Biomedical subjects

B Rossi

Publications and source records attributed to B Rossi.

At least 73 records · Page 4Linked to original sources

PubMed1999

Cytosine deaminase/5-fluorocytosine-based vaccination against liver tumors: evidence of distant bystander effect.

BACKGROUND: The cytosine deaminase gene of Escherichia coli converts the nontoxic compound 5-fluorocytosine into 5-fluorouracil (5-FU), thereby acting as a suicide gene when introduced into cancer cells, killing the cells when they are exposed to 5-fluorocytosine. We analyzed the efficacy of using cytosine deaminase-bearing cancer cells as an autologous tumor vaccine in a rat model that mimics liver metastasis from colon carcinoma. METHODS: We introduced a plasmid vector containing the E. coli cytosine deaminase gene into a BDIX rat colon carcinoma cell line. Intrahepatic injection of the modified cells in syngeneic animals generates a single experimental liver "suicide tumor." We then analyzed the effect of 5-fluorocytosine treatment in terms of regression of cytosine deaminase-expressing cells in vivo as well as protection against wild-type cancer cells. RESULTS: Treatment with 5-fluorocytosine induced regression of cytosine deaminase-expressing (CD+) tumors, with seven of 11 treated animals being tumor free at the end of 30 days and a statistically significant difference in tumor volumes between treated and control animals (two-sided P<.0001). Intrahepatic injection of CD+ cells followed by 5-fluorocytosine treatment rendered the treated animals resistant to challenge with wild-type tumor cells, with no (zero of seven) treated animals developing wild-type tumors in contrast to all (four of four) control animals. Moreover, in animals with established wild-type liver tumors, injection of CD+ tumor cells followed by 5-fluorocytosine treatment produced a statistically significant increase in survival time (two-sided P<.0001). In vivo immunodepletion and immunohistologic analysis of experimental tumors indicate that natural killer cells are the major immune component involved in this antitumor effect. CONCLUSIONS AND IMPLICATIONS: Taken together, these results suggest the potential use of suicide gene-modified tumor cells as therapeutic vaccines against liver metastasis from colon carcinoma.

Animals↗

PubMed1999

Src-regulated extracellular signal-related kinase and Syk-regulated c-Jun N-terminal kinase pathways act in conjunction to induce IL-1 synthesis in response to microtubule disruption in HL60 cells.

A microtubule reorganization is often observed during cellular contacts that are associated to IL-1 production. Here, we show that in HL60 cells, vincristine, a microtubule-disrupting agent that induces a strong production of IL-1, triggers the activation of both extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK-1). While ERK activation is rapid and transient, peaking at 10 min, the JNK1 activation is delayed and more sustained reaching a maximum at 2 h. ERK activation was blocked by CP 118556, indicating it is regulated by a Src-like kinase, while JNK1 was inhibited by piceatannol, revealing an upstream regulation by Syk. Each kind of the nonreceptor tyrosine kinase blockers efficiently inhibits the vincristine-induced IL-1 production and diminishes the level of IL-1 transcripts, indicating that the ERK and JNK pathways act coordinately to elicit the transcription of the IL-1 gene. Furthermore, we found that pertussis toxin, a blocker of Go/Gi proteins, abrogated the vincristine-induced activation of both Src and Syk. Our data support a model where the status of microtubule polymerization influences the activity of Go or Gi proteins that control, in turn, two independent Src/ERK and Syk/JNK1 cascades that are both necessary to sustain IL-1 synthesis.

Enzyme Activation↗

PubMed1999

Evidence for a p23 caspase-cleaved form of p27[KIP1] involved in G1 growth arrest.

p27[KIP1] (p27) is a cyclin dependent kinase inhibitor, involved in the negative regulation of G1 progression in response to a number of anti-proliferative signals. In this study we show, in growing mouse hybridoma (7TD1) and human myeloma (U266) cell lines, that p27 is highly expressed but slightly upregulated when cells are arrested, regardless to the phases of the cell cycle. In contrast, the specific blockade of these cells in early G1 phase reveals the induction of a protein of 23 kDa (p23) specifically recognized by polyclonal anti-p27 antibodies raised against the NH2 terminal part of p27 but not by anti-p21[CIP1] antibodies. Experiments using caspase inhibitors strongly suggest that p23 results from the proteolysis of p27 by a 'caspase-3-like' protease. This cleavage leads to the cytosolic sequestration of p23 but does not alter its binding properties to CDK2 and CDK4 kinases. Indeed, p23 associated in vivo with high molecular weight complexes and coprecipitated with CDK2 and CDK4. We demonstrate by transfection experiments in SaOS-2 cells that p23 induces a G1 phase growth arrest by inhibition of cyclin/CDK2 activity. In summary we describe here a caspase-cleaved form of p27, induced in absence of detectable apoptosis and likely involved in cell cycle regulation.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1999

