order Go 6976 Biofilm formation is one of the ways S aureus
Biofilm formation is one of the ways S. aureus expresses its pathogenesis through the colonization of infection sites. In the current study, results (Figure 2) showed that S. aureus (control) was able to form a biofilm throughout the 60 hours of incubation. Growth pattern of the biofilm was in good agreement with the results of a previous study, which suggested that the biofilm established itself in the first 24 hours of incubation prior to reaching a state of dynamic equilibrium. After 24 hours of incubation, cyclical maturation and dispersal of the biofilm took place as the biofilm reached a critical mass, eventually unable to sustain the bacteria encased within the matrix. Bacteria on the outermost layers of the biofilm would then dissociate from it, leading to better availability of nutrients to stimulate further growth until the condition became favorable for the bacteria to form the biofilm again, which occurred at 60 hours in this study.
Results of this study (Figure 2) successfully proved that LAB extracts can inhibit the biofilm formation of S. aureus; the growth of biofilm in the presence of L. bulgaricus FTDC 8611 (A30) CFS was significantly lower (p < 0.05) than that in the presence of a control. Antimicrobial compounds in the CFS were believed to work synergistically to halt the growth of the pathogen and even cause death in the cells, rendering the aggregation of order Go 6976 to form the biofilm unsuccessful. Bacteriocins produced by LAB may alter the physical and chemical conditions of the culture conditions, and thus development of the biofilm becomes unfavourable.
In conclusion, results of the present study illustrated that LAB have the ability to synthesize antimicrobial compounds that can inhibit the growth of the pathogen S. aureus. The biofilm formed by S. aureus was successfully inhibited by the extracellular extracts of LAB, proving that LAB can serve as a potential alternative in dermatological applications.
Acknowledgments This work was financially supported by the Science Fund grant (305/PTEKIND/613222), provided by the Malaysian Ministry of Science, Technology and Innovation (MOSTI); Fundamental Research Grant Scheme (FRGS) grant (203/PTEKIND/6711239), provided by the Malaysian Ministry of Higher Education (MOHE); Universiti Sains Malaysia (USM) Research University (RU) grants (1001/PKIMIA/855006, 1001/PTEKIND/815085); BioAsie grant, provided by the French Government under the Bio-Asia Program; and USM Fellowship provided by Universiti Sains Malaysia.
Introduction Primary cutaneous lymphomas represent a rare heterogeneous entity of T- and B-cell lymphomas, with mycosis fungoides (MF) comprising the majority of cases. MF accounts for 65% of cutaneous T-cell lymphoma (CTCL). MF is characterized by an indolent clinical course, a long-term evolution, and typical manifestations in the patch-or-plaque stage, with variable progression to the tumor stage and erythroderma. Approximately 30% of patients present with cutaneous tumors or erythroderma at disease onset. A confident diagnosis of MF needs to take both clinical and histopathologic findings into consideration. Characteristic histopathologic and immunohistochemical features include skin-homing CD4+ lymphocytes with epidermotropism or formation of Pautrier\'s microabscesses, cytologically atypical lymphocytes with hyperchromatic, cerebriform or vesicular nuclei, a band-like upper dermal infiltration of cytologically atypical cells, and papillary dermal fibrosis. Several epidemiologic and laboratory factors were previously reported to correlate with poor prognosis in patients with MF including male sex, advanced disease age, blood eosinophilia, elevated serum lactate dehydrogenase (LDH) levels, and advanced stages. Histopathologic variables that correlated with poor prognosis include follicular mucinosis, folliculotropic variant, moderate-to-marked dermal lymphocyte atypia, large-sized Pautrier\'s microabscesses with more than 10 atypical lymphocytes per cluster, and diminished proportion of CD7+ and CD8+ cells in the dermal infiltrate.