Figure 5: Summary of mechanisms of adaptation to host lungs by Pneumocystis. | Nature Communications

Figure 5: Summary of mechanisms of adaptation to host lungs by Pneumocystis.

From: Genome analysis of three Pneumocystis species reveals adaptation mechanisms to life exclusively in mammalian hosts

Figure 5

Different mechanisms are highlighted by different colours. Potential mechanisms of uptake of nutrients (which cannot be synthesized de novo) include the use of plasma membrane-localized transporters (indicated by T), conversion of other metabolites scavenged from hosts (indicated by C), endocytosis (indicated by E) and unknown (indicated by U). §Potential uptake of haem or haemoglobin from lungs by endocytosis mediated by CFEM domain-containing proteins. *Cholesterol biosynthesis pathway is retained in P. jirovecii but lost in P. murina and P. carinii. ¶β-glucan is present in cysts and absent in trophic forms. β-glucan as well as chitin and mannan in other fungal pathogens are known pathogen-associated molecular patterns (PAMP) involved in host immune recognition; none of these components is detected in Pneumocystis organisms except for the presence of β-glucan in the cyst form (Figs 6 and 7; Supplementary Fig. 13). Pneumocystis is the only fungus identified to date that cannot synthesize chitin.

Back to article page