasma gondii, an intracellular protozoan parasite that infects one-third of the world's population, has been reported to hijack host cell apoptotic machinery and promote either an anti- or proapoptotic program depending on the parasite virulence and load and the host cell type. However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.

• 한국패류학회지
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• 제31권4호
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• pp.267-272
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• 2015

This study was conducted in order to elucidate the dissemination mechanism of P. olseni using field and laboratory experiments. For this purpose, we quantified the level of P. olseni infection in buried (healthy) and surfaced (gapped) R. philippinarum from a clam bed on Wi-do Island on the west coast of Korea. In addition, the levels of internal and released P. olseni cells from artificially infected (and later dead) R. philippinarum were monitored for 8 days using the RFTM-2 M NaOH lysis method. Our results indicate that P. olseni cells in buried R. philippinarum was $2,655,625{\pm}1,536,936cells/clam$; the level in gapped R. philippinarum was considerably lower, $28,203{\pm}24,889cells/clam$ (p < 0.05). In the laboratory experiment, the P. olseni cells remained in the host tissue 2 days after death was approximately 50% lower than the level of infection measured in living clams. The level dropped to 20% 4 days after death and to 1.5% 6 days after death; eight days after death, P. olseni cells were undetectable since the R. philippinarum flesh had completely decomposed. The level of released cells on the day of death was only 0.05% of the internal level in live R. philippinarum; however, the level increased to 2.3% 5 days after death then gradually decreased and no released cells were detected 8 days after death. Therefore, our laboratory experiment suggest that the low level of P. olseni infection observed in gapped R. philippinarum at Wi-do Island could be caused by lysis of the most of P. olseni cells during the decomposition of dead R. philippinarum tissues. Until the end of decomposition of R. philippinarum, 6.68% of the total amount of P. olseni was released within 8 days. Our study showed that the amount of P. olseni cells from dead host is a considerably higher level than naturally released from healthy R. philippinarum, suggesting that death of the host plays an important role in the dissemination of P. olseni.

• 한국안광학회지
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• 제18권4호
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• pp.541-548
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• 2013

목적: 골수기질세포는 생체 내 외에서 신경세포와 신경교세포로 교차분화 할 수 있는 능력을 가지고 있는 것으로 밝혀져 있다. 발생 중인 숙주 환경에 따라 이식된 골수기질세포의 생존여부, 형태학적 그리고 분자적 분화영향을 조사하기 위해 브라질산 주머니쥐 안구에 마우스 골수기질세포를 이식하였다. 방법: GFP를 발현하는 골수기질세포를 발생 중인 브라질산 주머니쥐의 각 시기별로 이식하여, 이식 후 최대 4주까지 생존시킨 후 각 시기별로 면역조직화학법을 시행하였다. 결과: 이식한 골수기질세포의 일부는 숙주동물의 유리체 내에서 생존하며 일부 돌기를 내는 신경세포로 형태학적 분화가 됨을 관찰할 수 있었다. 또한 유리체에 존재하는 일부 세포는 신경세포 표지인자인 TuJ1(class III ${\beta}$-tubulin), 신경교세포 표지인자인 GFAP(glial fibrillary acidic protein), 또는 신경줄기세포 표지인자인 Nestin 단백질을 발현하였다. 게다가, 일부 골수기질세포는 신경절세포층으로 이동함을 관찰했으나, 이동한 세포들은 형태학적 또는 분자적 분화를 나타내지는 않았다. 결론: 이번 연구에서 가장 효율적인 이식시기는 생후 16일째의 포유류 망막으로, 이는 망막세포의 분화양상과 층분화 패턴으로 미뤄볼 때 생후 4~5일 정도의 마우스 망막과 발생학적으로 상동함을 알 수 있었다. 또한 이식 받은 숙주 망막의 미세환경이 이식된 세포운명에 영향을 미치는 것을 확인할 수 있었다.

• Parasites, Hosts and Diseases
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• 제38권1호
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• pp.17-23
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• 2000

Eosinophils are important effector cells in host defense against parasites. Excretory-secretory product (ESP) produced by helminthic worms plays important roles in the uptake of nutrients, migration in the host tissue, and in immune modulation. However little is known about the ability of the ESP to directly trigger eosinophil apoptosis. This study investigated whether the ESP of newly excysted metacercariae of Paragonimus westermani could induce apoptosis in human eosinophils. Apoptosis was assayed by staining the cells with FITC-annexin V, and the cells were analyzed by flow cytometry. It was found that the ESP of newly excysted metacercariae of P. westemani induced a direct time- and concentration-dependent increase in the rate of constitutive apoptosis in mature human eosinophils. Eosinophil apoptosis was first apparent 3 hr after treatment with the ESP and continued to increase after 6 hr of incubation with respect to the cells cultured in the absence of the ESP. While only 2.8% of the eosinophils incubated in the medium for 3 hr were apoptotic, 7.6%, 10.9% and 22.6% of the eosinophils treated with 10. 30 and $100{\;}\mu\textrm{g}/ml$ ESP were apoptotic, respectively. This result suggests that the ESP of newly excysted metacercariae of P. westermani directly induce eosinophil apoptosis, which may be important for the survival of the parasites and the reduction of eosinophilic inflammation in vivo.