Hypobaric hypoxia-related impairment of pulmonary surfactant proteins A and D did not favour<i>Pneumocystis carinii</i>Frenkel 1999 growth in non-immunocompromised rats

Vives, Marta; Caspar-Bauguil, Sylvie; Aliouat, El Moukhtar; Escamilla, R.; Perret, Bertrand; Dei‐Cas, Eduardo; Prévost, Marie-Claude

doi:10.1051/parasite/2008151053

Cited by 11 publications

(3 citation statements)

References 79 publications

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“…In nonimmunocompromised laboratory rats, hypobaric hypoxia weakened host immune mechanisms and significantly impaired the surfactant composition. Such changes were not enough, however, to favor Pneumocystis growth or to inhibit Pneumocystis clearing from their lungs (95).…”

Section: Discussionmentioning

confidence: 99%

“…The almost exponential decline of the atmospheric pressure is accompanied by a parallel decline of the oxygen pressure in the inspired air, which induces hyperventilation. Thus, altitude could directly impact on respiratory physiology and host defense mechanisms (95) and indirectly act on the development of Pneumocystis organisms in the alveolar microenvironment. These aspects were not explored in bats.…”

Section: Discussionmentioning

confidence: 99%

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Characterizing Pneumocystis in the Lungs of Bats: Understanding Pneumocystis Evolution and the Spread of Pneumocystis Organisms in Mammal Populations

Akbar

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Aliouat-Denis

et al. 2012

Appl Environ Microbiol

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Bats belong to a wide variety of species and occupy diversified habitats, from cities to the countryside. Their different diets (i.e., nectarivore, frugivore, insectivore, hematophage) lead Chiroptera to colonize a range of ecological niches. These flying mammals exert an undisputable impact on both ecosystems and circulation of pathogens that they harbor. Pneumocystis species are recognized as major opportunistic fungal pathogens which cause life-threatening pneumonia in severely immunocompromised or weakened mammals. Pneumocystis consists of a heterogeneous group of highly adapted host-specific fungal parasites that colonize a wide range of mammalian hosts. In the present study, 216 lungs of 19 bat species, sampled from diverse biotopes in the New and Old Worlds, were examined. Each bat species may be harboring a specific Pneumocystis species. We report 32.9% of Pneumocystis carriage in wild bats (41.9% in Microchiroptera). Ecological and behavioral factors (elevation, crowding, migration) seemed to influence the Pneumocystis carriage. This study suggests that Pneumocystis-host association may yield much information on Pneumocystis transmission, phylogeny, and biology in mammals. Moreover, the link between genetic variability of Pneumocystis isolated from populations of the same bat species and their geographic area could be exploited in terms of phylogeography.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Characterizing Pneumocystis in the Lungs of Bats: Understanding Pneumocystis Evolution and the Spread of Pneumocystis Organisms in Mammal Populations

Akbar

Pinçon

Aliouat-Denis

et al. 2012

Appl Environ Microbiol

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“…Specific properties of SP‐A include direct antimicrobial activity, non‐immune opsonization, and/or modulation of the host immune response (Santo and Kuroki 2004). We and other investigators have shown that immunosuppressed SP‐A knockout (KO) mice develop higher levels of PCP than immunosuppressed wild‐type (WT) mice (Atochina et al 2004a; Linke et al 2001, 2005; Vives et al 2008). Upon removal of the immunosuppression, SP‐A does not appear to affect the clearance of P. murina , but does alter the host immune response (Linke et al 2006a, b).…”

mentioning

confidence: 98%

Effects of Surfactant Protein‐A on the Interaction of Pneumocystis murina with its Host at Different Stages of the Infection in Mice

Linke

Ashbaugh

Koch

et al. 2009

J Eukaryotic Microbiology

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ABSTRACT. We examined the effects of surfactant protein A (SP-A), a collectin, on the interaction of Pneumocystis murina with its host at the beginning, early to middle, and late stages of infection. Pneumocystis murina from SP-A wild-type (WT) mice inoculated intractracheally into WT mice (WT S -WT R ) adhered well to alveolar macrophages, whereas organisms from SP-A knockout (KO) mice inoculated into KO mice (KO S -KO R ) did not. Substitution of WT mice as the source of organisms (WT S -KO R ) or recipient host macrophages (KO S -WT R ) restored adherence to that found with WT S -WT R mice. In contrast, when immunosuppressed KO and WT mice were inoculated with P. murina from a homologous source (KO S -KO R , WT S -WT R ) or heterologous source (WT S -KO R , KO S -WT R ) and followed sequentially, WT S -KO R mice had the highest levels of infection at weeks 3 and 4; these mice also had the highest levels of the chemokine macrophage inflammatory protein-2 and neutrophils in lavage fluid at week 3. Surfactant protein-A administered to immunosuppressed KO S -KO R mice with Pneumocystis pneumonia for 8 wk as a therapeutic agent failed to lower the organism burden. We conclude that SP-A can correct the host immune defect in the beginning of P. murina infection, but not in the middle or late stages of the infection.

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Evolution, Development, and Function of the Pulmonary Surfactant System in Normal and Perturbed Environments

Orgeig

Morrison

Daniels

2015

Comprehensive Physiology

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Surfactant lipids and proteins form a surface active film at the air-liquid interface of internal gas exchange organs, including swim bladders and lungs. The system is uniquely positioned to meet both the physical challenges associated with a dynamically changing internal air-liquid interface, and the environmental challenges associated with the foreign pathogens and particles to which the internal surface is exposed. Lungs range from simple, transparent, bag-like units to complex, multilobed, compartmentalized structures. Despite this anatomical variability, the surfactant system is remarkably conserved. Here, we discuss the evolutionary origin of the surfactant system, which likely predates lungs. We describe the evolution of surfactant structure and function in invertebrates and vertebrates. We focus on changes in lipid and protein composition and surfactant function from its antiadhesive and innate immune to its alveolar stability and structural integrity functions. We discuss the biochemical, hormonal, autonomic, and mechanical factors that regulate normal surfactant secretion in mature animals. We present an analysis of the ontogeny of surfactant development among the vertebrates and the contribution of different regulatory mechanisms that control this development. We also discuss environmental (oxygen), hormonal and biochemical (glucocorticoids and glucose) and pollutant (maternal smoking, alcohol, and common "recreational" drugs) effects that impact surfactant development. On the adult surfactant system, we focus on environmental variables including temperature, pressure, and hypoxia that have shaped its evolution and we discuss the resultant biochemical, biophysical, and cellular adaptations. Finally, we discuss the effect of major modern gaseous and particulate pollutants on the lung and surfactant system.

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

Cited by 11 publications

References 79 publications

Characterizing Pneumocystis in the Lungs of Bats: Understanding Pneumocystis Evolution and the Spread of Pneumocystis Organisms in Mammal Populations

Characterizing Pneumocystis in the Lungs of Bats: Understanding Pneumocystis Evolution and the Spread of Pneumocystis Organisms in Mammal Populations

Effects of Surfactant Protein‐A on the Interaction of Pneumocystis murina with its Host at Different Stages of the Infection in Mice

Evolution, Development, and Function of the Pulmonary Surfactant System in Normal and Perturbed Environments

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