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1.
The disease outcome in malaria caused by the protozoan parasite Plasmodium is influenced by host genetic factors. To identify host genes conferring resistance to infection with the malaria parasite, we undertook chromosomal mapping using a whole-genome scanning approach in cross-bred mice. NC/Jic mice all died with high parasitemia within 8 days of infection with 1 x 10(5) parasitized erythrocytes. In contrast, 129/SvJ mice all completely excluded malaria parasites from the circulation and remained alive 21 days after infection. We performed linkage analysis in backcross [(NC/Jic x 129/SvJ)xNC/Jic] mice. The Pymr ( Plasmodium yoelii malaria resistance) locus was mapped to the telomeric portion of mouse Chromosome (Chr) 9. This locus controls host survival and parasitemia after infection. The Char1 locus ( P. chabaudi resistance locus 1), controlling host survival and peak parasitemia in P. chabaudi infection, was previously mapped to the same region. This host resistance locus mapping to Chr 9 may represent a ubiquitous locus controlling susceptibility to rodent malaria. Elucidation of the function of this gene will provide valuable insights into the mechanism of host defense against malaria parasite infection. 相似文献
2.
Two actin genes, actA from the hemibiotrophic anthracnose fungus, Colletotrichum gloeosporioides (Penz.) Penz. & Sacc. f. sp. malvae, and act1 from its host, Malva pusilla (Sm.) were cloned from a cDNA library developed from infected host tissue. The actin gene, actA, of C. gloeosporioides f. sp. malvae, which is similar to that of other euascomycetes, appears to be expressed constitutively. The actin gene of M. pusilla is most similar to one of the actin genes of Arabidopsis thaliana that is unique in being responsive to environmental stimuli such as wounding. Expression of actA was used to follow the growth of the fungus in the plant tissue. Low actA expression occurred until 72–96 h after inoculation and then increased rapidly, corresponding with the timing of the shift
from slower biotrophic fungal growth to much more rapid necrotrophic growth. In contrast, expression of act1 approximately doubled during the biotrophic phase and then rapidly declined during the necrotrophic phase. Increased host
actin expression could be due to host cytoskeleton rearrangement in response to biotrophic infection, and the subsequent decrease
in host actin expression could be due to host cell disruption resulting from tissue maceration during necrosis. This is the
first report of a host actin gene that can increase in expression during a compatible plant-pathogen interaction.
Received: 15 March 1999 / Accepted: 1 May 1999 相似文献
3.
Strain variation in the level of resistance to malaria was investigated in inbred mice after infection with Plasmodium chabaudi. Following intraperitoneal infection with the typing dose of parasitized erythrocytes, mice of 11 inbred strains could be separated using survival time as the criterium into resistant and susceptible groups. Genetic analysis of F1 hybrid and backcross progeny derived from one of the most resistant (B10.A) and from the most susceptible (A/J) strains as parents suggested that host resistance in this strain combination was genetically controlled by a dominant, non-H-2-linked, autosomal gene or closely linked genes. Analysis of the mechanisms of resistance to P chabaudi showed (1) phenotypic expression of the resistance gene was apparent within 6 days of infection as a significant difference between resistant and susceptible mice in the level of parasitemia; (2) the level of host NK cell activity was not related to the level of host resistance to malaria; (3) compared with susceptible A/J mice, resistant B1O.A hosts had an augmented erythropoietic response during the course of malaria as well as during phenylhydrazine-induced anemia and (4) treatment with BCG or P acnes resulted in an equal degree of protection, measured by parasitemia and survival, in both resistant and susceptible mice. 相似文献
4.
【背景】2型猪链球菌(Streptococcus suis serotype 2, S. suis 2)可感染宿主引起严重的脑膜炎,对养猪业和人类公共卫生安全构成重大威胁。【目的】构建S. suis 2感染小鼠脑膜炎模型,并对其脑组织进行转录组学分析,为揭示S.suis2感染宿主后引起脑膜炎的分子机制和发现潜在的治疗靶点提供理论依据。【方法】采用S. suis 2感染小鼠,并对其脑组织进行病理组织学分析确认构建脑膜炎小鼠后,对其脑组织进行转录组学分析,对比S.suis2感染和未感染小鼠的差异表达基因,并对差异表达基因进行基因本体论(geneontology,GO)功能、京都基因和基因组百科全书(Kyoto encyclopedia of genes and genomes, KEGG)通路富集和韦恩分析。【结果】脑病理组织学分析结果显示,S. suis 2感染的小鼠脑膜中有大量的炎症细胞浸润,并且血管周围出现“袖套”现象,并能从感染小鼠的组织器官中再分离出攻毒的S. suis 2菌株,结果证明构建了S. suis 2感染脑膜炎小鼠模型。转录组学分析结果表明,感染S.suis2与未感染的... 相似文献
5.
