Surface Modification of Film Chitosan Materials With Aldehydes for Wettability and Biodegradation Control

Chitosan is one of prospective polymer for use in regenerative medicine which has unique properties such as biocompatibility, biodegradability, antimicrobial, anti-inflammatory, and antitumor potency. In this article, we study the peculiarities of the surface modification of chitosan films with carbonyl-containing compounds, which differed both in molecular characteristics and in their hydrophilic and hydrophobic properties. The potential for controlling the biodegradation of the resulting materials has been established, which can be used in the creation of wound dressings. Both the destruction time and lyophilic properties of the surface depend on the length of the modifier's hydrocarbon radical. The contact angle and water absorption of obtained film materials correlate with hydrophobicity, which estimated by the calculated value of the hydrophilic–lipophilic balance (HLB). The cytotoxicity of modified chitosan films was studied, and it was found that they are non-toxic (cytotoxic index of <50%) for human skin cell cultures, which shows their potential for use in the creation of materials for skin protection and external wound healing.

Evaluation of The Pathogenic Potential of Insecticidal Serratia marcescens Strains to Humans

We observed the death of insect caterpillars of Spodoptera exigua in the laboratory culture line and identified Serratia marcescens as the bacterial causative agent of the insect death. We confirmed that S. marcescens had insecticidal activity against S. exigua and caused high mortality of larvae. The LC50 values of S. marcescens CFU per 1cm2 of insect diet surface were similar for all isolates. Our research reports novel strains with high pesticidal activity as candidates for future research on a new bioinsecticide. As bioinsecticides cannot be harmful to non-target organisms, we determined the pathogenic properties of S. marcescens to humans. We proved the ability of S. marcescens todamage mammalian epithelial cells. All strains had cytopathic effects to Vero cells with a cytotoxic index ranging from 51.2% ± 3.8%to 79.2% ± 4.1%. We found that all of the strains excreted catecholate siderophore – enterobactin. All isolates were resistant to sulfamethoxazole, tobramycin, gentamicin, cefepime, and aztreonam. We did not observe the ESBL phenotype and the integrons’ integrase genes. Resistance to sulfamethoxazole was due to the presence of the sul1 or sul2 gene. The use of resistant S. marcescens strains that are pathogenic to humans in plant protection may cause infections difficult to cure and lead to the spread of resistance genes. The results of our study emphasize the necessity of determination of the safety to vertebrates of the bacteria that are proposed to serve as biocontrol agents. The novelty of our study lies in the demonstration of the indispensability of the bacteria verification towards the lack of hazardous properties to humans.

Surfactant protein A prevents silica-mediated toxicity to rat alveolar macrophages

Silicosis is a serious occupational lung disease associated with irreversible pulmonary fibrosis. The interaction between inhaled crystalline silica and the alveolar macrophage (AM) is thought to be a key event in the development of silicosis and fibrosis. Silica can cause direct injury to AMs and can induce AMs to release various inflammatory mediators. Acute silicosis is also characterized by a marked elevation in surfactant apoprotein A (SP-A); however, the role of SP-A in silicosis is unknown. We investigated whether SP-A directly affects the response of AMs to silica. In this study, the degree of silica toxicity to cultured rat AMs as assessed by a 51Cr cytotoxicity assay was shown to be dependent on the time of exposure and the concentration and size of the silica particles. Silica directly injured rat AMs as evidenced by a cytotoxic index of 32.9 ± 2.5, whereas the addition of rat SP-A (5 μg/ml) significantly reduced the cytotoxic index to 16.6 ± 1.2 ( P < 0.001). This effect was reversed when SP-A was incubated with either polyclonal rabbit anti-rat SP-A antibody ord-mannose. These data indicate that SP-A mitigates the effect of silica on AM viability, and this effect may involve the carbohydrate recognition domain of SP-A. The elevation of SP-A in acute silicosis may serve as a normal host response to prevent lung cell injury after exposure to silica.

«In vitro» Cytotoxic Activity of Normal and Leukemic Anti-Leukocyte Murine Sera

These experiments were designed to evaluate the specificity of cytotoxic antibodies for normal and leukemic leukocytes from mice with different genotypes. C57BL and C3Hf/Gs mice were immunized with allogeneic splenic cells from C3Hf/Gs, C57BL and (C3Hf/Gs x CBA T6T6) F1 donors. The animals were injected intraperitoneally once a week for 6–7 weeks and serum was obtained 7 days after the last injection. The cytotoxic effect of the sera on leukocytes was evaluated using the Terasaki test, which is based on direct phase contrast observation of refraction modification in damaged cellular elements. By using donors and recipients with dissimilar H-2 locus, an increase in the cytotoxic index was observed which was related to the number of immunizing injections. Values were fairly uniform for the different combinations tested. The maximum antibody titer was obtained 7 days after the last injection with notable decrease after 14 and 30 days. Cross tests between antisera and leukocytes with the same or different H-2 allele have demonstrated a high specificity of the isoantisera for the different H-2 locus alleles (k, b). In another group of experiments, the effect of isoantisera on leukocytes from animals with generalized leukemia was tested. The leukemia was induced by inoculation at birth with either Graffi or Gross virus. In the 12 cases studied, the cytotoxic effect on leukemic cells was always less than on normal cells of the same strain. Finally, a group of experiments was carried out using leukemic anti-leukocyte sera obtained by immunizing C57BL animals with cells derived from 2 Graffi virus-induced leukemias grafted into (C3Hf/Gs x CBA T6T6) F1 mice. These sera presented maximum cytotoxic index values on leukocytes of (C3Hf/Gs x CBA T6T6) F1 animals with Graffi virus-induced leukemia. Lower values were observed for normal leukocytes of the same strain. (C3Hf/Gs x CBA T6T6) F1 cells originating from Gross virus-induced leukemia were less sensitive to these sera, not only in comparison with Graffi virus-induced leukemia leukocytes but with normal (C3Hf/Gs x CBA T6T6) F1 leukocytes as well. It was also possible to demonstrate positivity in the cytotoxic response with C57BL leukemic leukocytes (Graffi virus-induced). These data seem to indicate that a reduction in the histocompatibility antigens of the leukemic leukocyte occurs contemporaneously with the appearance of tumor-specific antigens, and both phenomena are most likely related to neoplastic transformation. The following hypotheses are discussed as possible explanations of these phenomena: the possibility of true antigen deletion; the spreading out of membrane antigenic receptors as a consequence of increased cellular volume; the appearance of the TL antigen in the leukemic cells causing a partial loss of H-2 antigens.