Abstract
The host immune response is critical in Pneumocystis pneumonia (PCP). Immunocompetent hosts can eliminate the fungus without symptoms, while immunodeficient hosts develop PCP with an unsuitable excessive inflammatory response leading to lung damage. From studies based on rodent models or clinical studies, this review aimed to better understand the pathophysiology of Pneumocystis infection by analysing the role of immune cells, mostly lymphocytes, according to the immune status of the infected host. Hence, this review first describes the immune physiological response in infected immunocompetent hosts that are able to eliminate the fungus. The objective of the second part is to identify the immune elements required for the control of the fungus, focusing on specific immune deficiencies. Finally, the third part concentrates on the effect of the different immune elements in immunocompromised subjects during PCP, to better understand which cells are detrimental, and which, on the contrary, are beneficial once the disease has started. This work highlights that the immune response associated with a favourable outcome of the infection may differ according to the immune status of the host. In the case of immunocompetency, a close communication between B cells and TCD4 within tertiary lymphocyte structures appears critical to activate M2 macrophages without much inflammation. Conversely, in the case of immunodeficiency, a pro-inflammatory response including Th1 CD4, cytotoxic CD8, NK cells, and IFNγ release seems beneficial for M1 macrophage activation, despite the impact of inflammation on lung tissue.
Highlights
Pneumocystis jirovecii pneumonia (PCP), otherwise known as pneumocystosis, remains nowadays one of the most frequent fungal infections in immunocompromised subjects with a worldwide prevalence of over 500,000 cases per year [1]
When rodents are infected with Pneumocystis sp through the respiratory tract, the Antigen Presenting Cells (APC) available in the lungs can recognise several wall or membrane compounds of the fungus, such as Major Surface Glycoprotein (MSG) or beta-D glucan (BDG)
A study performed on non-immuno-depressed patients with chronic bronchial disease colonized by P. jirovecii, showed an increase in the blood number of total lymphocytes and TCD4, confirming the results observed in the lungs and lymph nodes of infected immunocompetent mice [36]
Summary
Pneumocystis jirovecii pneumonia (PCP), otherwise known as pneumocystosis, remains nowadays one of the most frequent fungal infections in immunocompromised subjects with a worldwide prevalence of over 500,000 cases per year [1]. This micro-organism, initially identified as a protozoan parasite and designated as Pneumocystis carinii, has been classified as a fungus over the years and been renamed Pneumocystis jirovecii for the species infecting humans [3] This atypical fungus remains impossible to cultivate in vitro, slowing down progress in understanding PCP, including its pathophysiology. Humans and rodents notably share the dichotomous asymptomatic infection or interstitial pneumonia in immunocompetent or immunosuppressed hosts, respectively, and the type of immunosuppression at risk of PCP [4] Both clinical studies and rodent models underline a critical role of the host immune response in the disease. It focuses on specific immune deficiencies in human diseases or in rodent experiments and their consequences on Pneumocystis infection. It should be noted that the vast majority of these rodent experiments concern primary infections without any Pneumocystis-specific immunity, unlike most of the Pneumocystis infections in humans
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