HIV-1 nef expression inhibits the activity of a Ca2+-dependent K+ channel involved in the control of the resting potential in CEM lymphocytes.

The HIV-1 Nef protein plays an important role in the development of the pathology associated with AIDS. Despite various studies that have dealt with different aspects of Nef function, the complete mechanism by which it alters the physiology of infected cells remains to be established. Nef can associate with cell membranes, therefore supporting the hypothesis that it might interact with membrane proteins as ionic channels and modify their electrical properties. By using the patch-clamp technique, we found that Nef expression determines a 25-mV depolarization of lymphoblastoid CEM cells. Both charybdotoxin (CTX) and the membrane-permeable Ca2+ chelator BAPTA/AM depolarized the membrane of native cells without modifying that of Nef-transfected cells. These data suggested that the resting potential in native CEM cells is settled by a CTX- and Ca2+-sensitive K+ channel (KCa,CTX), whose activity is absent in Nef-expressing cells. This was confirmed by direct measurements of whole-cell KCa,CTX currents. Single-channel recordings on excised patches showed that a KCa,CTX channel of 35 pS with a half-activation near 400 nM Ca2+ was present in both native and Nef-transfected cells. The measurements of free intracellular Ca2+ were not different in the two cell lines, but Nef-transfected cells displayed an increased Ca2+ content in ionomycin-sensitive stores. Taken together, these results indicate that Nef expression alters the resting membrane potential of the T lymphocyte cell line by inhibiting a KCa,CTX channel, possibly by intervening in the regulation of intracellular Ca2+ homeostasis.

Alkaline Phosphatase↗

PubMed1999

Measurement of the anorectal angle by defecography for the diagnosis of fecal incontinence.

We assessed the reliability of anorectal angle (ARA) measurement as an index of fecal incontinence. The "posterior" ARA was measured at rest, squeezing, and straining in 69 continent and 82 incontinent subjects all complaining of various evacuation dysfunctions. The two groups were homogeneous with regard to sex distribution (48.6% vs. 51.4% men and 44.7% vs. 55.3% women, n.s.) and age (56.5 +/- 10.2 vs. 59.3 +/- 9.7 years, n.s.). The incidence of rectal prolapse was the same in the two groups (40 each). The intraobserver agreement index from two independent measurements (Pearson's correlation coefficient), age, and gender interaction [T2 Hotelling test in multivariate analysis of variance (ANOVA)] and the most discriminating category of ARA measurement (Fisher's F test in ANOVA) were calculated. In addition, the relationship between ARA and severity of incontinence was assessed by the eta coefficient. Pearson's correlation coefficient was between 0.78 and 0.98 (P < 0.01). The mean ARA differed significantly between the continent and incontinent subjects (104.5 +/- 10.3 degrees vs. 116.2 +/- 23.6 degrees at rest, 84.5 +/- 14.2 degrees vs. 95.1 +/- 20.1 degrees on squeezing, and 133.7 +/- 21.7 degrees vs. 141.7 +/- 25.9 degrees on straining; T2 0.066, P < 0.05 in multivariate ANOVA). No interaction was noted between groups and gender (T2 = 0.023; F = 1.11, n.s.). Resting ARA was shown by ANOVA to be the most discriminating index (F = 9.4 P < 0.01) between the two groups. Overall, ARA measurement was correlated with the severity of fecal incontinence (eta coefficient: 0.894 at rest; 0.811 on squeezing; 0.695 on straining); its accuracy was 79%, the false-positive rate was 15.3% and the false-negative rate 26.5%. Irrespective of the underlying abnormality, namely rectal prolapse, ARA measurement by defecography can: (a) be reinterpreted reliably by the same observer and (b) differentiate continent from incontinent subjects.

