Biomedical subjects

P Cappello

Publications and source records attributed to P Cappello.

9 recordsLinked to original sources

PubMed2000

Tumor rejection and immune memory elicited by locally released LEC chemokine are associated with an impressive recruitment of APCs, lymphocytes, and granulocytes.

The human beta chemokine known as LEC (also called NCC-4, HCC-4, or LMC) displays chemotactic activity for monocytes and dendritic cells. The possibility that its local presence increases tumor immunogenicity is addressed in this paper. TSA parental cells (TSA-pc) are poorly immunogenic adenocarcinoma cells that grow progressively, kill both nu/nu and syngeneic BALB/c mice, and give rise to lung metastases. TSA cells engineered to release LEC (TSA-LEC) are still able to grow in nu/nu mice, but are promptly rejected and display a marginal metastatic phenotype in BALB/c mice. Rejection is associated with a marked T lymphocyte and granulocyte infiltration, along with extensive macrophage and dendritic cell recruitment. NK cells and CD4+ T lymphocytes are uninfluential in TSA-LEC cell rejection, whereas both CD8+ lymphocytes and polymorphonuclear leukocytes play a major role. An antitumor immune memory is established very quickly after rejection, since 6 days later 75% of BALB/c mice were already resistant to a TSA-pc challenge. Spleen cells from rejecting mice display specific cytotoxic activity against TSA-pc and secrete IFN-gamma and IL-2 when restimulated by TSA-pc. The ability of LEC to markedly improve recognition of poorly immunogenic cells by promoting APC-T cell cross-talk suggests that it could be an effective component of antitumor vaccines.

Adenocarcinoma↗

PubMed1999

A "stealth effect": adenocarcinoma cells engineered to express TRAIL elude tumor-specific and allogeneic T cell reactions.

BALB/c mammary adenocarcinoma cells engineered to express TNF-related apoptosis-inducing ligand (TRAIL)/APO-2 ligand (APO-2L) on their membrane (TSA-TRAIL) grow with kinetics similar to that of parental cells (TSA-pc) in vitro and in nu/nu mice. In contrast, TSA-TRAIL cells grow faster than TSA-pc in normal BALB/c mice. In DBA/2 mice, which differ from BALB/c mice at minor histocompatibility Ags, they also grow faster and display a higher percentage of tumor takes than TSA-pc. In fully histoincompatible C57BL/6 (B6) mice, TSA-TRAIL cells form evident tumors that are slowly rejected by most mice, but outgrow in a few. In contrast, TSA-pc cells are rejected at once by B6 mice. Since TRAIL/APO-2L induces apoptosis by interacting with a variety of specific receptors, this rapid growth in both syngeneic and allogeneic mice may be the result of an immunosuppressive mechanism. The following evidence supports this hypothesis: 1) TSA-TRAIL cells overcome the strong immunity against TSA-pc cells elicited in BALB/c mice by preimmunization with TSA cells engineered to release IL-4; 2) their rejection by B6 mice does not prime a CTL-mediated memory; 3) thymidine uptake by T lymphocytes unstimulated or stimulated by allogeneic cells is inhibited when TSA-TRAIL cells are added as third party cells; 4) CTL kill TSA-pc but not TSA-TRAIL cells in 48-h assays; and 5) activated lymphocytes interacting with TSA-TRAIL cells in vivo and in vitro undergo apoptosis.

Adenocarcinoma↗

PubMed1999

Apoptosis in the development of the mouse olfactory epithelium.

Apoptotic cells were detected in the mouse olfactory epithelium (OE) at different embryonic and postnatal stages by in situ nick translation (ISNT) and Tdt-mediated dUTP nick end-labeling (TUNEL) techniques. During development, the apoptotic process presented two peaks. One at E12 during the invagination of the olfactory placode and the second at E16 corresponding to olfactory axon synaptogenesis. Then, from E18, a sharp decrease in the number of apoptotic cells was observed and at E19 the apoptotic index reached low values that were maintained in postnatal stages, P1 and P8, and in the adult. Apoptotic nuclei belonged to mature as well as immature olfactory receptor neurons (ORNs). Indeed, double-labeling experiments evidenced apoptotic neurons immunopositive for olfactory marker protein (OMP), carnosine and GAP-43. According to our data, two apoptotic phases occur during early development. One is involved in the morphogenesis of the OE when this last is not yet, or poorly, connected to its target, the olfactory bulb (OB). The second peak of apoptosis is more closely dependent on the interplay between OE and OB.

Animals↗

PubMed1999

Proliferation and apoptosis in the mouse vomeronasal organ during ontogeny.

