Pulmonary infections caused by Pseudomonas aeruginosa and Acinetobacter baumannii pose significant clinical challenges, especially in immunocompromised and critically ill patients. These ESKAPE Gram-negative bacteria are notorious for their intrinsic and acquired resistance to antibiotics, leading to high morbidity and mortality rates. The lung, as the primary site of infection, faces a complex interplay between the invading pathogens and the host's innate immune system. Understanding the intricacies of this interaction, particularly the early recognition and response mechanisms, is crucial for developing effective therapeutic strategies. This Research Topic aims to explore the latest advancements in our understanding of innate immune responses to these pathogens in the pulmonary environment.

Despite advancements in critical care, multidrug-resistant P. aeruginosa and A. baumannii pathogens continue to exploit vulnerabilities in the host's innate immune system, resulting in severe lung damage and systemic complications. Our goal is to consolidate and expand knowledge on the mechanisms by which the innate immune system, including alveolar macrophages, neutrophils, and epithelial cells, recognizes and responds to these bacteria. We seek to highlight recent advances in understanding pattern recognition receptor signaling, cytokine and chemokine production, and the role of cellular effectors like NETs in controlling these infections. By focusing on the dynamic interplay between pathogen virulence factors and host defense mechanisms, we aim to identify novel therapeutic targets and strategies to enhance innate immunity and improve patient outcomes.

This Research Topic focuses on the innate immune responses to P. aeruginosa and A. baumannii specifically within the lung. Authors are invited to submit original research articles, reviews, mini-reviews, and perspectives that contribute to a deeper understanding of this critical area of research. We welcome submissions that address the following themes:

• Mechanisms of pathogen recognition by pulmonary innate immune cells (e.g., TLRs, NLRs, CLRs).
• Role of alveolar macrophages, neutrophils in the initial response.
• Formation and function of neutrophil extracellular traps (NETs) in the lung.
• Lung epithelial cells utilized in vitro as infection models.
• Cytokine and chemokine signaling pathways involved in pulmonary inflammation.
• Impact of bacterial virulence factors on innate immune evasion.

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ESKAPE Gram-negative bacteria