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Biomedical subjects

E Lechapt-Zalcman

Publications and source records attributed to E Lechapt-Zalcman.

11 recordsLinked to original sources
PubMed2006

Transforming growth factor-beta1 increases airway wound repair via MMP-2 upregulation: a new pathway for epithelial wound repair?

In vivo, transforming growth factor (TGF)-beta1 and matrix metalloproteinases (MMPs) present at the site of airway injury are thought to contribute to epithelial wound repair. As TGF-beta1 can modulate MMP expression and MMPs play an important role in wound repair, we hypothesized that TGF-beta1 may enhance airway epithelial repair via MMPs secreted by epithelial cells. We evaluated the in vitro influence of TGF-beta1 on wound repair in human airway epithelial cells cultured under conditions allowing differentiation. The results showed that TGF-beta1 accelerated in vitro airway wound repair, whereas MMP inhibitors prevented this acceleration. In parallel, we examined the effect of TGF-beta1 on the expression of MMP-2 and MMP-9. TGF-beta1 induced a dramatic increase of MMP-2 expression with an increased steady-state level of MMP-2 mRNA, contrasting with a slight increase in MMP-9 expression. To confirm the role of MMP-2, we subsequently evaluated the effect of MMP-2 on in vitro airway wound repair and demonstrated that the addition of MMP-2 reproduced the acceleration of wound repair induced by TGF-beta1. These results strongly suggest that TGF-beta1 increases in vitro airway wound repair via MMP-2 upregulation. It also raises the issue of a different in vivo biological role of MMP-2 and MMP-9 depending on the cytokine microenvironment.

Gelatinases↗
PubMed2006

Matrix metalloproteinase-2 and -9 expression in sinonasal inverted papilloma.

STATEMENT OF PROBLEM: Inverted papilloma (IP) is a proliferative lesion of the epithelium lining the sinonasal tract, characterized by marked propensity for recurrence and association with carcinoma. To determine a putative role of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the establishment of IP, their expression was studied in IP. METHODS: Archived surgical specimens from 15 IPs were studied using immunohistochemistry and compared to 12 nasal polyps (NP), a model of chronic respiratory mucosal inflammation, and to 6 control nasal mucosa (CM) samples obtained from snorers during turbinectomy. Within IP, MMP-2 and -9 expression was compared between tumoral areas with hyperplastic epithelium and non tumoral areas with nonhyperplastic epithelium. RESULTS: In IP, MMP-2 and MMP-9 epithelial expression was not different compared to CM and NP. MMP-9 expression in submucosal inflammatory cells was not different between IP and CM or NP. However, within IP, a significantly increased number of MMP-9 positive inflammatory cells in the lamina propria adjacent to the hyperplastic epithelium was observed compared to the lamina propria adjacent to nonhyperplastic epithelium. CONCLUSION: Our findings suggest that MMP 9 expressing inflammatory cells may be involved in the pathophysiology of IP.

Case-Control Studies↗
PubMed2001

Increased expression of matrix metalloproteinase-9 in nasal polyps.

To investigate the role of gelatinases in nasal polyposis, a common and disabling airway disease characterized by chronic inflammation and tissue remodelling, matrix metalloproteinase-2 (MMP-2) and MMP-9 expression was investigated in the nasal polyps (NP) of 24 patients undergoing ethmoidectomy and compared with 15 control nasal mucosal (CM) samples obtained from snorers during turbinectomy. Tissue samples were either frozen for enzymatic analysis or paraffin wax-embedded for immunohistochemistry. Zymography and quantitative image analysis showed that MMP-9 active forms were significantly increased (p<0.05) in NPs compared to CM (44 +/- 40 versus 13 +/- 19x10(3) AU/10 microg protein), while MMP-2 expression was similar in both tissues. Concomitant studies of gelatinase immunoexpression showed that MMP-9 expression was enhanced (4- to 16-fold) in surface epithelium, glands (p<0.05), and submucosal inflammatory cells (p<0.05). In addition, MMP-9 positivity was markedly increased in endothelial cells (p<0.01). In situ zymography demonstrated marked gelatinolytic activity, consistent with the immunolocalization of MMP-2 and MMP-9. These results suggest up-regulation of active MMP-9 in the glands and vessels characteristic of NPs. It is concluded that MMP-9 may play a role in the upper airway remodelling observed during nasal polyposis.

Adult↗
PubMed2001

Association of primary pleural effusion lymphoma of T-cell origin and human herpesvirus 8 in a human immunodeficiency virus-seronegative man.