Differential cell proliferation and apoptosis play a key role in organ morphogenesis. We have analyzed these two processes in the development of murine vomeronasal organ (VNO), an olfactory structure involved in the detection of pheromones. Using the TUNEL (TdT-mediated dUTP nick end labelling) method we demonstrate that dying cells are relatively more abundant in non sensory vomeronasal organ (NS-VNO) rather than in sensory epithelium (S-VNO), particularly in early stages of development. During ontogeny cell proliferation, studied with bromodeoxyuridine (BrdU) labelling, shows a broad pattern of localization, since proliferating cells are distributed throughout the VNO and not confined between NS-VNO and S-VNO. Quantification of BrdU-labelled cells indicates that proliferation is rather stable in both components.

Animals↗

PubMed1998

Prenatal differentiation of mouse vomeronasal neurones.

The vomeronasal organ (VNO) subserves basic chemosensory functions in rodents, mainly related to sexual behaviour. In order to understand early stages of the VNO structural maturation, we have undertaken an immunocytochemical analysis of the VNO of fetal mice. Our results demonstrate that Olfactory Marker Protein (OMP), a marker of differentiated chemosensory cells, is already expressed in vomeronasal neurones and their fibres projecting to the accessory olfactory bulb during the last week of gestation. However, in contrast to the adult, where its expression is restricted to the medial sensory neuronal component of the VNO, during fetal development OMP is also present in cells located in the lateral non-sensory epithelial component. Some other markers of nasal chemosensory neurones, such as GAP-43/B-50, Protein Gene Product 9.5 (PGP 9.5) and carnosine are also transiently expressed in this ectopic site. These results indicate that (i) significant morphological and biochemical maturation of the VNO is achieved before birth; (ii) transient cell populations, sharing the biochemical profile of the vomeronasal chemosensory receptors, occur in ectopic areas during fetal development.

Animals↗

PubMed1985

[Validity of the ABAC II system: applicability in the hospital laboratory and verification of breakpoint concentrations in the determination of antibiotic sensitivity].

Two different sensitivity testing methods were evaluated on 183 bacterial strains of Gram-negative clinical isolates in relation to 13 antimicrobial drugs. Comparison between both methods: conventional technique of disk diffusion (Kirby-Bauer) and the automated ABAC breakpoints system, has shown a good agreement of the results (91.1%) according to several investigators. The authors analyze the role of ABAC system and its achievement in routine work of a medium bacteriological hospital laboratory.

Anti-Bacterial Agents↗

PubMed1985

[Rapid identification of Enterobacteriaceae: evaluation of 3 commercial systems].

We have compared three rapid systems for the identification of Enterobacteriaceae: MS-2, Rapid 20E, Micro-ID. These methods allows to identifications of bacteria within 4-5 hours. We have chosen API 20E as reference system; because it is normally used in the clinical microbiology laboratories. We have noted good agreement of concordance for MS-2, Micro-ID and Rapid 20E towards API 20E, respectively 95, 90, 84%. We have, moreover, analysed significative difference about three systems biochemical tests in comparison with the same of API 20E.

Enterobacteriaceae↗

PubMed1981

[Triangular comparison of the agar diffusion method, the ABAC system and the Sensitre system for determination of bacterial sensitivity to aminoglycoside chemoantibiotics].

The in vitro activity of sisomicin, gentamicin, tobramycin and amikacin, four similar aminoglycosides, has been determined against 135 bacterial strains of Gram-negative bacilli representing 4 genera of common pathogens isolated from urinary tract infections. Comparison between three methods of antibiotic susceptibility tests: agar diffusion by Kirby-Bauer, semi-automatic technique using ABAC apparatus (Intertechnique, Sclavo) dilution method (MIC), has shown a considerable percentage of agreement, in almost all cases. The highest percentages of agreement have been shown for sisomicin and tobramycin. The authors analyze the role of the new techniques representing an advance in routine work.

Aminoglycosides↗

PubMedDate not supplied

IL-10 enhances CCL2 release and chemotaxis induced by CCL16 in human monocytes.

CCL16 is a CC chemokine originally identified as a liver-expressed chemokine. Its expression has been detected in activated monocytes where it is up-regulated by stimulation with IL-10. This is in contrast with IL-10's inhibition of the expression of most chemokines. CCL16 is chemotactic for monocytes, lymphocyte and dendritic cells. We investigated whether CCL16 displays biological activities other than chemotaxis and whether IL-10 affects monocyte response to CCL16. We show that CCL16 induces the expression of CCL2 at the mRNA and protein level, but does not affect that of CCL5, CCL18 and proinflammatory cytokines. This effect was prevented by treatment with pertussis toxin and may thus be mediated by G-protein-coupled receptors. IL-10 markedly increased CCL2 production induced by CCL16, but suppressed that of CXCL8. It also enhanced the chemotactic response to CCL16. Addition of antibodies blocking CCR1, but not CCR8, prevented this enhanced chemotactic response and suggested that CCR1 is primarily involved. We propose that IL-10 modulates the effects of CCL16 on monocytes by increasing their CCR1-dependent response. The coordinated secretion of CCL16 and IL-10 may thus enhance monocyte infiltration.

Cell Line↗