Inverse relationship between the apoptotic rate and the time elapsed from thermal injuries in deep partial thickness burns.

BACKGROUND: The purpose of this article was to further describe apoptotic behaviour in deep partial thickness burns, correlating the apoptotic rate of these lesions with the time elapsed from injury. METHODS: We used TUNEL and Fas immunohistochemistry in serial biopsies of deep partial thickness burns harvested from 1 to 23 days following injury. The apoptotic rate was defined as the number of apoptotic cells out of the total number of nucleated cells. RESULTS: We recruited 25 subjects. Apoptosis was present in all biopsies and showed an inverse relationship with the time elapsed from thermal injury, higher during the first days and lower in the third week (r=-0.518; p=0.008). No significant correlations were demonstrated with age, total burn surface area, deep partial thickness burns area, Baux UBS index. CONCLUSIONS: Our study demonstrates that apoptosis persists in deep partial thickness burns throughout the first 3 weeks and shows an inverse relationship with the time elapsed from injury. It provides, in our opinion, the basis for future investigations regarding correlation with local vascularity and perfusion status and with clinical outcomes of deep partial thickness burns.

BCL2 and BAX expression in hyperplastic and dysplastic rectal polyps.

BACKGROUND/AIMS: Members of the gene family that includes BCL2 and BAX are functionally antagonists in the apoptosis process and they have been observed in normal and neoplastic tissues. The aim of this study is to investigate the combined effects of BCL2 and BAX protein in normal mucosa, dysplastic and hyperplastic polyps of the rectum. METHODOLOGY: We studied BCL2 and BAX protein expression in 40 cases of adenomatous polyps all located in the rectum, with different dysplastic gradings, and the mean time in 10 cases of normal rectal mucosa. RESULTS: BCL2 expression was found more frequently in hyperplastic and in low dysplastic polyps with moderate and strong positivity compared to moderate and severe dysplasia. BAX expression was found in normal mucosa in hyperplastic and dysplastic polyps, the immunoreactivity was prevalently moderate and strong. CONCLUSIONS: These preliminary data suggest that BCL2 and BAX confirm a probably different role in apoptosis. Nevertheless, it is important to know the relation between the molecular pathways of apoptosis, the defective mismatch repair and the tumor suppressor genes associated with an increased mutation rate in cancerogenesis of the colorectum.

Adhesion molecules and lymphocyte recruitment in lymphocytic thyroiditis, thyroid papillary carcinoma and parotid adenolymphoma.

Lymphocytic infiltrates are usually present in chronic lymphocytic thyroiditis, thyroid papillary carcinoma and parotid adenolymphoma. We selected these conditions to investigate the mechanisms of recruitment and organization of lymphocytic infiltrates in extranodal tissues. MoAbs in immunoperoxidase were used to identify the expression of ICAM-1 and VCAM-1 on endothelial cells (EC), and of their ligands LFA-1 and VLA-4 on lymphocytes and accessory cells. VCAM-1 positive EC were rarely observed in thyroids devoid of lymphocyte infiltration. Conversely, EC in chronic lymphocytic thyroiditis and in papillary carcinoma showed positive immunostaining for VCAM-1 and ICAM-1. These findings were associated with the presence of lymphocytes positive for the ligands VLA-4 and LFA-1. The upregulated expression of VCAM-1 on perifollicular capillaries was co-distributed with an accumulation of VLA-4 positive lymphocytes. In adenolymphoma, all EC were ICAM-1 positive, whereas the majority of vessels were VCAM-1 negative. Consequently the majority of lymphoid cells were LFA-1 positive and VLA-4 negative. We suggest that ICAM-1 and VCAM-1 expression on EC play a role in the recruitment of lymphocyte infiltration in chronic lymphocytic thyroiditis and papillary carcinoma. Furthermore, the upregulation of VCAM-1 and VLA-4 in thyroid reactive and neoplastic conditions may be linked to an immune response possibly related to thyroid tissue antigens.

Cytokine production and expression of adhesion molecules and integrins in tumor infiltrating lymphomononuclear cells of non-small cell carcinomas of the lung.

Localization of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, and of their ligands, lymphocyte function-associated antigen-1 and very late activation antigen-4, was determined in non-small cell lung carcinomas and tumor-free lung. Messenger RNA expression for interleukins (IL) IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, tumor necrosis factor-alpha, transforming growth factor-beta, interferon-gamma, granulocyte-macrophages colony stimulating factor, and human perforin-1 was assessed by in situ hybridization on the same tissues. Intercellular adhesion molecule-1 was expressed in all blood vessels, whereas only a low number of vessels displayed vascular cell adhesion molecule-1 immunoreactivity. Tumor infiltrating lymphomononuclear cells consisted of lymphocyte function-associated antigen-1-positive cells and of a lower number of very late activation antigen-4-positive cells. All squamous cell carcinomas consisted of intercellular adhesion molecule-1-positive neoplastic cells infiltrated by lymphocyte function-associated antigen-1-positive tumor infiltrating lymphomononuclear and CD-la-positive Langerhans cells, whereas only a minor number of adenocarcinomas displayed a consistent number of intercellular adhesion molecule-1-positive neoplastic cells. Tumor infiltrating lymphomononuclear cells showed a wider production of cytokines when compared to bronchus-associated lymphoid tissue of tumor-free lung. Moreover, cells producing interferon-gamma, IL-4, and IL-5 were more numerous in squamous cell carcinomas than in adenocarcinomas. These findings indicate that the lung squamous cell carcinoma might represent a neoplastic microenvironment able to induce activation of tumor infiltrating lymphomononuclear cells more efficiently than the adenocarcinoma.