Observations on the fine structure of two species of the peritrich ciliate genus Scyphidia and on their mode of attachment to their host.
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Adaptation, Biological↗
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Attachment and invasion of host cells by Toxoplasma gondii.
Recent studies indicate that Toxoplasma gondii attachment is mediated via a parasite ligand-host cell receptor interaction. Lloyd Kosper and Jose Mineo here survey factors involved in the attachment to and penetration and invasion of host cells by T. gondii.
Journal Article↗
The attachment sites of T5-host range temperate coliphages.
The attachment sites of 13 temperate coliphages were determined. Specialized transduction of proAB mutants was shown by eight isolates and of a his mutant by another two. Two isolates were concluded to integrate at atthtt and the integration site of one isolate remained undetermined.
Base Sequence↗
Miracidia of Schistosoma japonicum: approach and attachment to the snail host.
Schistosoma japonicum miracidia swim directed along a chemical gradient toward the snails Oncomelania hupensis and Biomphalaria glabrata, and they turn back when the concentration of attractive chemicals decreases. The host signal for this chemotactic response has a molecular weight of more than 30,000. When swimming miracidia encounter the surface of O. hupensis or agar containing O. hupensis snail-conditioned water (SCW) they perform the host-specific responses "contact with return," "repeated investigation," and "attachment," but they do not exhibit such behavior when encountering B. glabrata surface or agar containing B. glabrata SCW. Thus S. japonicum miracidia respond to different host signals when they approach snails than when they attach to snails.
Animals↗
Signal transduction in the protozoan host Hartmannella vermiformis upon attachment and invasion by Legionella micdadei.
The intracellular pathogens Legionella micdadei and Legionella pneumophila are the two most common Legionella species that cause Legionnaires' disease. Intracellular replication within pulmonary cells is the hallmark of Legionnaires' disease. In the environment, legionellae are parasites of protozoans, and intracellular bacterial replication within protozoans plays a major role in the transmission of Legionnaires' disease. In this study, we characterized the initial host signal transduction mechanisms involved during attachment to and invasion of the protozoan host Hartmannella vermiformis by L. micdadei. Bacterial attachment prior to invasion of H. vermiformis by L. micdadei is associated with tyrosine dephosphorylation of multiple host cell proteins, including a 170-kDa protein. We have previously shown that this 170-kDa protein is the galactose N-acetylgalactosamine (Gal/GalNAc)-inhibitable lectin receptor that mediates attachment to and invasion of H. vermiformis by L. pneumophila. Subsequent bacterial entry targets L. micdadei into a phagosome that is not surrounded by the rough endoplasmic reticulum (RER). In contrast, uptake of L. pneumophila mediated by attachment to the Gal/GalNAc lectin is followed by targeting of the bacterium into an RER-surrounded phagosome. These results indicate that despite similarities in the L. micdadei and L. pneumophila attachment-mediated signal transduction mechanisms in H. vermiformis, the two bacterial species are targeted into morphologically distinct phagosomes in their natural protozoan host.
Acetylgalactosamine↗
Striatal xenotransplantation of human retinal pigment epithelial cells attached to microcarriers in hemiparkinsonian rats ameliorates behavioral deficits without provoking a host immune response.
Attachment of donor cells to microcarriers has been reported to make them more tolerable for transplantation into the brain. Human retinal pigment epithelial (hRPE) cells have been previously reported to contain enzymes for the production of dopa. Therefore, we examined the host immune response and behavioral effects of xenotransplantation of hRPE cells attached to microcarriers (hRPE-M) into the striatum of unilateral dopamine-depleted rats. Thirty-four adult rats were lesioned with 6-OHDA injections into the medial forebrain bundle on the right side. After 5 weeks of testing for apomorphine-induced rotations (AIR), animals were randomized for right striatal surgery into the following four groups: hRPE-M (group 1), hRPE alone (group 2), microcarriers alone (group 3), or needle tract alone (group 4). Following surgery, animals were tested for AIR every 4 weeks for a period of 12-18 weeks and thereafter euthanized. There was a significant reduction in AIR scores posttransplantation in all groups of animals in the initial observation points at 4 weeks and 8 weeks. However, there was a gradual return to baseline scores in groups 2, 3, and 4 animals at 12 weeks and at 18 weeks only group 1 animals had statistically significant (p = 0.001, repeated measures ANOVA, means comparison, predetermined contrasts) reduction in AIR scores. Brain tissue from representative animals from each group was cut into 30-microm coronal sections, stained for cresyl violet, tyrosine hydroxylase (TH), and markers for host immune activation. Sections through the striatum from group 1 animals revealed microcarriers with attached cells resembling RPE cells. No evidence of transplanted hRPE cells could be detected in sections from group 2 animals while those from groups 3 and 4 animals showed microcarriers and a needle tract alone, respectively. There was no host TH-immunoreactive sprouting response in the striatum in any of the groups and the host immune response was minimal. These results suggest that intrastriatal hRPE-M xenotransplantation into rats is well tolerated without systemic immunosuppression and that such transplants may provide behavioral benefit for parkinsonism.
