Surfactant protein A limits Pneumocystis murina infection in immunosuppressed C3H/HeN mice and modulates host response during infection

Characterization of a Distinct Host Response Profile to Pneumocystismurina Asci during Clearance of Pneumocystis Pneumonia

“…Cells in the BALF were enumerated on a Z2 Coulter Counter (Beckman Coulter, Hialeah, FL). Slides for differential counting of the leukocyte subsets were prepared from BALF using a Cytospin II (Thermo Shandon, Inc., Pittsburgh, PA) to concentrate a standard volume, as previously described (42). Cells were stained with modified Wright-Giemsa stain, and the percentages of macrophages, lymphocytes, eosinophils, and neutrophils were determined by counting a total of 200 cells on each slide.…”

Hypobaric hypoxia-related impairment of pulmonary surfactant proteins A and D did not favourPneumocystis cariniiFrenkel 1999 growth in non-immunocompromised rats

“…In a transgenic SP-D-overexpression mouse model, which developed PcP after antibody-induced CD4 + -cell depletion and inoculation of P. murina Keely et al 2004, it was observed that both P. murina infection and lung inflammatory changes were increased (Vuk-Pavlovic et al, 2006). With regard with SP-A, in the pulmonary lavage fluid of SP-A deficient mice with corticosteroid-induced PcP were observed higher concentrations of TNF-α, IFN-γ and MIP-2 than in wild-type mice (Linke et al, 2005). The authors suggested that SP-A could exert a protective role against P. murina.…”

“…Both strong increase of SP-A associated with Pneumocystis infection (Phelps & Rose, 1991;Atochina et al, 2001;Schmidt et al, 2006) and the apparent absence of influence of this protein on Pneumocystis clearance (Linke et al, 2006, and present results) suggest that SP-A might somewhat protect Pneumocystis organisms from host defence mechanisms. Although, alternatively, recent observations suggest that SP-A plays a role in the protection of the host against Pneumocystis infection (Atochina et al, 2004;Linke et al, 2005), in an earlier work Koziel et al (1998) showed that increased levels of SP-A, through binding to the surface of P. carinii organisms, may interfere with alveolar macrophage recognition making phagocytosis more difficult. In the same way, though by a different mechanism, Yong et al (2003) showed that SP-D dodecamers mediate optimal aggregation of P. carinii, which was shown to be responsible for the impaired phagocytosis of the organisms by alveolar macrophages.…”

Pneumocystis murina MSG gene family and the structure of the locus associated with its transcription

“…Infected lungs were Xash frozen in liquid nitrogen and ground into a Wne powder and stored at ¡70°C (Linke et al, 2005). Approximately 50 mgs of frozen powdered lung tissue were placed in 1.0 ml Trizol ® Reagent (Invitrogen, Carlsbad, CA) and total RNA was isolated according to the manufacturer's directions.…”

“…Pneumocystis murina, the species of Pneumocystis found in laboratory mice (Keely et al, 2004), is of interest because the laboratory mouse provides an advanced animal model of host response to Pneumocystis infection (Wright et al, 2001;Lund et al, 2003;An et al, 2003;Qureshi et al, 2003;McAllister et al, 2004;Empey et al, 2004;Qureshi et al, 2005;Linke et al, 2005Linke et al, , 2006a. P. murina is a close relative of Pneumocystis carinii and Pneumocystis wakeWeldiae, both found in rats, and a more distant relative of the human pathogen, P. jirovecii (Frenkel, 1976(Frenkel, , 1999Stringer et al, , 2002Redhead et al, 2006).…”