Biomedical subjects

M Ströbel

Publications and source records attributed to M Ströbel.

17 recordsLinked to original sources

PubMed1995

Schistosoma mansoni and S. haematobium: miracidial host-finding behaviour is stimulated by macromolecules.

The miracidia of Schistosoma mansoni and S. haematobium approach their host snails by increasing their rate of change of direction (RCD) in increasing gradients of snail-conditioned water (SCW), and they perform a turnback response in decreasing gradients. After contact with the host "repeated investigation" is the typical host-specific response. Both species show no significant directed chemotactical orientation towards their snail hosts. All three host-finding responses (increased RCD, turnback response, and "repeated investigation") seem to be stimulated in both species by a similar component of SCW, a macromolecular glycoconjugate with a molecular weight > 30,000. The saccharide chains seem to be O-glycosidically linked via serine and N-acetylgalactosamine. The glycoconjugate is sensitive to lysozyme which may suggest that muramic acid as a gastropod-specific component is involved in the recognition process. Small molecular components of SCW, as well as magnesium chloride offered as pure chemical, may cause a moderate increase in the RCD. Therefore a minor contribution of these components to the host-finding response of schistosome miracidia cannot be excluded. That schistosome miracidia respond to complex macromolecules as host cues may indicate an adaptation to avoid interference of the host-finding with ubiquitous small molecular mud components and it might enable the miracidia to achieve a high degree of host-specificity in their host-finding.

Animals↗

PubMed1994

Tolerance to lipopolysaccharide involves mobilization of nuclear factor kappa B with predominance of p50 homodimers.

Stimulation of the human monocytic cell line Mono Mac 6 with lipopolysaccharide (LPS) leads to rapid and transient expression of cytokines like tumor necrosis factor (TNF). When such cells are precultured for 2 days with a low dose of LPS (20 ng/ml) followed by stimulation with a high dose of LPS (1 microgram/ml), expression of the TNF gene is minimal, i.e. the cells are tolerant. In nuclear run-on analysis, such tolerant cells show only a low degree of transcription, indicating that tolerance operates at or upstream of the transcription level. The CD14 LPS receptor is, however, up-regulated (not down-regulated) in tolerant cells, and LPS can, in fact, still lead to activation of tolerant cells as evidenced by mobilization of the transcription factor nuclear factor kappa B (NF-kappa B). Resolution of the NF-kappa B complex in gel shift analysis shows that the binding protein, mobilized in naive Mono Mac 6 cells, consists mainly of p50-p65 heterodimers, while in tolerant cells, the p50 homodimer is predominant. This increase in p50 homodimers coincides with an increase in p105 mRNA, suggestive of a transcriptional up-regulation of p50. Reporter gene analysis reveals that the NF-kappa B complex mobilized in tolerant cells is functionally inactive in that NF-kappa B-dependent luciferase constructs containing the human immunodeficiency virus long terminal repeat or the TNF 5'-region show only minimal transactivation after LPS stimulation. Similar to Mono Mac 6 cells, primary blood monocytes, when precultured with a low dose of LPS, also become tolerant and produce little TNF after LPS stimulation. The tolerant blood monocytes also up-regulate CD14, and they mobilize NF-kappa B with a predominance of p50 homodimers. Taken together, these results demonstrate that tolerance to LPS is determined by post-receptor mechanisms that involve an altered composition of the NF-kappa B complex.

Antigens, CD↗

PubMed1994

Expression of properdin in human monocytes.

Properdin is the only known positive regulator of the alternative pathway of complement activation. Northern blot analysis of cell lines derived from fibroblasts, B-cells, hepatoma cells, and cells of the monocyte-macrophage lineage revealed properdin expression only in the myelomonocytic cell line HL-60, in the monoblastic cell line U-937 and in the monocytic line Mono Mac 6. Culture of Mono Mac 6 cells for 24 h with phorbol 12-myristate 13-acetate, bacterial lipopolysaccharide and the cytokines interleukin-1 beta and tumour necrosis factor-alpha enhanced mRNA abundance, with the strongest effect (tenfold) being observed with the lipopolysaccharide. In contrast, recombinant interferon-gamma consistently halved properdin mRNA abundance. The same pattern was found for the secretion of properdin as detected by ELISA of Mono Mac 6 supernatants. The suppressive effect of interferon-gamma on properdin mRNA abundance was also demonstrated for primary blood monocytes. The data suggest that the expression and secretion of this complement regulatory protein by monocytes is differentially regulated by cytokines and link the immune response with alternative pathway activation.