Animals↗
Signal transduction in the protozoan host Hartmannella vermiformis upon attachment to Legionella pneumophila.
Intracellular replication of the Legionnaires' disease bacterium, Legionella pneumophila, within protozoa plays a major role in bacterial ecology and pathogenesis. Invasion of the protozoan host Hartmannella vermiformis by L. pneumophila is mediated by attachment to the Gal/GalNAc lectin receptor, which is similar to the beta(2) integrin transmembrane receptors of mammalian cells. Bacterial invasion is associated with induction of a protein tyrosine phosphatase (PTPase) activity in H. vermiformis that results in tyrosine dephosphorylation of the lectin receptor and several cytoskeletal proteins. In this report, we show that entry of L. pneumophila into H. vermiformis is not required to induce tyrosine dephosphorylation of one of the cytoskeletal proteins, paxillin. Tyrosine dephosphorylation of paxillin is mediated at the level of bacterial attachment to the lectin receptor, and is blocked by inhibiting bacterial attachment to the lectin receptor. Attachment of L. pneumophila to the lectin receptor is not mediated by the type IV pilus, which is one of the bacterial ligands involved in attachment to protozoa. Interestingly, the lectin receptor in resting H. vermiformis is associated with several phosphorylated proteins that are dissociated upon bacterial attachment and invasion. We show that the L. pneumophila-induced PTPase activity in H. vermiformis and the associated tyrosine dephosphorylation of host proteins can be mimicked by the cytoskeletal disrupting agent, cytochalasin D. Taken together, our data indicate that attachment of L. pneumophila to the lectin receptor of H. vermiformis induces a PTPase activity, tyrosine dephosphorylation of the lectin and cytoskeletal proteins, dissociation of the lectin from its associated phosphorylated proteins, and most probably disassembly of the cytoskeleton. This novel L. pneumophila-protozoa interaction may be a bacterial strategy to invade protozoa and to be trafficked into a replicative 'niche', or to block differentiation of the protozoan host into a cyst in which L. pneumophila cannot replicate.
Actin Cytoskeleton↗
An attack of the plant parasite Cuscuta reflexa induces the expression of attAGP, an attachment protein of the host tomato.
Dodder or Cuscutaceae are holoparasitic plants subsisting on other dicotyledonous plants. The infection process is initiated by adherence of Cuscuta prehaustoria to the host surface, followed by penetration attempts by hyphae. In the case of a successful infection, these organs connect the parasite's vascular tissue to that of the host. Here we show that contact of Cuscuta reflexa prehaustoria to tomato induces the expression of a new arabinogalactan protein (AGP), attAGP, in the tomato precisely at the site of dodder attack. We show that attAGP is a plasma membrane-bound cell wall-localized protein. Using the RNAi technique and attAGP-targeted virus-induced gene silencing, we observed a correlation between attAGP expression level and force of attachment of the parasite to host tomatoes. If the expression level of attAGP was reduced, the C. reflexa attachment capability was significantly reduced, too. We conclude that C. reflexa infection induced a signal in the host leading to expression of tomato attAGP, which promotes the parasite's adherence.
Cuscuta↗
Isolation and characterization of a mutant Chinese hamster ovary cell line that is resistant to Chlamydia trachomatis infection at a novel step in the attachment process.
