About this Research Topic
Lower respiratory tract infections caused by bacteria in hospital settings constitute a major concern worldwide because they cause a high mortality and there are limited therapeutic tools available. Gram-negative bacteria such as Acinetobacter baumanii, Pseudomonas aeruginosa, Klebsiella pneumoniae and other Enterobacteriaceae are important pathogens. Furthermore, treatment is increasingly difficult due to the widespread dissemination of antimicrobial resistance genes.
Once these bacteria transit the respiratory tract to reach the alveolar space, an immune response characterized by the rapid recruitment and activity of phagocytes such as neutrophils and monocytes, and the fast activity of the complement system, is coordinated in order to eliminate the invading pathogen. Although a robust immune response is critical for bacterial elimination and host survival, the response must be tightly regulated to prevent excessive lung injury caused by the action of the immune system, which can contribute to lung damage and host death.
An efficient immune response is characterized by a balanced immune response with both pro-inflammatory factors that promote the clearance of the pathogenic bacteria and by anti-inflammatory factors that assures lung integrity. However, host immune deficiencies that can break this balance, leading to higher susceptibility to infections that can translate into chronic and persistent infections or hyper-inflammatory syndromes with high mortality.
In this Research Topic, we invite the authors to submit manuscripts aimed to (I) identify and describe new genetic, as well as acquired deficiencies in humans that impair the innate immune response against Gram-negative bacteria; and (II) to study the cellular and molecular mechanisms by which host factors participate in the immune response during acute lung infections caused by Gram-negative bacteria in mouse models.
Hence, the scope of this Research Topic is to provide novel and compelling evidence regarding the regulatory mechanisms that allow the development of an efficient immune response during pulmonary Gram-negative bacteria infections with particular focus on:
- The identification of host and microbial factors that promote the expansion of anti-inflammatory phenotypes in innate cells.
- The identification and study of novel anti-inflammatory molecules produced by innate cells in order to modulate the pro-inflammatory response.
- The study of host and microbial factors that mediate the activation, modulation and evasion of the complement system.
- The discovery of new mechanisms used by pathogens to amplify lung inflammation, as well as the host molecules that counteract this phenomenon.
The submission of Original Research, Brief Research Report, Review and Mini Review articles that cover these topics are welcome.
Once these bacteria transit the respiratory tract to reach the alveolar space, an immune response characterized by the rapid recruitment and activity of phagocytes such as neutrophils and monocytes, and the fast activity of the complement system, is coordinated in order to eliminate the invading pathogen. Although a robust immune response is critical for bacterial elimination and host survival, the response must be tightly regulated to prevent excessive lung injury caused by the action of the immune system, which can contribute to lung damage and host death.
An efficient immune response is characterized by a balanced immune response with both pro-inflammatory factors that promote the clearance of the pathogenic bacteria and by anti-inflammatory factors that assures lung integrity. However, host immune deficiencies that can break this balance, leading to higher susceptibility to infections that can translate into chronic and persistent infections or hyper-inflammatory syndromes with high mortality.
In this Research Topic, we invite the authors to submit manuscripts aimed to (I) identify and describe new genetic, as well as acquired deficiencies in humans that impair the innate immune response against Gram-negative bacteria; and (II) to study the cellular and molecular mechanisms by which host factors participate in the immune response during acute lung infections caused by Gram-negative bacteria in mouse models.
Hence, the scope of this Research Topic is to provide novel and compelling evidence regarding the regulatory mechanisms that allow the development of an efficient immune response during pulmonary Gram-negative bacteria infections with particular focus on:
- The identification of host and microbial factors that promote the expansion of anti-inflammatory phenotypes in innate cells.
- The identification and study of novel anti-inflammatory molecules produced by innate cells in order to modulate the pro-inflammatory response.
- The study of host and microbial factors that mediate the activation, modulation and evasion of the complement system.
- The discovery of new mechanisms used by pathogens to amplify lung inflammation, as well as the host molecules that counteract this phenomenon.
The submission of Original Research, Brief Research Report, Review and Mini Review articles that cover these topics are welcome.
Keywords: Lung bacterial infection, Innate Immunity, Immune response dysregulation, Immunomodulation, Host genetic deficiencies
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