Adam J.W. Paige Brent W. Kiernan Anabel Varela Michael J.C. Rogers David Hughes Karen P. Steel Steve D.M. Brown 《Mammalian genome》2000,11(1):51-57
Whirler (wi) mice display profound deafness and a head-tossing and circling phenotype, showing an autosomal recessive mode of inheritance.
The wi mutation has been shown to map close to the Orm gene cluster on mouse Chromosome (Chr) 4. We have, therefore, investigated the Orm loci as candidates for the whirler gene. Detailed mapping and analysis of the Orm gene cluster in both normal and whirler mice indicates the presence of a <48-kb deletion in whirler mice that disrupts the
Orm1 locus. The Orm1 locus is also deleted in the CE/J mouse strain, and we discuss the candidature of Orm1 for the whirler gene.
Received: 22 June 1999 / Accepted: 17 September 1999 相似文献
6.
EDELBERTO J. CABRERA NELDA E. ALGER PAUL H. SILVERMAN 《The Journal of eukaryotic microbiology》1973,20(3):449-452
SYNOPSIS. Adoptive immunity to Plasmodium berghei was transferred by intraperitoneal injections into rats, never before exposed to this parasite, of either 2 × 107 or 2 × 108, but not of 2 × 106, spleen cells from syngenic rats which had recovered from a primary P. berghei infection. When the spleen cells from the latter animals were kept at 47 C for 45 min they remained alive, but no longer were able to transfer protection. The capacity to transfer adoptive immunity was not found in spleen cells from adult rats capable of age immunity. On the other hand, this capacity was found in spleen cells from rats that had suffered a very transient parasitemia (> 1% peak parasitemia). 相似文献
7.
Linkages among three biochemical loci (Acol, Ahd2, and Mup1) and four microsatellite loci (A8, Glut1, Jun, and Pnd) were determined to construct a linkage map of rat Chromosome (Chr) 5. Consequently, an extensive linkage map on rat Chr 5 was constructed with the following gene order: A8-Aco1-Mup1-Jun-Glut1-Ahd2-Pnd. In this linkage map, the Jun and A8 loci are newly placed, and two previously reported linkage groups on rat Chr 5 are connected by the Jun locus. The linkage map indicates an extensive linkage conservation between the loci on rat Chr 5 and those on mouse Chr 4. 相似文献
8.
Malaria continues to be a serious threat to global health. The malaria problem is compounded by the absence of an efficacious vaccine and widespread drug resistance in the Plasmodium malarial parasite. The host factors and parasite virulence determinants that regulate early response to infection and subsequent onset of protective immunity are poorly understood. The molecular characterization of this early host:pathogen interface may identify novel targets for prophylactic or therapeutic intervention. Genetic analyses in mouse model of malaria show that inactivation of the enzyme pantetheinase (Char9 locus) causes susceptibility to blood-stage infection. The pantetheinase product cysteamine is an inexpensive and non-toxic aminothiol that is approved for lifelong clinical management of nephropathic cystinosis. In mouse models of infection, cysteamine not only displays anti-malarial activity of its own, but also dramatically potentiates the anti-malarial activity of artemisinin, at doses currently used for the clinical management of cystinosis. Therefore, the inclusion of cysteamine in current artemisinin combination therapies may significantly increase efficacy and may also prove effective against emerging artemisinin-resistant human Plasmodium parasite. 相似文献
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11.
