Biofilm has garnered a lot of interest due to concerns in various sectors such as public health, medicine, and the pharmaceutical industry. Biofilm-producing bacteria show a remarkable drug resistance capability, leading to an increase in morbidity and mortality. This results in enormous economic pressure on the healthcare sector. The development of biofilms is a complex phenomenon governed by multiple factors. Several attempts have been made to unravel the events of biofilm formation; and, such efforts have provided insights into the mechanisms to target for the therapy. Owing to the fact that the biofilm-state makes the bacterial pathogens significantly resistant to antibiotics, targeting pathogens within biofilm is indeed a lucrative prospect. The available drugs can be repurposed to eradicate the pathogen, and as a result, ease the antimicrobial treatment burden. Biofilm formers and their infections have also been found in plants, livestock, and humans. The advent of novel strategies such as bioinformatics tools in treating, as well as preventing, biofilm formation has gained a great deal of attention. Development of newfangled anti-biofilm agents, such as silver nanoparticles, may be accomplished through omics approaches such as transcriptomics, metabolomics, and proteomics. Nanoparticles’ anti-biofilm properties could help to reduce antimicrobial resistance (AMR). This approach may also be integrated for a better understanding of biofilm biology, guided by mechanistic understanding, virtual screening, and machine learning in silico techniques for discovering small molecules in order to inhibit key biofilm regulators. This stimulated research is a rapidly growing field for applicable control measures to prevent biofilm formation. Therefore, the current article discusses the current understanding of biofilm formation, antibiotic resistance mechanisms in bacterial biofilm, and the novel therapeutic strategies to combat biofilm-mediated infections.

Autophagy is a lysosomal protein degradation system that eliminates cytoplasmic components such as protein aggregates, damaged organelles, and even invading pathogens. Autophagy is an evolutionarily conserved homoeostatic strategy for cell survival in stressful conditions and has been linked to a variety of biological processes and disorders. It is vital for the homeostasis and survival of renal cells such as podocytes and tubular epithelial cells, as well as immune cells in the healthy kidney. Autophagy activation protects renal cells under stressed conditions, whereas autophagy deficiency increases the vulnerability of the kidney to injury, resulting in several aberrant processes that ultimately lead to renal failure. Renal fibrosis is a condition that, if chronic, will progress to end-stage kidney disease, which at this point is incurable. Chronic Kidney Disease (CKD) is linked to significant alterations in cell signaling such as the activation of the pleiotropic cytokine transforming growth factor-β1 (TGF-β1). While the expression of TGF-β1 can promote fibrogenesis, it can also activate autophagy, which suppresses renal tubulointerstitial fibrosis. Autophagy has a complex variety of impacts depending on the context, cell types, and pathological circumstances, and can be profibrotic or antifibrotic. Induction of autophagy in tubular cells, particularly in the proximal tubular epithelial cells (PTECs) protects cells against stresses such as proteinuria-induced apoptosis and ischemia-induced acute kidney injury (AKI), whereas the loss of autophagy in renal cells scores a significant increase in sensitivity to several renal diseases. In this review, we discuss new findings that emphasize the various functions of TGF-β1 in producing not just renal fibrosis but also the beneficial TGF-β1 signaling mechanisms in autophagy.

Breast cancer (BC) is one of the most common types of cancer in women. Triple-negative breast cancer (TNBC), characterized by the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), exhibits a highly aggressive phenotype with increased metastasis and resistance to conventional treatments. Nanocarrier technology is consistently employed to overcome limitations associated with traditional breast cancer therapy. The targeted drug delivery approach using nanocarriers enhances bioavailability, prolongs circulation, and facilitates effective drug accumulation at the tumor site through active or passive targeting. Currently, the FDA has approved a few nanocarrier systems, and numerous nano formulations are undergoing preclinical and clinical development for breast cancer targeting. Common nanocarrier types include polymeric micelles, microemulsions, magnetic microemulsions, liposomes, dendrimers, carbon nanotubes, and magnetic nanoparticles (NPs). This review extensively explores the targeting potential of nanocarriers in breast cancer. This study will provide a concise summary of current advances in treatment of breast cancer and diagnostics.