Host factors involved in Chlamydia trachomatis pathogenesis were investigated by random chemical mutagenesis of Chinese hamster ovary (CHO-K1) cells followed by selection for clones resistant to chlamydial infection. A clonal mutant cell line, D4.1-3, refractory to infection by the C. trachomatis L2 serovar was isolated. The D4.1-3 cell line appears to be lacking in a previously undescribed temperature-dependent and heparin-resistant binding step that occurs subsequent to engagement of cell surface heparan sulfate by L2 elementary bodies. This novel binding step differentiates the lymphogranuloma venereum (LGV) serovar from other serovars and may contribute the different pathologies associated with LGV and non-LGV strains.
Animals↗
Host susceptibility to the attaching and effacing bacterial pathogen Citrobacter rodentium.
Many studies have shown that genetic susceptibility plays a key role in determining whether bacterial pathogens successfully infect and cause disease in potential hosts. Surprisingly, whether host genetics influence the pathogenesis of attaching and effacing (A/E) bacteria such as enteropathogenic and enterohemorrhagic Escherichia coli has not been examined. To address this issue, we infected various mouse strains with Citrobacter rodentium, a member of the A/E pathogen family. Of the strains tested, the lipopolysaccharide (LPS) nonresponder C3H/HeJ mouse strain experienced more rapid and extensive bacterial colonization than did other strains. Moreover, the high bacterial load in these mice was associated with accelerated crypt hyperplasia, mucosal ulceration, and bleeding, together with very high mortality rates. Interestingly, the basis for the increased susceptibility was not due to LPS hyporesponsiveness, as the genetically related but LPS-responsive C3H/HeOuJ and C3H/HeN mouse strains were also susceptible to infection. Analysis of the intestinal pathology in these susceptible strains revealed significant crypt epithelial cell apoptosis (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end label staining) as well as bacterial translocation to the mesenteric lymph nodes. Further studies with infection of SCID (T- and B-lymphocyte-deficient) C3H/HeJ mice demonstrated that loss of lymphocytes had no effect on bacterial numbers but did reduce crypt cell apoptosis and delayed mortality. These studies thus identify the adaptive immune system, crypt cell apoptosis, and bacterial translocation but not LPS responsiveness as contributing to the tissue pathology and mortality seen during C. rodentium infection of highly susceptible mouse strains. Determining the basis for these strains' susceptibility to intestinal colonization by an A/E pathogen will be the focus of future studies.
Animals↗
Attaching and effacing of host cells by enteropathogenic Escherichia coli in the absence of detectable tyrosine kinase mediated signal transduction.
An unusual mutant of enteropathogenic E. coli (EPEC), deficient in its ability to invade host cells, was evaluated. The gene interrupted by the transposon in this mutant was located within a region of the EPEC chromosome devoted to secretion of proteins required for signal transduction. The mutant did not secrete detectable levels of the EspB protein, previously shown to be required for attaching and effacing, and did not induce detectable tyrosine phosphorylation of a 90 kDa host cell protein, previously associated with attaching and effacing and invasion. No quantitative or qualitative defect in the ability of the mutant to induce attaching and effacing effects was observed. Moreover, attaching and effacing by wild-type EPEC was unaffected by high doses of the tyrosine kinase inhibitor genistein. These results indicate that attaching and effacing activity can occur in the absence of detectable EspB secretion and tyrosine kinase mediated signal transduction.
Actins↗
[Interaction of extracellular matrix macromolecules between host and metastatic tumor cells].
