Abstract

Mucosal bacterial infections pose a significant global health burden, affecting various anatomical sites such as the respiratory, gastrointestinal, and genitourinary tracts. Understanding the mechanisms by which bacteria interact with the mucosal surfaces and elicit immune responses is crucial for developing effective therapeutic strategies. This abstract provides a concise overview of the current knowledge regarding mucosal bacterial infections, including the pathogenesis, host immune responses, and emerging therapeutic approaches. Mucosal surfaces serve as the primary entry points for bacterial pathogens, which exploit host colonization and invasion strategies to establish infection. The interactions between bacteria and the mucosa involve adhesion, colonization, and subsequent evasion of host defenses, leading to tissue damage and inflammation. Bacterial factors, such as virulence factors, adhesins, and toxins, play critical roles in the pathogenesis of mucosal infections. The host immune response to mucosal bacterial infections is multifaceted and involves both innate and adaptive immune components. Epithelial cells at the mucosal surfaces act as physical barriers and secrete antimicrobial peptides, mucus, and immunoglobulins to limit bacterial invasion. Innate immune cells, such as macrophages, neutrophils, and dendritic cells, recognize and phagocytose bacteria, initiating pro-inflammatory responses. Furthermore, adaptive immune cells, including T and B lymphocytes, generate specific immune responses, resulting in the production of antibodies and memory cells that confer protection against future infections. Despite the existence of host defense mechanisms, bacterial pathogens have evolved various mechanisms to evade or subvert the immune response, contributing to chronic infections and disease progression. Understanding these immune evasion strategies is crucial for the development of novel therapeutic approaches. Recent advances in mucosal immunology research have identified potential targets for intervention, including the modulation of host immune responses, inhibition of bacterial adhesion and colonization, and the development of vaccines targeting specific bacterial antigens.