Abstract
The lung is under constant pressure to protect the body from invading bacteria. An effective inflammatory immune response must be tightly orchestrated to ensure complete clearance of any invading bacteria, while simultaneously ensuring that inflammation is kept under strict control to preserve lung viability. Chronic bacterial lung infections are seen as a major threat to human life with the treatment of these infections becoming more arduous as the prevalence of antibiotic resistance becomes increasingly commonplace. In order to survive within the lung bacteria target the host immune system to prevent eradication. Many bacteria directly target inflammatory cells and cytokines to impair inflammatory responses. However, bacteria also have the capacity to take advantage of and strongly promote anti-inflammatory immune responses in the host lung to inhibit local pro-inflammatory responses that are critical to bacterial elimination. Host cells such as T regulatory cells and myeloid-derived suppressor cells are often enhanced in number and activity during chronic pulmonary infection. By increasing suppressive cell populations and cytokines, bacteria promote a permissive environment suitable for their prolonged survival. This review will explore the anti-inflammatory aspects of the lung immune system that are targeted by bacteria and how bacterial-induced immunosuppression could be inhibited through the use of host-directed therapies to improve treatment options for chronic lung infections.
Highlights
The respiratory tract is in constant contact with a myriad of bacterial species
There are still major gaps in our understanding of how Bregs and their immunosuppressive effects are being hijacked by pulmonary bacteria, it seems likely that these cells are important in suppressing inflammatory immune responses in the lung through their production of the anti-inflammatory cytokines IL-10 and potentially IL-35
In a murine model of M. bovis pulmonary infection the inhibition of TGF-β by the administration of latency associated peptide (LAP) inhibited TGF-β activity in the lung, enhanced IFN-γ production and improved antigen-specific effector T cell responses in cells isolated from mediastinal lymph nodes of mice administered with LAP compared to PBS-treated mice
Summary
The respiratory tract is in constant contact with a myriad of bacterial species. To maintain homeostasis the healthy lung must efficiently and precisely identify friend from foe, and defend from infection without any long lasting inflammation or immunopathology occurring. By promoting tolerogenic phenotypes of AMs and DCs in the lung bacteria can promote early IL10 production and reduced antigen-presentation resulting in the prevention of effective protective pro-inflammatory adaptive responses leading to undisturbed bacterial growth. There are still major gaps in our understanding of how Bregs and their immunosuppressive effects are being hijacked by pulmonary bacteria, it seems likely that these cells are important in suppressing inflammatory immune responses in the lung through their production of the anti-inflammatory cytokines IL-10 and potentially IL-35.
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