Arantes JM Francisco AF de Abreu Vieira PM Silva M Araújo MS de Carvalho AT Pedrosa ML Carneiro CM Tafuri WL Martins-Filho OA Elói-Santos SM 《Experimental parasitology》2011,(4):401-408
Desferrioxamine (DFO) is a potent iron chelator that is also known to modulate inflammation and act as an efficient antioxidant under normal conditions and under oxidative stress. Many in vitro and in vivo studies have shown the efficacy of DFO in the treatment of viral, bacterial and protozoan infections. DFO is known to reduce the intensity of Trypanosoma cruzi infections in mice even during a course of therapy that is not effective in maintaining anaemia or low iron levels. To further clarify these findings, we investigated the action of DFO on mouse T. cruzi infection outcomes and the direct impact of DFO on parasites.Infected animals treated with DFO (5 mg/animal/day) for 35 days, beginning 14 days prior to infection, presented lower parasitemia and lower cumulative mortality rate. No significant effect was observed on iron metabolism markers, erythrograms, leukograms or lymphocyte subsets.In the rapid method for testing in vivo T. cruzi susceptibility, DFO also induced lower parasitemia.In regard to its direct impact on parasites, DFO slightly inhibited the growth of amastigotes and trypomastigotes in fibroblast culture. Trypan blue staining showed no effects of DFO on parasite viability, and only minor apoptosis in trypomastigotes was observed. Nevertheless, a clear decrease in parasite mobility was detected.In conclusion, the beneficial actions of DFO on mice T. cruzi infection seem to be independent of host iron metabolism and free of significant haematological side effects. Through direct action on the parasite, DFO has more effective trypanostatic than trypanocidal properties. 相似文献
12.
Singhania NA Dyer KD Zhang J Deming MS Bonville CA Domachowske JB Rosenberg HF 《Journal of molecular evolution》1999,49(6):721-728
The two eosinophil ribonucleases, eosinophil-derived neurotoxin (EDN/RNase 2) and eosinophil cationic protein (ECP/RNase
3), are among the most rapidly evolving coding sequences known among primates. The eight mouse genes identified as orthologs
of EDN and ECP form a highly divergent, species-limited cluster. We present here the rat ribonuclease cluster, a group of
eight distinct ribonuclease A superfamily genes that are more closely related to one another than they are to their murine
counterparts. The existence of independent gene clusters suggests that numerous duplications and diversification events have
occurred at these loci recently, sometime after the divergence of these two rodent species (∼10–15 million years ago). Nonsynonymous
substitutions per site (d
N) calculated for the 64 mouse/rat gene pairs indicate that these ribonucleases are incorporating nonsilent mutations at accelerated
rates, and comparisons of nonsynonymous to synonymous substitution (d
N / d
S) suggest that diversity in the mouse ribonuclease cluster is promoted by positive (Darwinian) selection. Although the pressures
promoting similar but clearly independent styles of rapid diversification among these primate and rodent genes remain uncertain,
our recent findings regarding the function of human EDN suggest a role for these ribonucleases in antiviral host defense.
Received: 8 April 1999 / Accepted: 22 June 1999 相似文献
13.
Human cerebral malaria (CM) during acute Plasmodium falciparum infection is a serious neurological complication that leads to coma and death. P. berghei ANKA infection of CBA mice is a useful experimental model of CM. To identify host susceptibility loci, we performed chromosomal mapping in crossbred populations of both CM-susceptible CBA and CM-resistant DBA/2 mice. One significant region for a CM-susceptible locus in CBA mice was mapped to H2 region on Chromosome 17, tentatively designated cmsc. cmsc was mapped to a different chromosomal region from that previously reported in the C57BL/6 mouse model of CM. It is possible that different loci contribute to CM in CBA and C57BL/6 mouse strains. Comparison of the function of CM susceptibility loci between CBA and C57BL/6 mice could have important implications for the study of the complex pathogenesis of CM in humans. 相似文献
14.
