Bandita Dutta

Bacteria use quorum sensing (QS), a high-level signaling process employing autoinducer (AI) molecules, to control virulence, biofilm formation, and population-level behaviors. The process is crucial for both Gram-positive and Gram-negative bacteria, affecting their capacity to thrive in diverse environments. In addition, host-derived stress hormones play important roles in the pathogenicity of bacteria through enhanced growth, virulence, and immune evasion. Catecholamines act as siderophores that assist in the acquisition of iron and increase bacterial resistance. QS in Gram-negative bacteria is mediated by acyl-homoserine lactones that trigger synchronized gene expression at elevated cell density. In contrast, Gram-positive bacteria utilize a peptide-based signaling system for similar regulatory purposes. The disruption of QS by quorum-quenching mechanisms like enzymatic degradation of AI molecules, receptor antagonists, or the inhibition of gene activation are very promising avenues for controlling bacterial infections and antimicrobial resistance. Additionally, bacterial QS systems interact with host endocrine signaling, enabling pathogens to exploit stress-induced hormonal alterations for survival. This cross-kingdom communication underscores the need for targeted interventions, interfering with bacterial signaling without disrupting host–microbe homeostasis. It is critical to comprehend QS-host-derived hormone complex interaction in order to innovate novel anti-microbial strategies, particularly in the healthcare and aquaculture sectors, where bacterial infection poses a critical threat.

The interplay between the sugar-regulating hormones and the formation of biofilms has gained interest in recent decades. Hormones such as glucagon, insulin, epinephrine, cortisol and growth hormone (GH) aid in the modulation of biofilm formation by microbes. These hormones are primarily known for the maintenance of homoeostasis among humans, but they may also take part in influencing microbial pathogenesis and bacterial accumulation. This chapter deals with the way in which the levels of hormonal fluctuations, mainly in metabolic diseases like diabetes mellitus, can affect the development of biofilms, the expression of virulence factors, and the regulation of quorum sensing (QS) in bacterial cells. This chapter also refers to the change in microbiome that occurs due to the modification of hormonal levels within the human body. The conjunction of microbiology with endocrinology may open up new avenues for the study of the host–microbe interactions in another dimension, thereby developing interdisciplinary approaches for management of biofilm-associated infections among humans.

Biofilms, heterophilic microbial populations contained within a self-secreted extracellular polymeric matrix, are paradoxical due to their resistance to antibiotics and the immune system. Several factors, such as quorum-sensing molecules, environmental parameters, and scaffold proteins, control biofilm formation. Current research has emphasized an important intersection between peptide hormones, the main regulators of metabolic and physiological processes, and biofilm function. Hormones like insulin, somatostatin, natriuretic peptides, and others affect bacterial growth, virulence, and biofilm dynamics in both Gram-positive and Gram-negative species. Significantly, insulin and other peptide hormones have been reported to regulate biofilm formation in pathogens such as Pseudomonas aeruginosa and Escherichia coli, especially in chronic disease conditions like diabetes. Recent research indicates that some peptide hormones have inherent antimicrobial and antibiofilm activities, which can be potential candidates for novel therapeutics. In addition, the incorporation of the hormone-based approaches into medical device coatings provides opportunities in preventing biofilm-related infections. This chapter integrates existing knowledge on the mechanistic functions of peptide hormones in microbial biofilm control, their therapeutic applications, and their clinical implications.

Bacterial biofilms are sessile communities of microorganisms which pose a significant problem in clinical settings by resisting the antibiotics and host defense mechanisms. Recent studies have proclaimed the alteration of the bacterial biofilm formation by hormonal drugs, which has important implications for treatment outcomes. This chapter is mainly designated to discuss the impact of different hormonal drugs, like steroids, sex hormones, metabolic hormones, and gonadotropins in biofilm matrix formation for both Gram-positive and Gram-negative bacteria. Steroid drugs including glucocorticoids have been reported to increase the biofilm formation in pathogenic bacteria such as Staphylococcus aureus and Pseudomonas aeruginosa through suppressing host immune responses and inducing bacterial stress response pathways. Estrogen also increases the biofilm formation in Escherichia coli and Klebsiella pneumoniae resulting UTIs and in addition disrupts the biofilm of a protective bacteria Lactobacillus. Furthermore, drugs with thyroxine hormones are associated in the adherence and stability of bacterial biofilms leading to chronic infections. Bacterial biofilm formation is known to be facilitated by insulin especially in diabetic patients. Moreover, FSH and LH have been identified to induce biofilm formation in opportunistic pathogens thus increasing their pathogenicity. The knowledge of hormone-bacteria interactions is important in the design of effective hormonal drugs.