We describe a case of an 87-year-old human immunodeficiency virus (HIV)-negative man who developed a primary pleural lymphoma without any identifiable tumor mass associated with human herpesvirus 8 (HHV-8) infection. A large T-cell lymphoma was diagnosed based on morphologic, immunophenotypic, and molecular findings. The HHV-8 DNA sequences were detected using specific polymerase chain reaction amplification in the lymphomatous effusion. Study of the patient's serum confirmed the HHV-8 infection. This case report displays the characteristic features of HHV-8-related body cavity-based lymphoma/primary effusion lymphoma previously reported in HIV-seronegative patients, except that it is of T-cell origin. Whether this case may be included or not within the primary effusion lymphoma entity, the association of a pleural T-cell non-Hodgkin lymphoma with HHV-8 infection raises the question of the possible occurrence of T cells as the target of malignant transformation associated with HHV-8 infection.

Aged↗
PubMed2000

[Implication of extracellular matrix metalloproteinases in the course of chronic inflammatory airway diseases].

Matrix metalloproteinases (MMPs) are major proteolytic enzymes that are involved in extracellular matrix (ECM) turn over. MMP-2 (gelatinase A) and MMP-9 (gelatinase B) cleave type IV collagen, which is an important constituent of basement membrane. These enzymes play an important role in normal tissue homeostasis, but imbalance between MMPs and their tissue inhibitors (TIMPs) is thought to be a critical factor in regulating tissue remodeling. MMP-2 is produced by fibroblasts, endothelial, and epithelial cells, while MMP-9 is mainly produced by inflammatory cells. The role of MMPs was investigated through biochemical analysis or in situ expression, in the pathogenesis of two chronic inflammatory airway diseases, asthma and nasal polyposis. Both are characterized with the accumulation of active inflammatory cells, matrix remodeling and epithelial changes. Increased levels of MMP-9 and TIMP-1 were found in asthmatic subjects and NP. In NP, MMP-9 expression was detected in epithelial, endothelial and inflammatory cells. In this setting, MMP-9 could play a crucial role in the transmigration of basement membrane components by inflammatory cells leading to inflammatory cell accumulation and maintenance of inflammation in airway. Moreover, MMP-9 may contribute to cell migration, an important mechanism involved in the repair of the respiratory epithelium.

Asthma↗
PubMed1999

Labial salivary gland biopsy for diagnosis of amyloid polyneuropathy.

Biopsies of peroneal nerve and labial salivary gland (LSG) were performed in 32 patients with polyneuropathy of unknown origin. Amyloid deposits were detected in 7 LSG (transthyretin=5; amyloid, light chain derived=2) and 6 nerve biopsies. Familial amyloid and light chain amyloid polyneuropathies were subsequently confirmed by relevant tests. We propose that LSG biopsy, a minimally invasive test that may document both sicca syndrome and amyloidosis, should be systematically performed in the investigation of patients with axonal polyneuropathies.

Amyloid↗
PubMed1999

Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) and its receptor flt-1 in microcystic meningiomas.

We investigated the immunohistochemical expression of vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) and of its endothelial cell receptor flt-1 in relationship to microcyst formation in meningiomas. Expression of VPF/VEGF was studied in 60 meningiomas (6 microcystic, 38 partially microcystic and 16 with no microcystic areas) and 30 meningiomas from these three subgroups were evaluated for flt-1 expression. VPF/VEGF immunoreactivity was mainly observed in vessel endothelium. Positive vessels were present in 75% (33/44) of meningiomas with any amount of microcystic pattern and in 38% (6/16) of the solid meningiomas (P < 0.02). Densities and percentages of both VPF/VEGF-positive and flt-1-positive vessels were higher in meningiomas with microcystic areas than in solid meningiomas (P </= 0.002). The 6 microcystic meningiomas showed the highest densities and percentages of both VPF/VEGF-positive (P </= 0.0002) and flt-1-positive vessels (P </= 0. 01). Vessel expression of VPF/VEGF and flt-1 were positively correlated (r >/= 0.75, P < 0.0001). A strong positive correlation between VPF/VEGF-positive vessel density and proportion of microcystic pattern in all 60 specimens was found (r = 0.75, P < 0. 0001). We conclude that accumulation of flt-1-bound VPF/VEGF on endothelial cells of meningiomas is associated with microcyst formation that leads to the histologic appearance of microcystic meningiomas.