Background: Probiotics have been found to be beneficial for human beings through the modulation of intestinal bacteria and inhibition of pathogens. In light of the increased prevalence of multidrug resistant uropathogens, there is a need for alternative therapies than antibiotics. Objectives: This study assessed the capacity of three probiotics (Lactobacillus acidophilus, Lactic Acid Bacillus and Probiotic Consortium) to inhibit three important uropathogens; Escherichia coli, Klebsiella and Staphylococcus aureus with a view of understanding their antibacterial mechanism of action. Methods: In vitro co-cultures were set up to monitor the growth of the pathogens, the development of biofilms and acidification of the culture media for 24 hours. Biofilm biomass inhibition was assessed using crystal violet microtiter plate assays. The molecular responses to probiotics of Escherichia coli was also assessed by analysis of transcriptomics of cell envelope stress genes (omp) and molecular chaperones (dnaK, chap). Results: The efficacy of biofilm inhibition was highly strain-dependent, such that Lactobacillus acidophilus always showed significantly greater broad spectrum biofilm inhibition than both the probiotic consortium and Lactic Acid Bacillus. Escherichia coli Biofilm Inhibition: L. acidophilus gave the highest inhibition of 66.67%, whereas the probiotic consortium inhibited 59.05% of the biofilms and Lactic Acid Bacillus 3.81%. Klebsiella Biofilm Inhibition: The best biofilm inhibition was observed with L. acidophilus with 78.00% compared to the probiotic consortium (61.11%) and Lactic Acid Bacillus (42.50%). Staphylococcus aureus Biofilm Inhibition: L. acidophilus showed maximal biofilm inhibition of 69.09% compared to 54.55% inhibition from the probiotic consortium. Inhibition showed high correlation with medium acidification and antimicrobial metabolite production. Transcriptome analysis: treatment with L. acidophilus caused severe cell envelope stress in E. coli (5.4-fold increase in expression of omp) and impaired intracellular stress response in E. coli with the inhibition of molecular chaperone (dnaK -4.0-fold and chap -2.6-fold. Conclusion: Lactobacillus acidophilus is a strong broad spectrum antibiofilm agent that targets Gram-negative and Gram-positive uropathogens. Antimicrobial activity of this bacterium is exerted through acidification, metabolite production, cell envelope stress induction, and regulation of stress response mechanisms.

Nowadays, acute kidney damage (AKI) is seen as a serious public health risk. Exposure to lipopolysaccharide (LPS), the primary outer membrane component of Gram-negative bacteria, causes a significant increase in AKI that is generated by sepsis. In this work, we attempted to show how LPS affects the kidneys by creating a mouse model of AKI generated by LPS. Three different dosages of LPS were injected: 125ug/kg (i.p.), 250ug/kg (i.p.), and 1 mg/kg (i.p.). The experiment was completed after 24 hours. Mice exposed to LPS had different BUN responses at the same dosages. Significant LPS-induced damage was seen in the kidney tissue, including renal tubules that had epithelial cell degeneration and necrosis, tubules that showed total obliteration or enlargement, blood vessel congestion, and a slight thickening of the glomerular basement membrane, overall, a perfect AKI model with unusual BUN levels in kidney injury resistant mice model. The expression of core autophagy genes in the kidneys showed distinct patterns during LPS-induced AKI: ATG5 and Beclin 1 levels decreased, indicating inhibition of autophagic initiation, but LC3B levels remained unchanged. On the other hand, there was a significant increase in ATG4 expression (p < 0.001). Dysregulation resulting in a deficient autophagic flux during AKI development is indicated by this imbalance, which showed a drop in initiation components and an increase in processing components (ATG4). Based on the blood chemistry, histopathological findings, and autophagy genes expression, this study prompts future researchers to modify the LPS dosage as well as animal strain (BALB/c) which is a resistant strain for kidney damage and its impact on autophagy.

Chronic obstructive pulmonary disease (COPD) is a prevalent and debilitating condition with significant social and public health implications due to its high morbidity and mortality rates. The World Health Organization recognizes COPD as a major global health challenge. Despite extensive research, the complex pathophysiology of COPD has hindered the development of precise treatments. Recent advancements in understanding the gut-lung axis and immunological mechanisms have opened new avenues for COPD management. This review delves into the pathophysiological aspects of COPD, highlighting the interplay between genetic predispositions, environmental exposures, and lifestyle factors. It emphasizes the critical role of the gut-lung axis in modulating pulmonary immunity and disease progression, presenting dysbiosis as a key factor exacerbating inflammation and COPD symptoms. Emerging therapeutic approaches, including the modulation of gut microbiota through probiotics, prebiotics, and dietary changes, show promise in improving COPD outcomes. Additionally, advancements in immunotherapies, such as monoclonal antibodies targeting specific cytokines and immune checkpoint inhibitors, offer the potential for reducing inflammation and enhancing lung function. Precision medicine, which customizes treatment based on individual genetic, environmental, and lifestyle factors, represents a significant stride toward more effective COPD management. This review also identifies crucial research gaps, such as the need for a comprehensive understanding of non-smoking-related COPD, reliable biomarkers for early diagnosis, and the long-term effects of novel therapies. Future research can pave the way for innovative therapeutic strategies and improved patient care by addressing these gaps. This comprehensive analysis underscores the importance of an integrative approach to COPD, combining pathophysiological insights, immunological perspectives, and cutting-edge therapies to enhance the quality of life for individuals affected by this chronic disease.