Jianhe Wang Chao Wang Hong‐Bing Yu Stephen Dela Ahator Xiaoyan Wu Shumei Lv Lian‐Hui Zhang 《Cellular microbiology》2019,21(10)
Pseudomonas aeruginosa, an opportunistic life‐threatening human bacterial pathogen, employs quorum‐sensing (QS) signal molecules to modulate virulence gene expression. 2‐(2‐hydroxyphenyl)‐thiazole‐4‐carbaldehyde (IQS) is a recently identified QS signal that integrates the canonical lasR‐type QS of P. aeruginosa and host phosphate stress response to fine‐tune its virulence production for a successful infection. To address the role of IQS in pathogen–host interaction, we here present that IQS inhibits host cell growth and stimulates apoptosis in a dosage‐dependent manner. By downregulating the telomere‐protecting protein POT1 in host cells, IQS activates CHK1, CHK2, and p53 in an Ataxia telangiectasia mutated (ATM)/ATM and RAD3‐related (ATR)‐dependent manner and induces DNA damage response. Overexpression of POT1 in host cells presents a resistance to IQS treatment. These results suggest a pivotal role of IQS in host apoptosis, highlighting the complexity of pathogenesis mechanisms developed by P. aeruginosa during infection. 相似文献
15.
Genome‐wide DNA methylation signatures of infection status in Trinidadian guppies (Poecilia reticulata)
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Juntao Hu Felipe Pérez‐Jvostov Léa Blondel Rowan D. H. Barrett 《Molecular ecology》2018,27(15):3087-3102
Epigenetic modification, especially DNA methylation, can play an important role in mediating gene regulatory response to environmental stressors and may be a key process affecting phenotypic plasticity and adaptation. Parasites are potent stressors with profound physiological and ecological effects on their hosts, yet it remains unclear how parasites influence host methylation patterns. Here, we used a well‐studied host–parasite system, the guppy Poecilia reticulata and its ectoparasitic monogenean Gyrodactylus turnbulli to gain mechanistic insight into the dynamics of DNA methylation in host–parasite interactions. To explore this, we quantitatively measured genome‐wide DNA methylation in guppy skin tissue using reduced representation bisulphite sequencing and characterized differential methylation patterns in guppies during distinct phases of infection. We identified 365, 313, and 741 differentially methylated regions (DMRs) between infected and control fish in early infection, peak infection and recovery phases, respectively. The magnitude of the methylation difference was moderate in DMRs, with an average of 29% (early infection), 27% (peak infection) and 30% (recovery) differential methylation per DMR. Approximately 50% of DMRs overlapped with CpG islands, and over half of the DMRs overlapped with gene bodies, several of which encode proteins relevant to immune response. These findings provide the first evidence of an epigenetic signature of infection by ectoparasites and demonstrate the changing relationship between epigenetic variation and immune response in distinct phases of infection. 相似文献
16.
TGFα is a mitogenic polypeptide found in the conditioned media of transformed cell lines as well as in various solid tumors. Although its physiological role in normal tissues is uncertain, the autocrine action of TGFα on the EGF receptor is postulated to play a role in tumorigenesis. To explore the possibility that pre-existing mouse mutants might have concordance with the mouse TGFα locus (Tgfa) we sought to establish the chromosomal localization of the murine TGFα gene. Using Southern analysis we have detected NcoI and PvuII RFLP in the TGFα gene of progenitor RI mouse strains. These RFLPs have been used to analyze four different RI sets of DNA and to assign Tgfa to the 35-cM region of chromosome 6. Linkage has been established and the data suggest that the distance between Igk and wa-1 anchor loci may be less than 8 cM and that the gene order for the proximal to mid region of mouse chromosome 6 may be: Ggc-Xmmv27-[Brp-1, Lvp-1, Ms6-4]-[Igk, Ly2, Ly3 Odc-rs5, Rn7s-6, Fabp1]-[Tgfa/wa-1]-IL5-R. Homology of synteny has been further defined between the proximal region of mouse chromosome 6 and with the 2p 13-p11 region of human chromosome 2 encompassing TGFA, IGK, CD8A, and FABP1 . 相似文献
17.