Adult↗

PubMed1994

CD14 is expressed and functional in human B cells.

The human B cell line RPMI 8226 exhibits variable staining with the CD14 antibody My4. We have isolated three stable clones from this line with clones 1 and 2 being My4 positive and clone 3 My4 negative. Similar to previous results in monocytes, immunoprecipitation with the My4 antibody revealed a 54-kDa cell surface molecule, analysis of supernatants showed soluble CD14, and Northern blotting demonstrated a 1.4-kb transcript in clones 1 and 2, but not in clone 3, which suggests that the My4 antibody detects CD14 in clones 1 and 2. This CD14 molecule was functional in that lipopolysaccharide stimulation induced interleukin (IL)-6 and IL-10 in clones 1 and 2 but not in clone 3. Furthermore, the My4 antibody was capable of blocking these responses at the transcript and protein levels. Finally, peripheral blood B cells were highly purified by cell sorting (> 98% CD19 positive). These cells produced IL-6 in response to lipopolysaccharide, and this response was blocked by anti-CD14 antiserum. Thus, our findings demonstrated that human B cells can express functionally active CD14.

Antigens, CD↗

PubMed1994

Distinct patterns of differentiation induced in the monocytic cell line Mono Mac 6.

The human Mono Mac 6 cell line exhibits many characteristics of mature blood monocytes including expression of the CD14 molecule and production of cytokines, such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor. To determine whether these cells can be further differentiated, we treated the cells for up to 3 days with either prostaglandin E2 (PGE2; 10(-5) or 10(-6) M), lipopolysaccharide (LPS; 10-20 ng/ml), or tetradecanoylphorbol-13-acetate (TPA; 10-50 ng/ml). All three reagents reduced proliferation and expression of the early myelomonocytic antigen CD33, and all increased phagocytosis of staphylococci and constitutive expression of mRNA for the macrophage colony-stimulating factor (M-CSF) receptor. By contrast, with respect to CD23 (Fc epsilon RII) expression, CD14 expression, and production of O2-, the three reagents induced distinct responses. Expression of CD23 (Fc epsilon RII) on Mono Mac 6 cells (36%) was not increased by LPS and TPA but was increased by PGE2 treatment to 48%, with a 50% increase of fluorescence intensity. The CD14 antibody My4 stained more than 75% of untreated Mono Mac 6 cells with a specific mean fluorescence intensity of 87.5 channels. This staining was increased more than twofold by both PGE2 and LPS. Staining with the CD14 antibody UCHM1 (6%) was increased to 43% by PGE2 and to 43% by LPS. This increase in CD14 cell surface expression was accompanied by a rise in soluble CD14 and enhancement of CD14 mRNA. By contrast, TPA treatment resulted in a twofold decrease of CD14 cell surface staining with no significant change in sCD14, while CD14 mRNA was transiently down-regulated. Secretion of O2- (stimulated by TPA) was already detectable in untreated Mono Mac 6 cells (6.1 mmol/10(6) cells/30 min), and this response was enhanced 10-fold by pretreatment with LPS but not with PGE2 or TPA. The kinetics of M-CSF receptor mRNA, CD14 expression, and O2- production revealed that these monocytic features started to increase at 6-24 h and were maximal at 2 days. These data suggest that the three reagents induce maturation of the Mono Mac 6 cells to different levels or into different branches of the monocyte system with the notable differences that PGE2 enhances CD23 expression, LPS enhances O2- secretion, and TPA down-regulates CD14.

Antigens, CD↗

PubMed1994

Increased levels of soluble serum interleukin-2 receptor in extrinsic allergic alveolitis correlate with interleukin-2 receptor expression on alveolar macrophages.

