β-Glucans, <em>Pneumocystis jirovecii</em> and Atherogenic Inflammation: From Pulmonary Immunity to Cardiovascular Risk

The interaction between Pneumocystis jirovecii and systemic inflammation has emerged as a potential modulator of cardiovascular risk. This review describes the potential of β-glucans to contribute to atherogenic inflammation. A narrative review was developed on the PubMed/MEDLINE, Scopus, Web of Science and Google Scholar databases. The inflammatory pathways induced by β-glucans from P. jirovecii contrast with the immunometabolic effects of dietary β-glucans. The relevance of serum (1→3)-β-D-glucans as a marker of systemic exposure was also described. P. jirovecii β-glucans activate Syk–CARD9–NFκB, MAPK and STAT3 signalling pathways. This signalling promotes proinflammatory monocyte/macrophage polarization and a systemic microenvironment of low-grade inflammation with proatherogenic potential. The serum persistence of (1→3)-β-D-glucan indicates prolonged exposure, even in the absence of overt clinical manifestations of colonisation. Conversely, dietary β-glucans have been observed to elicit regulatory effects facilitated by microbiota and metabolism. Using murine models and cell systems, a causal link has been established between fungal β-glucans and atherosclerosis. P. jirovecii β-glucans act as immunological mediators capable of amplifying pulmonary and systemic inflammation, constituting a possible modulator of cardiovascular risk. Distinguishing between fungal and dietary β-glucans is imperative for comprehending emerging mechanisms of vascular inflammation.