Adolescent↗

PubMed1999

A hybrid approach to EMG pattern analysis for classification of arm movements using statistical and fuzzy techniques.

In this paper, a hybrid approach is presented for discriminating a few upper limb movements by processing the electromyographic (EMG) signals from selected shoulder muscles. Statistical techniques, such as the Generalized Likelihood Ratio test, the Principal Component Analysis, autoregressive parametric modeling techniques and cepstral analysis techniques, combined with a fuzzy logic based classifier (the Abe-Lan network) are used to construct low-dimensional feature spaces with high classification rates. The experimental results show the ability of the algorithm to correctly classify all the EMG patterns related to the selected planar arm pointing movements. Moreover, the structure presented offers promise for real-time applications because of the low computation costs of the overall algorithm.

Adult↗

PubMed1999

Lack of internucleosomal DNA fragmentation is related to Cl(-) efflux impairment in hematopoietic cell apoptosis.

The heterodimeric DNA fragmentation factor (DFF) is responsible for DNA degradation into nucleosomal units during apoptosis. This process needs the caspase-dependent release of ICAD/DFF-45, the inhibitory subunit of DFF. Here we report that triggering apoptosis via a hyperosmotic shock in hematopoietic cells causes the appearance of mitochondrial and cytosolic alterations, activation of caspases, chromatin condensation, nuclear disruption, and DNA fragmentation. However, oligonucleosomal but not high molecular weight (50-150 kb) DNA cleavage is abolished if Cl(-) efflux is prevented by using NaCl to raise extracellular osmolarity or by Cl(-) channel blockers, even when apoptosis is initiated by other agents (staurosporine, anti-Fas antibody). In these conditions, all the apoptosis hallmarks investigated remain detectable, including the cleavage of ICAD/DFF-45. In vitro assays with lysates of cells in which Cl(-) efflux is blocked confirm the lack of internucleosomal DNA degradation. These findings establish that neither caspase activation nor ICAD/DFF-45 processing per se is sufficient to induce oligonucleosomal DNA fragmentation and that high molecular weight DNA degradation and chromatin condensation appear independently of it. Finally, they suggest that Cl(-) efflux is a necessary cofactor that intervenes specifically in the activation of the DFF endonuclease.

Apoptosis↗

PubMed1999

Adhesion of human monocytic THP-1 cells to endothelial cell adhesion molecules or extracellular matrix proteins via beta1 integrins regulates heparin binding epidermal growth factor-like growth factor (HB-EGF) expression.

Adherence to endothelium and then to the extracellular matrix is a prerequisite for extravasation of monocytes into injured tissues. There, monocytes differentiate into macrophages and express heparin binding epidermal growth factor-like growth factor (HB-EGF), a key growth factor involved in normal wound healing. We investigated whether the interaction of human monocytic THP-1 cells with the endothelial cell adhesion molecules (vascular CAM-1, VCAM-1; intercellular adhesion molecule-1 ICAM-1 and endothelial-selectin, E-selectin), or the extracellular matrix (ECM) proteins (fibronectin, FN; laminin, LN and fibrinogen, FG) regulate HB-EGF expression. We have shown that adherence of THP-1 cells via VCAM-1, E-selectin or FN, which are all overexpressed at sites of inflammation, potentiates HB-EGF mRNA expression. In contrast, adhesion of THP-1 cells via ICAM-1 or FG, has no significant effect. Since THP-1 cells interact with ICAM-1 and FG through beta2 integrins, and with VCAM-1 and FN via beta1 integrins, regulation of HB-EGF expression appears to be specific to beta1 integrin ligation. In addition, we demonstrate that THP-1 binding to LN, through the beta1 integrin VLA-6, down regulates HB-EGF expression. Thus physiologically, transient destruction of LN and expression of VCAM-1, E-selectin and fibronectin at sites of inflammation, may locally induce HB-EGF overexpression.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1999

Neutrophil F-actin and myosin but not microtubules functionally regulate transepithelial migration induced by interleukin 8 across a cultured intestinal epithelial monolayer.