In a group of 20 patients with extrinsic allergic alveolitis (10 with farmer's lung, 9 with bird-breeder's lung, and 1 with humidifier's lung), we observed increased levels of soluble serum interleukin-2 receptor (ssIL-2R) with an average of 75.2 pmol (control group average, 40.6 pmol). Analysis of bronchoalveolar lavage cells by immunocytochemistry with a CD25 antibody revealed only a slight increase to 4.2% IL-2R+ cells among alveolar lymphocytes but a pronounced rise to 21.2% IL-2R+ cells among alveolar macrophages. Furthermore, cytometry revealed a fourfold higher IL-2R expression on a per cell basis for alveolar macrophages as compared with alveolar lymphocytes. A clear-cut positive correlation (p = 0.006) was found for ssIL-2R and IL-2R+ alveolar macrophages, but only a borderline correlation was found for ssIL-2R and IL-2R+ alveolar lymphocytes (p = 0.04). The finding of a concomitant decrease of IL-2R+ alveolar macrophages and of ssIL-2R on allergen avoidance further supports the notion that alveolar macrophages may be the main source of the increased ssIL-2R in patients with extrinsic allergic alveolitis.

Adult↗

PubMed1994

Antioxidants inhibit monocyte adhesion by suppressing nuclear factor-kappa B mobilization and induction of vascular cell adhesion molecule-1 in endothelial cells stimulated to generate radicals.

Cell adhesion to endothelial cells stimulated by tumor necrosis factor-alpha (TNF) is due to induction of surface receptors, such as vascular cell adhesion molecule-1 (VCAM-1). The antioxidant pyrrolidine dithiocarbamate (PDTC) specifically inhibits activation of nuclear factor-kappa B (NF-kappa B). Since kappa B motifs are present in VCAM-1 and intercellular adhesion molecule-1 (ICAM-1) promoters, we used PDTC to study the regulatory mechanisms of VCAM-1 and ICAM-1 induction and subsequent monocyte adhesion in TNF-treated human umbilical vein endothelial cells (HUVECs). PDTC or N-acetylcysteine dose dependently reduced TNF-induced VCAM-1 but not ICAM-1 surface protein (also in human umbilical arterial endothelial cells) and mRNA expression (by 70% at 100 mumol/L PDTC) in HUVECs as assessed by flow cytometry and polymerase chain reaction. Gel-shift analysis in HUVECs demonstrated that PDTC prevented NF-kappa B mobilization by TNF, suggesting that only VCAM-1 induction was controlled by NF-kappa B. Since HUVECs released superoxide anions in response to TNF, and H2O2 induces VCAM-1, PDTC may act as a radical scavenger. Although ICAM-1 induction was unaffected, inhibitors of NADPH oxidase (apocynin) or cytochrome P-450 (SKF525a) suppressed VCAM-1 induction by TNF, revealing that several radical-generating systems are involved in its regulation. PDTC, apocynin, or SKF525a decreased adhesion of monocytic U937 cells to TNF-treated HUVECs (by 75% at 100 mumol/L PDTC). Inhibition by anti-VCAM-1 monoclonal antibody 1G11 indicated that U937 adhesion was VCAM-1 dependent and suppression by antioxidants was due to reduced VCAM-1 induction.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗

PubMed1993

Pyrrolidine dithiocarbamate inhibits NF-kappa B mobilization and TNF production in human monocytes.

The human TNF promoter contains four potential nuclear factor-kappa B (NF-kappa B)-binding sites, with the strongest binding seen for the -605 motif. Nuclear extracts from unstimulated cells of the human monocytic cell line, Mono Mac 6, contain one specific binding protein (complex II), consistent with a constitutive p50 homodimer. Stimulation of Mono Mac 6 cells with LPS will increase complex II and will strongly induce a second specific complex (complex I), which represents the p50/65 heterodimer. Treatment of Mono Mac 6 cells with pyrrolidine-dithiocarbamate (PDTC) at 300 microM will block the LPS-induced complex I almost completely and will reduce complex II to the constitutive level. Binding activity of other nuclear factors that recognize the SP-1 and c/EBP motifs of the human TNF promoter is not affected by such treatment. Northern blot analysis demonstrates that PDTC treatment will strongly reduce LPS-induced TNF transcripts. Secreted TNF protein as detected in the Wehi 164S/ActD bioassay and in a sandwich immunoassay was similarly reduced by PDTC. Kinetic analyses show that after LPS stimulation, NF-kappa B will peak at 1 h, TNF transcript prevalence at 2 h, and TNF protein at 4 h. PDTC did not shift this response to LPS to a later time, but suppressed NF-kappa B mobilization, TNF transcripts, and TNF protein over the entire 8-h observation period. Analysis of freshly isolated, LPS-stimulated blood monocytes showed a similar blockade of NF-kappa B. Furthermore, in these primary cells, induction of TNF transcripts, as determined by Northern blot analysis and by quantitative polymerase chain reaction, was prevented by PDTC as was TNF protein production. These data show that dithiocarbamates can profoundly affect cytokine expression and suggest that NF-kappa B is involved in LPS-induced TNF gene expression in human monocytes.

