Modulation of macrophage survival during Klebsiella pneumoniae infections

<i>Klebsiella pneumoniae</i>, a facultative anaerobe and Gram-negative bacterium, has high clinical significance in public health concerns. <i>K. pneumoniae</i> is given its name in recognition of the German-Swiss microbiologist Edwin Klebs. Carl Friedlander first identified <i>K. pneumoniae</i> as a bacterium isolated from the lungs of individuals who had died from pneumonia. <i>K. pneumoniae</i> is a prominent member of the <i>Enterobacteriaceae</i> family, an opportunistic pathogen, and one of the pathogens sweeping the world in the antibiotic resistance pandemic. This organism accounts for approximately one-third of all Gram-negative infections, including pneumonia, urinary tract infections, liver abscesses, and bacteremia. Classically, these infections commonly occur in individuals who are hospitalized or immunocompromised and regularly treated with <i>β</i>-lactams along with other antibiotics effective against <i>Enterobacteriaceae</i>. Unfortunately, the emergence of multidrug-resistant infections in patients treated at intensive care units (ICUs) has been a serious problem faced by clinicians globally. <i>K. pneumoniae</i> has been recently added to the critical list of microorganisms by the World Health Organization (WHO), highlighting the urgent requirement for new therapeutic options to combat this bacterium. Developing new therapeutic interventions requires a comprehensive understanding of host-pathogen interactions and the role of immune cells in clearing the bacteria. To that end, macrophages play a crucial role in safeguarding our body against infectious agents, as well as contributing to processes such as pathogen clearance and tissue homeostasis. Calcium, a secondary messenger, refines the macrophage protective responses and influences cell survival. Many pathogens have evolved tactics to circumvent the innate immune clearance mechanisms exerted by macrophages. Therefore, this review will focus on the modulation of macrophage innate immune responses and survival upon <i>K. pneumoniae</i> infection.