Immune Responses to Pseudomonas aeruginosa Biofilm Infections - PubMed (original) (raw)

Review

Immune Responses to Pseudomonas aeruginosa Biofilm Infections

Claus Moser et al. Front Immunol. 2021.

Abstract

Pseudomonas aeruginosa is a key pathogen of chronic infections in the lungs of cystic fibrosis patients and in patients suffering from chronic wounds of diverse etiology. In these infections the bacteria congregate in biofilms and cannot be eradicated by standard antibiotic treatment or host immune responses. The persistent biofilms induce a hyper inflammatory state that results in collateral damage of the adjacent host tissue. The host fails to eradicate the biofilm infection, resulting in hindered remodeling and healing. In the present review we describe our current understanding of innate and adaptive immune responses elicited by P. aeruginosa biofilms in cystic fibrosis lung infections and chronic wounds. This includes the mechanisms that are involved in the activation of the immune responses, as well as the effector functions, the antimicrobial components and the associated tissue destruction. The mechanisms by which the biofilms evade immune responses, and potential treatment targets of the immune response are also discussed.

Keywords: Pseudomonas aeruginosa; adaptive immune response; biofilm infections; innate immune response; novel treatment possibilities.

Copyright © 2021 Moser, Jensen, Thomsen, Kolpen, Rybtke, Lauland, Trøstrup and Tolker-Nielsen.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1

Figure 1

Schematic presentation of biofilm stages and host response. Applies for non-foreign body-related biofilm infections, which is the main focus of the present review. Modified from Moser et al. (5) with permission from John Wiley & Sons, Inc.

Figure 2

Figure 2

Local immune response to infectious P. aeruginosa biofilm. The innate immune response recognizes pathogen associated molecular patterns (PAMPs) expressed on P. aeruginosa, and biofilm-associated molecular patterns (BAMPs) present in the biofilm matrix. Detection of BAMPs and PAMPs by PMNs and macrophages is mediated by pattern recognition receptors (PRRs). Binding of BAMPs and PAMPs to PRRs stimulates the PMNs and macrophages resulting in consumption of O2 for liberation of tissue-toxic reactive oxygen species (ROS) and nitric oxide (NO). Additional responses by the PMNs include secretion of proteases that may cause proteolytic tissue lesions while the macrophage may further enhance the inflammation by emitting pro-inflammatory cytokines such as TNF-α, Il-1, IL-6, IL-8, and IL-12. The effector cells of the adaptive immune response mainly reside distantly such as the T-cells and the B-cells in the secondary lymphoid organs and the plasma cells in the bone marrow. Activated T-cells may release cytokines that further reinforces the inflammation by stimulating the accumulation and activation of PMNs and production of IgG. The contribution of the increased accumulation of activated PMNs to the local inflammation is further accelerated by binding of antigens to IgG, leading to immune complex mediated stimulation of the PMNs and activation of the classical complement pathway.

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