Binding Sites↗

PubMed1993

The novel subset of CD14+/CD16+ blood monocytes is expanded in sepsis patients.

Staining with CD14 and CD16 monoclonal antibodies will identify two monocyte subpopulations in human blood: a major population of regular monocytes, which strongly expresses the CD14 antigen (CD14++), and a minor population with weak expression of CD14 and expression of the CD16 antigen (CD14+/CD16+ cells). As shown herein, the latter cells account for 45 +/- 22 cells/microL and 9% +/- 5% of the monocytes in healthy control donors (n = 35). In septicemia patients, the CD14+/CD16+ cells can become a major population, with more than 50% of all monocytes in 3 of 18 patients and with more than 500 cells in 4 of 18 cases. There was no correlation of CD14+/CD16+ cells to any clinical parameter except for CD14+/CD16+ percentage and body temperature (P = .013). The CD14++ regular monocytes showed a substantial decrease in CD14 antigen density in 9 of 11 patients. Three-color immunofluorescence shows that the CD14+/CD16+ monocytes in septicemia patients when compared with the CD14++ monocytes exhibit a higher level of class II antigen and a lower level of CD11b and CD33 antigens, consistent with a more mature nature of the CD14+/CD16+ cells. Levels of interleukin-6 (IL-6) were increased in septicemia patients; 3 of 5 patients with high numbers of CD14+/CD16+ cells (> 200/microL) had high levels of IL-6 (> 250/U/mL). These data suggest that septicemia may lead to substantial changes in blood monocyte composition and this may be related to elevated levels of cytokines such as IL-6.

Adult↗

PubMed1993

The novel subset of CD14+/CD16+ blood monocytes exhibits features of tissue macrophages.

The CD14+/CD16+ cells account for about 10% of all blood monocytes. They are characterized by a low level expression of the CD14 molecule and a high level expression of the CD16 (Fc gamma R III) molecule. Polymerase chain reaction analysis of mRNA prevalence in CD14+/CD16+ cells (compared to the regular CD14++ blood monocytes) demonstrates low levels of CD14 transcripts and high levels of CD16 transcripts, suggestive of a transcriptional control for both of these proteins. Analysis of additional cell surface molecules in three-color immunofluorescence reveals that CD14+/CD16+ cells express the Fc gamma R II in all, and Fc gamma R I and ICAM-1 in some donors. Furthermore, class II antigens are expressed at fourfold higher levels, while both, CD11b and CD33 cell surface proteins, are decreased by a factor of two. Transcript levels were reduced in CD14+/CD16+ cells for all three cell surface molecules. Since these phenotypic markers of the CD14+/CD16+ blood monocytes are reminiscent of tissue macrophages, we performed a comparative analysis with alveolar macrophages (AM). These cells are similar to the CD14+/CD16+ monocytes in that they show low levels of CD14 and strong expression of CD16. Furthermore, similar to the CD14+/CD16+ cells, the AM also exhibit higher levels of class II and lower levels of CD11b and CD33 when compared to the regular CD14++ blood monocytes. In vitro induction of maturation of blood monocytes by 5 day culture of peripheral blood mononuclear cells in 10% human serum will result in decreased CD14 and increased CD16 cell surface expression on the monocyte derived macrophages. At the same time, these cells acquire increased levels of class II and decreased levels of CD11b and CD33. Taken together, these data show that CD14+/CD16+ monocytes, while still in circulation, have acquired features in common with mature tissue macrophages.

Antigens, CD↗

PubMed1993

Concomitant modulation of serum-soluble interleukin-2 receptor and alveolar macrophage interleukin-2 receptor in sarcoidosis.