The role of the polymorphonuclear leukocyte (PMN) cytoskeleton during the transmigration across colonic epithelial cells is not very well understood. In order to study the role of different components of the PMN cytoskeleton during transepithelial migration across a colonic epithelial cell monolayer (T84), PMN were preincubated with drugs affecting either the actin cytoskeleton (cytochalasin B, iota toxin of Clostridium perfringens, and phalloidin) or the microtubules (colchicine and taxol). The role of PMN myosin during transepithelial migration was investigated using the inhibitor 2,3-butanedione monoxime (BDM) and DC3B toxin. PMN intracellular Ca2+, during neutrophil adhesion and translocation across the epithelium, was assessed by the Ca2+ chelator 1, 2bis-(2-aminophenoxy)-ethane-N,N,N', N'-tetra-acetic acid tetrakis (acetoxymethyl) ester (BAPTA-AM). Transmigration of PMN was initiated by applying either interleukin-8 or formyl-met-leu-phe (fMLP). While colchicine and taxol preexposure did not influence PMN transepithelial migration, treatment with cytochalasin B, iota toxin, phalloidin, BDM, DC3B toxin and BAPTA-AM greatly diminished migration of PMN across T84 monolayers. Similarly, cell-cell contacts established between PMN and epithelial cells during the transmigration were diminished after treatment of PMN with iota toxin or cytochalasin B. These data show that the neutrophil actin cytokeleton and myosin, but not the microtubules, evoke a Ca2+ -dependent motility that facilitates migration across the colonic epithelial barrier.

ADP Ribose Transferases↗

PubMed1999

Impairment of HIV polymorphonuclear leukocyte transmigration across T84 cell monolayers: an alternative mechanisms for increased intestinal bacterial infections in AIDS?

Our objective was to study the influence of HIV infection of polymorphonuclear leukocytes (PMN) on transepithelial migration. To date, reports of functional PMN chemotaxis in AIDS are contradictory. This is the first attempt to assess this function via an in vitro model allowing transmigration of neutrophils through an intestinal epithelial barrier. PMN were isolated from 45 HIV-infected patients and 45 healthy volunteers. PMN transmigration across T84 epithelial cells was initiated by applying either various concentrations of formyl-met-leu-phe peptide (f-MLP) or interleukin-8 and assayed by quantification of myeloperoxidase activity. CD11b, CD18, and CD47 expression on PMN was compared before and after transepithelial migration by flow cytometry analysis. CD11b expression was studied by electron microscopy. Apoptosis of transmigrated HIV PMN and control PMN was investigated by morphology and DNA fragmentation characterization. Compared to control PMN, HIV PMN exhibited a decrease in transepithelial migration that directly correlated with CD4+ counts. Basal and transepithelial migration-mediated expression of CD11b, CD18, and CD47 were unmodified in HIV PMN compared to control PMN. Electron microscopy labeling confirmed no difference in CD11b expression on HIV and control PMN. The index of apoptosis in transmigrated HIV PMN and control PMN was identical. These data provide evidence of a defect in the f-MLP-induced chemotaxis of PMN from HIV-infected patients across an intestinal epithelial barrier. This defective migration is not due to a quantitative modification of CD11b, CD18 and CD47 on HIV PMN suggesting a more subtle alteration. The impairment in the transmigration function may contribute in vivo to an increased susceptibility to intestinal bacterial infection in HIV-infected patients.

Adult↗

PubMed1999

[The role of biological monitoring in the evaluation of the risk of from chemical compounds].

Over the years, the assessment of the risk to human health from occupational and environmental exposure to chemicals has become increasingly important. Exposure to chemicals, their biochemical effects and individual susceptibility can be estimated by biological monitoring carried out on potentially exposed subjects. Valid markers are needed to be effectively used within the framework of biological monitoring programs. Quality assurance, which includes all those activities necessary to provide adequate confidence that the results of laboratory test are reliable, is of the utmost importance. Among these activities the participation in external quality assessment schemes is strongly recommended. Biological monitoring has a key role also in the field of human reproduction since the level of exposure to many chemicals which are known or suspected to be reproductive toxicants can be assessed by specialized laboratories.

Environmental Monitoring↗

PubMed1998

Early G1 growth arrest of hybridoma B cells by DMSO involves cyclin D2 inhibition and p21[CIP1] induction.

