## 1 Introduction  
The human body harbors a complex and diverse microbiota that colonizes nearly all organs, including the gastrointestinal tract, skin, and respiratory system. Bacterial cells are estimated to be present in numbers roughly equal to human cells [1]. While many of these microorganisms contribute to host health through mutualistic relationships, humans are also frequently exposed to pathogenic bacteria capable of establishing infections. The human host employs multiple strategies to curb bacterial infections, including physical barriers, immune responses, and antimicrobial molecules [2]. For example, the skin and mucosal surfaces serve as the first line of defense, preventing bacterial entry through tight junctions and mucus secretion, which entraps pathogens such as _Pseudomonas aeruginosa_[3]. Innate immune responses further combat infections through the production of antimicrobial peptides (AMPs) like defensins and cathelicidins, which disrupt bacterial membranes, effectively targeting pathogens such as _Staphylococcus aureus_[4, 5] and _Mycobacterium tuberculosis_ (Mtb) and also aid protection against viruses including HumanImmunodeficiency Virus (HIV) [6]. In addition, the complement system enhances bacterial clearance by opsonization, and membrane attack complex formation, particularly against _Neisseria meningitidis_[7]. Furthermore, the host cells limit bacterial growth by sequestering essential nutrients, a strategy known as nutritional immunity; for instance, lactoferrin and calprotectin bind iron and zinc to restrict the proliferation of uropathogenic strains of _Escherichia coli_ and _Klebsiella pneumoniae_ in the urinary tract [8; 9; 10]. Adaptive immunity further strengthens bacterial control through antibody production and T-cell-mediated responses, which are critical for long-term protection against Mtb [11]. These multilayered defense mechanisms collectively work to prevent bacterial infections and maintain host homeostasis. To circumvent these host defenses and ensure their survival inside the host and establish an infection, the bacterial pathogens have evolved sophisticated virulence factors and immune evasion strategies [12; 13; 14]. These include spatiotemporal expression of virulence factors as well as stress-responsive pathways that equip the pathogen with the necessary adaptations needed to colonize and persist within the host. In addition, bacterial pathogens often communicate with each other through chemical messengers, which are collectively called quorum sensing [15; 16; 17; 18]. Bacterial quorum sensing regulates group behaviors such as biofilm formation, virulence factor expression, and antibiotic resistance. By sensing and responding to host-derived signals, bacteria can coordinate adaptive responses that enhance colonization, persistence, and immune evasion. Finally, the bacteria have evolved a series of strategies to curb the effect of antibiotics including modification of the lipid bilayer, expression of efflux pumps, and the inhibition of antibiotic uptake systems [19; 20; 21]. Together, the bacteria have developed a sophisticated system to evade host immunity, and studying the molecular mechanisms behind these processes could lead to new therapeutic advancements. Although the role of various proteins in virulence of these pathogens have been well characterized, the importance of bacterial small regulatory RNA was only recognized in the last decade or so. Bacterial sRNAs are a diverse class of molecules, typically ranging from 40 to 500 nucleotides, that play essential roles in posttranscriptional gene regulation by interacting with target mRNAs or proteins. Initially categorized as small non-coding RNAs, only a handful of these sRNAs such as SgrS from enteric species, SR1 from _Bacillus subtilis_, Pel RNA from _Streptococcus pyogenes_, RNAIII, and Psm-Mec from _Staphylococcus aureus_ have been found to encode small peptides [22].