Endothelial Growth Factors↗
PubMed1999

Overexpression of alveolar macrophage gelatinase B (MMP-9) in patients with idiopathic pulmonary fibrosis: effects of steroid and immunosuppressive treatment.

Alveolar macrophages (AM) express gelatinase B, a member of the matrix metalloproteinase family involved in the degradation and remodeling of extracellular matrix components. We evaluated the expression of gelatinase B in the course of idiopathic pulmonary fibrosis (IPF) by studying alveolar macrophages in culture AM and bronchoalveolar lavage fluid from 12 untreated patients with IPF, 11 patients with IPF under treatment with steroid and immunosuppressive agents, and 10 control subjects. By using zymography and quantitative image analysis, latent gelatinase B, as well an 88-kD active form, were investigated in culture medium (24 h) of AMs and were found to be significantly increased (P < 0.01) in untreated patients exhibiting severe IPF when compared with control subjects (4.1 +/- 1.7 versus 0.3 +/- 0.2 10(5) arbitrary units [AU]/10(4) AM for the 92-kD form). Concomitant studies of gelatinase B levels associated with cultured AM extracts or freshly harvested AM showed similar results, both at the mRNA and protein levels, respectively. Immunocytochemical studies on freshly harvested AM demonstrated that the enzyme was located mainly at the cell, suggesting some involvement of gelatinase B in AM migration. In contrast, gelatinase B activity secreted by AM tended to be normal in patients with IPF under steroid and immunosuppressive treatment. Simultaneously, level of the gelatinase B activity in epithelial lining fluid was increased in untreated IPF patients, whereas it was normal in treated patients. These results suggest that AM of patients with IPF are primed for gelatinase B expression and that steroid and immunosuppressive treatment induces negative modulation of the gelatinase B overexpression. We conclude that gelatinase B may play a role in lung remodeling in IPF.

Base Sequence↗
PubMed1997

MDR1-Pgp 170 expression in human bronchus.

MDR1 P-glycoprotein (Pgp 170), a member of the adenosine triphosphate (ATP) binding cassette transporters, acts as an efflux pump for various hydrophobic agents, particularly for xenobiotics such as benzo(a)pyrene. It has also been shown to regulate cell-volume activated chloride channels. Pgp 170 could, therefore, be of particular importance in cellular mechanisms of defence in the airways and in the control of mucus layer composition. For these reasons, we evaluated the precise localization of Pgp 170 in human adult airways. Fresh non-neoplastic bronchial specimens were collected from 33 patients (26 smokers, four exsmokers and three nonsmokers) who underwent surgery for lung carcinoma. The presence of MDR1 messenger ribonucleic acid (mRNA) was demonstrated by reverse transcriptase chain reaction (RT-PCR) in bronchial epithelial cells collected by gentle scraping from either smokers, exsmokers or nonsmokers. Immunodetection of Pgp 170 using a panel of monoclonal antibodies (MRK16, JSB1, C219, C494) was performed either on cryostat or paraffin-embedded sections of histologically normal bronchial tissue. Pgp 170 was constantly detected with intense labelling at the apical surface of ciliated epithelial cells from the surface epithelium or ciliated collecting ducts, and on apical and lateral surfaces of serous cells from bronchial glands. No staining of mucus-secreting cells was observed. Pgp 170 was also demonstrated at the luminal surface of endothelial cells of bronchial capillaries. In conclusion, the expression of MDR1 P-glycoprotein in bronchial structures, particularly at the epithelial apical surface, suggests important roles for this transmembrane protein in human airways.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Posttransplantation lymphoproliferative disorder mimicking a nonspecific lymphocytic pleural effusion in a bone marrow transplant recipient. A case report.

BACKGROUND: Serous effusions are rare complications of bone marrow transplantation (BMT) and result mainly from infections or tumor relapse. CASE: We report a case of posttransplantation lympho-proliferative disorder (PTLD) revealed by cytodiagnostic examination of serous effusions in a BMT recipient. The effusion was initially considered reactive, but morphologic, immunocytologic and molecular studies subsequently revealed PTLD. CONCLUSION: This case demonstrates the importance of cytologic examination of effusions in BMT or organ recipients. Since most PTLDs are Epstein-Barr virus (EBV)-associated B-cell lymphoproliferative disorders and T cells predominate in reactive effusions, appropriate initial immunostaining, including CD3, CD79a and EBV latent membrane protein, should aid in their early detection.

Acute Disease↗