Dimethylsulfoxide (DMSO) was shown to inhibit the proliferation of several B cell lines including Raji, Daudi, and SKW6-CL4 but the mechanisms involved in this growth arrest are still unclear. We show that in 7TD1 mouse hybridoma cells a DMSO-induced reversible G1 arrest involves inactivation of Rb kinases, cyclin D2/CDK4 and cyclin E/CDK2. This occurs by at least three distinct mechanisms. Inhibition of cyclin D2 neosynthesis leads to a dramatic decrease of cyclinD2/CDK4 complexes. This in turn enables the redistribution of p27[KIP1] from cyclin D2/CDK4 to cyclin E/CDK2 complexes. In addition, the simultaneous accumulation of p21[CIP1] entails increasing association with cyclin D3/CDK4 and cyclin E/CDK2. Thus, p21[CIP1] and p27[KIP1], act in concert to inhibit cyclin E/CDK2 activity which, together with CDK4 inactivation, confers a G1-phase arrest.

Administration, Topical↗

PubMed1998

SP220K is a novel matrix serine proteinase.

Matrix proteinases play a critical role in extracellular matrix remodeling, which is particularly involved in cancer invasion and metastasis. We have previously characterized and purified a new tetrameric serine proteinase (SP220K) from human kidney clear cell carcinoma plasma membranes. Here, we report that SP220K exhibits gelatinase activity as assessed both in solution and by zymography. Optimum gelatinase activity ranges between pH 7.5 to pH 9.0. Fibronectin and type I collagen were hydrolyzed by SP220K, at variance with laminin and type IV collagen. Like other trypsin-like fibronectin degrading proteinases, SP220K released the 29-kDa N-terminal heparin-binding domain of fibronectin. By using a panel of proteinase inhibitors, we found that the inhibition profile of SP220K was different from that of other known serine proteinases such as thrombin, trypsin, plasmin, plasminogen activators and tryptase. Altogether, our results indicate that SP220K corresponds to a novel matrix proteinase that exhibits a marked specificity for fibronectin and type I collagen.

Collagen↗

PubMed1998

Microtubule integrity regulates src-like and extracellular signal-regulated kinase activities in human pro-monocytic cells. Importance for interleukin-1 production.

We have demonstrated previously that microtubule depolymerization by colchicine in human monocytes induces selective production of interleukin-1 (IL-1) (Manié, S., Schmid-Alliana, A., Kubar, J., Ferrua, B., and Rossi, B. (1993) J. Biol. Chem. 268, 13675-13681). Here, we provide evidence that disruption of the microtubule structure rapidly triggers extracellular signal-regulated kinase (ERK) activation, whereas it was without effect on SAPK2 activity, which is commonly acknowledged to control pro-inflammatory cytokine production. This process involves the activation of the entire cascade including Ras, Raf-1, MEK1/2, ERK1, and ERK2. Activation of ERKs is followed by their nuclear translocation. Although other SAPK congeners might be activated upon microtubule depolymerization, the activation of ERK1 and ERK2 is mandatory for IL-1 production as shown by the blocking effect of PD 98059, a specific MEK1/2 inhibitor. Additionally, we provide evidence that microtubule disruption also induces the activation of c-Src and Hck activities. The importance of Src kinases in the mediation of the colchicine effect is underscored by the fact that CP 118556, a specific inhibitor of Src-like kinase, abrogates both the colchicine-induced ERK activation and IL-1 production. This is the first evidence that ERK activation is an absolute prerequisite for induction of this cytokine. Altogether, our data lend support to a model where the status of microtubule integrity controls the level of Src activities that subsequently activate the ERK kinase cascade, thus leading to IL-1 production.

Biological Transport↗

PubMed1998

T-lymphocyte interleukin 6 receptor binding in patients with dementia of Alzheimer type.

OBJECTIVE: To investigate some aspects of T-cell-dependent immune function in patients with dementia of the Alzheimer type (DAT). DESIGN: Assay of interleukin 6 binding on T lymphocytes from patients with DAT, compared with that in healthy controls. SETTING: The study included ambulatory patients in a tertiary care center who were diagnosed as having DAT according to the criteria of the National Institute of Neurologic and Communicative Disorders and Stroke. SUBJECTS: Thirty-five patients with DAT without depression (15 women and 20 men; mean +/- SD age, 68.6 +/- 15.8 years) were selected consecutively. They had not taken any medication for at least 3 weeks and did not smoke. Illness severity was evaluated according to the Clinical Dementia Rating Scale. Thirty-five age- and sex-matched healthy nonsmoking subjects with no family history of neuropsychiatric disorders formed the control group. RESULTS: A significant (P < .001) increase in T-lymphocyte interleukin 6 binding was found in patients with DAT compared with healthy controls (mean +/- SE receptors per cell, 305 +/- 7 vs 276 +/- 6, respectively), whereas the ligand-receptor affinity values were similar in the 2 groups (mean +/- SE, 25.9 +/- 0.9 and 25.3 +/- 0.6 nmol/L). CONCLUSION: These data indicate a derangement of the immune response in patients with DAT since cell-surface interleukin 6 receptors seem to be related to T-lymphocyte immune function.