Interleukin-2 receptor (IL-2R) expression on bronchoalveolar lavage (BAL) cells was studied in patients with sarcoidosis using immune cytochemistry and cytometric analysis. A low percentage of alveolar lymphocytes (AL) was found positive for IL-2R, with 7% in patients with impaired lung function and 6% in patients with normal lung function (0.4% in control subjects). Expression of IL-2R on alveolar macrophages (AM) was considerably higher, with 25% in patients with lung function impairment compared with 14% in patients without lung function impairment (1.5% in control subjects). Serum-soluble IL-2R (ssIL-2R) was significantly elevated only in patients with impaired lung function (140.0 pM), but not in patients with normal lung function (52.2 pM; control subjects, 40.0 pM). These elevated levels of ssIL-2R positively correlated with the percentage of IL-2R positive AM (p < 0.001). Immunosuppressive treatment in three patients resulted in a decrease of IL-2R+ AM and in a decrease of ssIL-2R, whereas IL-2R+ AL were unaffected. The positive correlation and the concomitant decrease of IL-2R+ AM and ssIL-2R are consistent with the idea that in sarcoidosis with clinically apparent lung involvement, elevated levels of ssIL-2R may be derived from AM and may thus be a useful indicator of the degree of activation of these cells.

Adult↗

PubMed1993

Increased expression of the monocyte differentiation antigen CD14 in extrinsic allergic alveolitis.

Expression of the CD14 antigen was studied on alveolar macrophages in extrinsic allergic alveolitis (EAA), using immunocytochemistry and cytometry. Compared to control donors, EAA patients had higher percentages of My4 positive cells (40 versus 22%), and the antigen density was fourfold higher (410 versus 92 channels). Levels of soluble CD14 (sCD14) in serum were found to be increased in EAA patients with an average of 4.6 +/- 1.5 micrograms.ml-1 compared to 3.2 +/- 0.7 micrograms.ml-1 in controls. Follow-up of patients with antigen avoidance revealed a concomitant decrease of CD14 staining of alveolar macrophages (AMs) and of sCD14 in serum, whilst allergen exposure induces both parameters. These data are consistent with the concept that antigen contact upregulates CD14 expression on AMs in EAA, followed by shedding and increase of sCD14 in serum.

Adult↗

PubMed1992

Constitutive monocyte-restricted activity of NF-M, a nuclear factor that binds to a C/EBP motif.

In a search for monocyte-specific nuclear factors, we analyzed in human cells the promoter of the chicken myelomonocytic growth factor, a gene that, in the chicken, is expressed in myeloid and myelomonocytic cells. Reporter gene constructs were active in monocytic Mono Mac 6 cells and in monoblastic THP-1 cells but not in the hematopoietic stem cell line K562. When a region with homology to the sequence recognized by CAAT enhancer-binding proteins (C/EBP) was inactivated by site-directed mutagenesis, the reporter activity was reduced by a factor of 10. Multimers of this region, termed F, in front of a heterologous promoter were active in Mono Mac 6 and THP-1 cells but not in K562 cells, WIL2 B cells, BT20 mammary carcinoma cells, MelJuso melanoma cells, or SK-Hep-1 hepatoma cells. Gel shift analysis with the F oligonucleotide identified DNA-binding activity in monocytic Mono Mac 6, monoblastic THP-1, and myelomonocytic HL60 cells. No binding was detected in myelomonocytic RC2A cells, in myeloid KG-1 cells, or in the hematopoietic stem cell line K562. Furthermore, a panel of solid tumor cell lines, representing various tissues, were also negative. Stimulation by PMA could not induce this binding factor in any of the negative cell lines. Analysis of primary cells (granulocytes, T cells, monocytes, and alveolar macrophages) revealed binding activity only in monocytes and macrophages. This DNA-binding factor, termed NF-M, was found to consist of two molecules, of 50 and 72 kDa, as determined by affinity cross-linking. Binding of NF-M was competed by the region F oligonucleotide and by the C/EBP motif from the albumin enhancer but not by an AP-2 motif. These data suggest that NF-M is a member of the C/EBP family of nuclear factors. The monocyte-restricted activity of NF-M suggests that this nuclear factor may be involved in regulation of monocyte-specific genes.

Base Sequence↗

PubMed1992

Gangliosides suppress tumor necrosis factor production in human monocytes.

