Strategies of Vibrio parahaemolyticus to acquire nutritional iron during host colonization

Iron is an essential element for the growth and development of virtually all living organisms. As iron acquisition is critical for the pathogenesis, a host defense strategy during infection is to sequester iron to restrict the growth of invading pathogens. To counteract this strategy, bacteria such as Vibrio parahaemolyticus have adapted to such an environment by developing mechanisms to obtain iron from human hosts. This review focuses on the multiple strategies employed by V. parahaemolyticus to obtain nutritional iron from host sources. In these strategies are included the use of siderophores and xenosiderophores, proteases and iron-protein receptor. The host sources used by V. parahaemolyticus are the iron-containing proteins transferrin, hemoglobin and hemin. The implications of iron acquisition systems in the virulence of V. parahaemolyticus are also discussed

Antitumor activity of bovine lactoferrin and its derived peptides against HepG2 liver cancer cells and Jurkat leukemia cells

Liver cancer and leukemia are the fourth and first causes, respectively, of cancer death in children and adults worldwide. Moreover, cancer treatments, although beneficial, remain expensive, invasive, toxic, and affect the patient’s quality of life. Therefore, new anticancer agents are needed to improve existing agents. Because bovine lactoferrin (bLF) and its derived peptides have antitumor properties, we investigated the anticancer effect of bLF and LF peptides (LFcin17-30, LFampin265-284 and LFchimera) on liver cancer HepG2 cells and leukemia Jurkat cells. HepG2 and Jurkat cells were incubated with bLF and LF peptides. Cell proliferation was quantified by an MTT assay, and cell morphology and damage were visualized by light microscopy or by phalloidin-TRITC/DAPI staining. The discrimination between apoptosis/necrosis was performed by staining with Annexin V-Alexa Fluor 488 and propidium iodide, and the expression of genes related to apoptosis was analyzed in Jurkat cells. Finally, the synergistic interaction of bLF and LF peptides with cisplatin or etoposide was assessed by an MTT assay and the combination index. The present study demonstrated that bLF and LF peptides inhibited the viability of HepG2 and Jurkat cells, inducing damage to the cell monolayer of HepG2 cells and morphological changes in both cell lines. bLF, LFcin17-30, and LFampin265-284 triggered apoptosis in both cell lines, whereas LFchimera induced necrosis. These results suggested that bLF and LF peptides activate apoptosis by increasing the expression of genes of the intrinsic pathway. Additionally, bLF and LF peptides synergistically interacted with cisplatin and etoposide. In conclusion, bLF and LF peptides display anticancer activity against liver cancer and leukemia cells, representing an alternative or improvement in cancer treatment

Outbreak of Serratia marcescens in the Neonatal Intensive Care Unit of a Tertiary Care Hospital in Mexico

Introduction. We describe an outbreak of Serratia marcescens (S. marcescens) infection in the neonatal intensive care unit at Women’s Hospital in Sinaloa, Mexico. Methods. In April 2021, an outbreak of S. marcescens infection was identified. A case was identified as any patient who tested positive for S. marcescens and showed signs of an infectious process. Results. S. marcescens was isolated from the blood cultures of 15 neonates with clinical signs of neonatal sepsis. Statistical analysis showed that all neonates had an invasive medical device. The problem was controlled after hospital hygiene and sanitation measures were strengthened. Conclusion. The study provides evidence of an outbreak of nosocomial bacteremia due to the cross-transmission of S. marcescens. The findings highlight the need for hospitals to implement strict hygiene measures, especially regarding hand washing, to prevent future outbreaks

Association of <i>PCSK1</i> and <i>PPARG1</i> Allelic Variants with Obesity and Metabolic Syndrome in Mexican Adults

Metabolic diseases, including obesity, diabetes, and metabolic syndrome, are among the most important public health challenges worldwide. Metabolic diseases are classified as multifactorial diseases in which genetic variants such as single-nucleotide polymorphisms (SNPs) may play an important role. The present study aimed to identify associations linking allelic variants of the PCSK1, TMEM18, GPX5, ZPR1, ZBTB16, and PPARG1 genes with anthropometric and biochemical traits and metabolic diseases (obesity or metabolic syndrome) in an adult population from northwestern Mexico. Methods: Blood samples were collected from 523 subjects, including 247 with normal weight, 276 with obesity, and 147 with metabolic syndrome. Anthropometric and biochemical characteristics were recorded, and single-nucleotide polymorphisms (SNPs) were genotyped by real-time PCR. Results: PCSK1 was significantly (p GPX5 was significantly associated with HDL cholesterol levels. In addition, PCSK1 was associated with obesity (p = 1.0 × 10−4) and metabolic syndrome (p = 3.0 × 10−3), whereas PPARG1 was associated with obesity (p = 0.044). Conclusions: The associations found in this study, mainly between allelic variants of PCSK1 and metabolic traits, obesity, and metabolic syndrome, may represent a risk for developing metabolic diseases in adult subjects from northwestern Mexico