Aged↗

PubMed1998

Altered surface myoelectric signals in peripheral vascular disease: correlations with muscle fiber composition.

Conduction velocity (CV) and median frequency (MDF) during tetanic electrical stimulation of the tibialis anterior muscle were evaluated in patients with uncomplicated peripheral arterial occlusive disease. Results were analyzed with respect to biopsy determination of diameter and proportion of types 1 and 2 muscles fibers. Initial MDF and CV correlated positively with type 2, but not type 1 fiber diameter. Initial MDF was reduced bilaterally in patients with unilateral peripheral arterial occlusive disease as compared to normal subjects, indicating that chronic ischemia alone cannot explain the altered myoelectric signal. Physical training increased pain-free walking distance and raised initial MDF, though CV remained unchanged. Fatigue indices were highly interrelated, but showed no correlation with any of the other evaluation variables. Thus, initial MDF, a correlate of type 2 muscle fiber distribution in chronically ischemic tibialis anterior muscles, is altered in peripheral vascular disease. However, muscle ischemia alone cannot explain all aspects of this abnormality.

Aged↗

PubMed1998

Sarcolemmal excitability in myotonic dystrophy: assessment through surface EMG.

A motor point stimulation protocol was carried out on the tibialis anterior of myotonic dystrophy (MyD) patients. The surface myoelectric signal was monitored to record average rectified value (ARV), median frequency of power spectrum (MDF), and conduction velocity (CV) parameters. The ARV curve showed a decreasing trend that reveals a reduction in the M-wave amplitude during stimulation. MDF presented a significant decrement in the first seconds of sustained contraction, probably caused by abnormal lengthening of the depolarization zone. CV was significantly lower in patients, suggesting reduced mean fiber size.

Electromyography↗

PubMed1998

CD10 inhibitors increase f-Met-Leu-Phe-induced neutrophil transmigration.

A variety of bacterial enterocolitis in their active stages are characterized by the migration of polymorphonuclear leukocytes (PMNs) across epithelial surfaces. These mechanisms could explain some effects of enterotoxins observed in the intestinal mucosae. Here, using specific inhibitors, we investigated the potential role of CD10 (E.C. 3.4.24.11), present at the surface of human neutrophils, on formyl-Met-Leu-Phe (fMLP)-induced PMN migration across cultured monolayers of the human intestinal cell line T84. Transmigration of human neutrophils across T84 epithelial cells was observed for concentrations of fMLP as low as 10(-9) M, whereas maximal effect was achieved at 10(-7) M as determined by transepithelial resistances and PMN myeloperoxidase assays. RB25, a CD10 inhibitor, reduced by two orders of magnitude the concentration of fMLP required to obtain full neutrophil transmigration across T84 epithelial cell line. RB25 response was concentration dependent with half-maximal and maximal effect occurring at 10(-9) and 10(-7) M, respectively. These concentrations of RB25 corresponded exactly to the half-maximal and maximal inhibition of endopeptidase 24.11 at the neutrophil cell surface. However, the effect of CD10 inhibitors on PMN transmigration cannot be accounted for by a direct action on T84 epithelial cells, since these cells fail to express any detectable endopeptidase 24.11 activity. Moreover, blocking of CD10 enzymatic activity by various and selective inhibitors potentiated the effect of low concentrations of fMLP on PMN transmigration. Finally, RB25 failed to affect interleukin-8 (IL-8)-induced PMN transmigration across T84 epithelial cells, in agreement with the preference of CD10 for small peptidic substrates. Taken together, these results demonstrate that inhibition of CD10 significantly reduced the concentration of fMLP needed for eliciting transmigration of PMN across intestinal epithelia.

Benzylidene Compounds↗