Kieran G. Meade Fernando Narciandi Sarah Cahalane Carla Reiman Brenda Allan Cliona O’Farrelly 《Immunogenetics》2009,61(2):101-110
Salmonella typhimurium and Campylobacter jejuni pose significant risks to human health and poultry are a major vector for infection. Comparative in vivo infection models were performed to compare the avian host immune response to both bacterial species. Forty-five commercial
broiler chickens were orally challenged with either C. jejuni or S. typhimurium whilst 60 similar control birds were mock challenged in parallel. Birds were sacrificed at 0, 6, 20 and 48 h post-infection
and cloacal swabs, blood and tissue samples taken. Peripheral blood leukocytes were isolated for flow cytometric analyses
and RNA was extracted for gene expression profiling. Colonisation patterns were markedly different between the two bacterial
species, with systemic colonisation of Campylobacter outside the gastrointestinal tract. Salmonella infection induced significant
changes in circulating heterophil and monocyte/macrophage populations, whilst Campylobacter infection had no effect on the
heterophil numbers but caused a significant early increase in circulating monocytes/macrophages. Toll-like receptor 1 (TLR1) gene expression was decreased, and avian β-defensin (AvBD) gene expression (AvBD3, AvBD10 and AvBD12) was significantly increased in response to Salmonella infection (P < 0.05). In contrast, Campylobacter infection induced increased TLR21 gene expression but significantly reduced expression of seven antimicrobial peptide (AMP) genes (AvBD3, AvBD4, AvBD8, AvBD13, AvBD14, CTHL2 and CTHL3; P < 0.05). Considered together, microbiological, cellular and gene expression profiles indicate that the innate immune system
responds differently to Salmonella and to Campylobacter infection. Furthermore, reduction in the expression of AMPs may play
a role in the persistence of high level colonisation of the host by Campylobacter.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
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19.
Simon Horvat Lutz Bünger Victoria M. Falconer Pamela Mackay Andy Law Grahame Bulfield Peter D. Keightley 《Mammalian genome》2000,11(1):2-7
A genome-wide quantitative trait locus (QTL) analysis was performed in a polygenic obesity mouse model resulting from a long-term
selection experiment. The parental lines were outbred lines divergently selected for 53 generations for high-fat (fat, F line)
or low-fat (lean, L line) percentage (fat%) that differed fivefold in fat% at 14 weeks of age. An F2 population of 436 mice was used for the QTL analysis with 71 markers distributed across the genome. The analysis revealed
significant QTLs Fob1 (for F-line obesity QTL 1), Fob2, Fob3, and Fob4, on Chromosomes (Chrs) 2, 12, 15, and X, respectively. None of these QTLs map to regions of known single gene obesity mutations
(Lep
ob
, Lepr
db
, Cpe
fat
, A
y
, tub), though they map to regions of previously described obesity QTLs and candidate genes. The effects of Fob1, Fob3, Fob4 were additive, and that of Fob2 was dominant. Fob2 also showed a significant female-specific effect. Fob1, Fob2, Fob3, and Fob4 explained 4.9%, 19.5%, 14.4%, and 7.3% of the F2 phenotypic variance for fat%, respectively. This study identified four loci that contributed to the response to divergent
selection and control a significant proportion of the difference in obesity between the F and L lines.
Received: 28 May 1999 / Accepted: 31 August 1999 相似文献
20.
Wesley G. Beamer Kathryn L. Shultz Gary A. Churchill Wayne N. Frankel David J. Baylink Clifford J. Rosen Leah Rae Donahue 《Mammalian genome》1999,10(11):1043-1049
Genetic analyses for loci regulating bone mineral density have been conducted in a cohort of F2 mice derived from intercross matings of (C57BL/6J × CAST/EiJ)F1 parents. Femurs were isolated from 714 4-month-old females when peak adult bone density had been achieved. Bone mineral density
(BMD) data were obtained by peripheral quantitative computed tomography (pQCT), and genotype data were obtained by Polymerase
Chain Reaction (PCR) assays for polymorphic markers carried in genomic DNA of each mouse. Genome-wide scans for co-segregation
of genetic marker data with high or low BMD revealed loci on eight different chromosomes, four of which (Chrs 1, 5, 13, and
15) achieved conservative statistical criteria for suggestive, significant, or highly significant linkage with BMD. These
four quantitative trait loci (QTLs) were confirmed by a linear regression model developed to describe the main effects; none
of the loci exhibited significant interaction effects by ANOVA. The four QTLs have been named Bmd1 (Chr 1), Bmd2 (Chr 5), Bmd3 (Chr 13), and Bmd4 (Chr 15). Additive effects were observed for Bmd1, recessive for Bmd3, and dominant effects for Bmd2 and Bmd4. The current large size of the QTL regions (6→31 cM) renders premature any discussion of candidate genes at this time. Fine
mapping of these QTLs is in progress to refine their genetic positions and to evaluate human homologies.
Received: 5 May 1999 / Accepted: 22 June 1999 相似文献