PMC:4503824 / 9129-10392 JSONTXT

{"project":"2_test","denotations":[{"id":"25498576-7642263-43267766","span":{"begin":113,"end":117},"obj":"7642263"},{"id":"25498576-18159253-43267767","span":{"begin":378,"end":382},"obj":"18159253"},{"id":"25498576-19451250-43267768","span":{"begin":750,"end":754},"obj":"19451250"},{"id":"25498576-22547543-43267769","span":{"begin":956,"end":960},"obj":"22547543"},{"id":"25498576-19451250-43267769","span":{"begin":956,"end":960},"obj":"19451250"},{"id":"25498576-24478083-43267770","span":{"begin":1257,"end":1261},"obj":"24478083"}],"text":"SP-A and SP-D are known to bind viral, bacterial and fungal pathogens, including C. neoformans (Schelenz et al., 1995). SP-A and SP-D bind both acapsular and encapsulated C. neoformans but the effect of binding differs. SP-A bound to encapsulated yeast was not beneficial to the host, as a murine SP-A knockout model showed no difference in survival to wild type (Giles et al., 2007). This suggests that SP-A will have little effect once C. neoformans has induced capsule synthesis and may be one mechanism by which the cryptococcal capsule promotes virulence through blocking the action of SP-A. Similarly, SP-D can bind both acapsular and encapsulated yeast but there is only increased phagocytosis of acapsular yeast in vivo (Geunes-Boyer et al., 2009). There is evidence that SP-D promotes virulence of encapsulated C. neoformans as SP-D knock-out mice were better able to control cryptococcal infection than wild-type mice (Geunes-Boyer et al., 2012, 2009). Two possible explanations for this are that SP-D protects cryptococci from macrophage mediated degradation (so far only demonstrated in vitro) and that SP-D promotes the recruitment of eosinophils that may be detrimental to the control and clearance of pulmonary cryptococcosis (Holmer et al., 2014)."}