Tumor cell attachment to host endothelium appears to be one of the specific steps occurring during the formation of distant metastasis, in which interactions of extracellular matrix molecules between tumor cells and endothelial cells are greatly involved. From mouse mammary carcinoma cells with no apparent lung-colonizing capacity (FM3A P-O), Honma et al. (Gann, 72, 898-905, 1981) selected two variant sublines, P-15A and P-10, for their ability to form lung tumor colonies with relatively high and low efficiencies, respectively. Comparison of their extracellular matrix products indicated that the rate of hyaluronic acid synthesis in both metastatic variants was about 60 times the rate in the parent cells and that there was no apparent association between metastatic ability and the rate of synthesis of other extracellular matrix molecules. Further analysis of the variant cells in vivo and in vitro indicated that the highly metastatic P-15A cells were surrounded by a hyaluronic acid-rich pericellular coat whereas the intermediately metastatic P-10 cells were not, suggesting the involvement of accumulation of hyaluronic acid in the pericellular regions in the potential for metastasis. The extracellular matrix molecules in host endothelium having a capacity to interact with hyaluronic acid were also studied. Bovine pulmonary arterial endothelial cells were metabolically labeled with 35S-methionine. Extraction and subsequent biochemical characterization of the labeled molecules suggested that PG-M-like chondroitin sulfate proteoglycan participated in the binding. These results provide a basis for further investigation of the potential role of interactions of extracellular matrix molecules between host and tumor cells during metastatic processes.
Animals↗
Virology of measles virus.
Measles virus is the prototypic member of the Morbillivirus genus of the family Paramyxoviridae. The viral genomic RNA is single-stranded, nonsegmented, and of negative polarity and encodes six major structural proteins. The two viral transmembrane glycoproteins, the hemagglutinin and fusion proteins, are both required for virus-host cell membrane fusion, while attachment to host cells is mediated by the hemagglutinin. The human CD46 molecule has been identified as a cellular receptor for measles virus. Antibodies raised against either viral glycoprotein neutralize measles virus in vitro and protect against infection. Although measles virus remains a single serotype (monotypic), nucleotide sequence analyses have identified distinct lineages among recent wild type isolates. These genetic changes were manifested by detectable antigenic variation between vaccine and wild type viruses and at some point may influence strategies for control, elimination, and eventual eradication of measles virus.
Animals↗
Fimbrial biogenesis genes of Pseudomonas aeruginosa: pilW and pilX increase the similarity of type 4 fimbriae to the GSP protein-secretion systems and pilY1 encodes a gonococcal PilC homologue.
Type 4 fimbriae of Pseudomonas aeruginosa are surface filaments involved in host colonization. They mediate both attachment to host epithelial cells and flagelia-independent twitching motility. Four additional genes, pilW, pilX, pilY1 and pilY2, are located on Spel fragment E in the 5 kb intergenic region between the previously characterized genes pilV and pilE, which encode prepilin-like proteins involved in type 4 fimbrial biogenesis. The phenotypes of a transposon insertion and other mutations constructed by allelic exchange show that these genes are involved in the assembly of type 4 fimbriae. The PilW and PilX proteins are membrane located, possess the hydrophobic N-terminus characteristic of prepilin-like proteins, and appear to belong to the GspJ and GspK group of proteins that are required for protein secretion in a wide range of Gram-negative bacteria. These findings increase the similarities between the fimbrial biogenesis and the Gsp-based protein-secretion supersystems. PilY1 is a large protein with C-terminal homology to the PilC2 protein of Neisseria gonorrhoeae, thought to be a fimbrial tip-associated adhesin, and which, like PilY1, is involved in fimbrial assembly. PilY1 appears to be located in both the membrane and the external fimbrial fractions. PilY2 is a small protein that appears to play a subtle role in fimbrial biogenesis and represents a new class of protein.
Alleles↗
Mode of host cell penetration by bacteriophage phi X174.
Bacteriophage phiX174 is an icosahedral phage which attaches to host cells without the aid of a complex tail assembly. When phiX174 was mixed with cell walls isolated from the bacterial host, the virions attached to the wall fragments and the phage deoxyribonucleic acid (DNA) was released. Attachment was prevented if the cell walls were treated with chloroform. Release of phage DNA, but not viral attachment, was prevented if the cell walls were incubated with lysozyme or if the virions were inactivated with formaldehyde. Treatment of the cell walls with lysozyme released structures which were of uniform size (6.5 by 25 nm). These structures attached phiX174 at the tip of one of its 12 vertices, but the viral DNA was not released. The virions attached to these structures were oriented with their fivefold axis of symmetry normal to the long axis of the structure. No virions were attached to these structures by more than one vertex. Freeze-etch preparations of phiX174 adsorbed to intact bacteria showed that the virions were submerged to one half their diameter into the host cell wall, and the fivefold axis of symmetry was normal to the cell surface. A second cell could not be attached to the outwardly facing vertex of the adsorbed phage and thus the phage could not cross-link two cells. When the virions were labeled with (3)H-leucine, purified, and adsorbed to Escherichia coli cells, about 15% of the radioactivity was recovered as low-molecular-weight material from spheroplasts formed by lysozyme-ethylenediaminetetraacetic acid. Other experiments revealed that about 7% of the total parental virus protein label could be recovered in newly formed progeny virus.