Both normal and malignant cells contain gangliosides as important cell membrane constituents that, after being shed, may influence cells of the immune system. We have studied the impact of gangliosides on the expression of TNF in blood monocytes and in the monocytic cell line Mono Mac 6. Although under standard culture conditions, bovine brain gangliosides (100 micrograms/ml) suppressed LPS-stimulated TNF production 5-fold in PBMC and 10-fold in Mono Mac 6 cells, suppression was more efficient under serum-free conditions. Looking at highly purified gangliosides, GD3, GD1a, GM3, GM2, and GM1 were all effective in reducing TNF production in PBMC, and in Mono Mac 6 by factor 10 to 50. The suppressive activity was lost in molecules, lacking the sugar moiety or the lipid moiety. Gangliosides appear to act at an early step of activation in that TNF transcripts were reduced and the mobilization of the nuclear factor kappa B was blocked. Furthermore, in time kinetics, gangliosides were effective for up to 30 min after addition of LPS, but not thereafter. However, the expression of the CD14 Ag, a receptor molecule for LPS-LPS binding protein complexes, was unaffected by gangliosides. Finally, when using Staphylococcus aureus or platelet activating factor as a stimulus, gangliosides were able to suppress TNF production in Mono Mac 6 cells by factor 5 to 10, as well. On the other hand, phorbol ester-induced production of O2- was similar in cells treated with and without gangliosides. Taken together, our data demonstrate that TNF gene expression in monocytes induced by different types of stimuli can be blocked by gangliosides at an early step of signal transduction.

Antigens, CD↗

PubMed1992

Differential expression of cytokines in human blood monocyte subpopulations.

Cytokine expression was analyzed in CD14++ regular monocytes and in the novel subset of CD14+/CD16+ small monocytes. Biologic activity for tumor necrosis factor (TNF), interleukin-1 (IL-1), and IL-6 in the supernatant of elutriator-enriched, cell sorter-purified small monocytes was about 10-fold lower compared with regular monocytes when stimulated with lipopolysaccharide (LPS) for 12 hours. In CD14++ regular monocytes levels were 1,157 U x 10(-3)/mL, 158 U/mL, and 1,337 U/mL for TNF, IL-1, and IL-6, respectively. By contrast, CD14+/CD16+ small monocytes exhibited 137 U x 10(-3)/mL, 14 U/mL, and 60 U/mL for TNF, IL-1, and IL-6, respectively. Additional treatment with interferon-gamma enhanced production of TNF in both subsets, but CD14+/CD16+ small monocytes still exhibited lower levels. Stimulation of the monocyte subsets by platelet-activating factor gave the same pattern of results. Hybridization with 32P-labeled oligonucleotides specific for the respective cytokine messenger RNAs (mRNAs) showed a 10-fold lower prevalence of transcripts for TNF, IL-1, and IL-6, as well. By contrast, the constitutive expression of Glyceraldehyde-3-phosphate-dehydrogenase mRNA was 1.7-fold higher in the CD14+/CD16+ small monocytes. These data indicate that the novel subset of small monocytes is selectively suppressed in the expression of the cytokines TNF, IL-1, and IL-6, suggesting that these cells may comprise a deactivated type of cell. The expression of class II transcripts in the small monocytes is, however, similar to the regular monocytes, and the cell surface expression of class II protein about threefold increased. Thus, the novel subset of small monocytes appears to be a functionally distinct type of cell.

Antigens, CD↗

PubMed1991

Small (CD14+/CD16+) monocytes and regular monocytes in human blood.

Compared to the obvious phenotypic and functional heterogeneity of tissue macrophages, little information is available on subsets of blood monocytes. We have employed two-color immunofluorescence and flow cytometry for the definition of regular and small monocytes, the latter characterized by the low-density expression of CD14 and the strong expression of the CD16 (Fcy-RIII) antigen. These cells comprise 15% of the blood monocytes and they appear to be similar in phenotype to the alveolar macrophage. The CD14+/CD16+ small monocytes can perform phagocytosis and they produce reactive oxygen, while their capacity for cytokine production is strongly reduced when compared to regular monocytes. At this point it is still unclear as to whether the CD14+/CD16+ small monocytes comprise a specific level of activation or differentiation or a distinct sublineage of human blood monocytes.

Antigens, CD↗

PubMed1991

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↗