Binding Sites↗
LcrQ/YscM1, regulators of the Yersinia yop virulon, are injected into host cells by a chaperone-dependent mechanism.
Pathogenic Yersinia species employ type III machines to secrete YopBDR into the extracellular milieu. After attaching to host cells, yersiniae transform the type III machinery into an injection device and target YopEHMNOPT into eukaryotic cells. Yersinia pseudotuberculosis LcrQ is a transcriptional regulator that prevents the expression of yop genes. We report that LcrQ is injected into eukaryotic cells. YscM1, the transciptional regulator of Yersinia enterocolitica, is also injected into eukaryotic cells, whereas the related YscM2 protein remains associated with bacterial cells. Type III targeting of YscM1 requires binding to the SycH chaperone. Chaperone binding as well as depletion of YscM1 and YscM2 from the cytoplasm of Y. enterocolitica causes an increase in yop expression, whereas a block in regulator export reduces expression. We propose a model whereby the chaperone-mediated injection of LcrQ/YscM1 functions as a regulatory switch for bacteria that are attached to host cells, triggering the expression of Yops that travel the type III targeting pathway.
Bacterial Proteins↗
Interacton of Bdellovibrio bacteriovorus and host bacteria. I. Kinetic studies of attachment and invasion of Escherichia coli B by Bdellovibrio bacteriovorus.
Quantitative methods were developed for the study of the early stages in the interaction of Bdellovibrio bacteriovorus and host bacteria. Attachment measurements were based on the differential filtration of host and parasite. Invasion was measured by estimation of radioactively labeled Bdellovibrio cells remaining attached to the host cells after mechanical agitation. The kinetics of attachment and the final number of Bdellovibrio cells attached were dependent on the multiplicity of the parasite, the composition and pH of the medium, and the incubation temperature. Inhibitors of Bdellovibrio motility, including chelating agents, NaN(3), and low pH, all inhibited attachment, as did anaerobiosis. Ultraviolet-killed host cells retained their competence for attachment of Bdellovibrio cells, whereas heat-killed cells lost it. Invasion was selectively inhibited by inhibitors of protein synthesis, such as streptomycin, puromycin, and chloramphenicol. These antibiotics had no effect on attachment.
Azides↗
Leptopilina heterotoma and L. boulardi: strategies to avoid cellular defense responses of Drosophila melanogaster.
Eggs of three strains of the cynipid parasitoid Leptopilina heterotoma and a Tunisian strain (G317) of L. boulardi are not encapsulated by hemocytes of Drosophila melanogaster hosts, but the eggs of a Congolese strain (L104) of L. boulardi are encapsulated. To determine the reason for the difference in host response against the parasitoid eggs, lamellocytes (hemocytes that encapsulate foreign objects and form capsules around endogenous tissues in melanotic tumor mutants) were examined in host larvae parasitized by the five Leptopilina strains. Parasitization by the three L. heterotoma strains affected the morphology of host lamellocytes and suppressed endogenous melanotic capsule formation in melanotic tumor hosts. L104 did not alter the morphology of host lamellocytes nor block tumor formation in melanotic tumor mutant hosts. The morphology of some lamellocytes was affected by G317 parasitization but host lamellocytes were still capable of forming melanotic tumors and encapsulating dead supernumerary parasitoid larvae. Therefore, the eggs of strains affecting lamellocyte morphology are protected from encapsulation by the host's blood cells. L. heterotoma eggs float freely in the host hemocoel but L. boulardi eggs are attached to host tissue surfaces. Lamellocytes cannot infiltrate the attachment site so the capsule around the L104 egg remains incomplete. The wasp larva uses this gap in the capsule as an escape hatch for emergence.
Animals↗