Impact of Surfactant Protein D, Interleukin-5, and Eosinophilia on Cryptococcosis

Holmer, Stephanie M.; Evans, Kathy S.; Asfaw, Yohannes G.; Saini, D.; Schell, Wiley A.; Ledford, Julie G.; Frothingham, Richard; Wright, Jo Rae; Sempowski, Gregory D.; Perfect, John R.

doi:10.1128/iai.00855-13

Cited by 33 publications

(42 citation statements)

References 49 publications

(48 reference statements)

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“…As an example, SP-D-deficient mice infected with the fungus Cryptococcus neoformans (CN) have decreased pulmonary eosinophils and lower IL-5 levels in lung lavage fluid compared with control wild-type (WT) mice. Moreover, CN-infected SP-D mice have decreased fungal burden and improved survival compared with the WT controls (20). These findings support the concept that SP-D is a virulence factor for CN and facilitates its infection in mice.…”

Section: Roles Of Sp-a/-d In Cell-mediated Immunitysupporting

confidence: 76%

“…In addition, reactive oxygen and nitrogen species may also affect posttranslational modifications of SP-D that alter its structure and function at sites of inflammation (39,113). For example, NO, produced locally by airway epithelial cells and increased in asthma (114), has been shown to S-nitrosylate two free Cys thiols in the N-terminus of dodecameric SP-D (Cys- [15][16][17][18][19][20] and to affect dissociation into SP-D trimers (115). Consequences of this structural perturbation include the activation of SP-D proinflammatory chemoattractant function and the loss of control TLR4 blockade (39).…”

Section: Alterations Of Sp-a/-d In Eosinophil-predominant Diseasesmentioning

confidence: 99%

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Eosinophil-Associated Lung Diseases. A Cry for Surfactant Proteins A and D Help?

Ledford

Addison

Foster

et al. 2014

Am J Respir Cell Mol Biol

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Surfactant proteins (SP)-A and SP-D (SP-A/-D) play important roles in numerous eosinophil-dominated diseases, including asthma, allergic bronchopulmonary aspergillosis, and allergic rhinitis. In these settings, SP-A/-D have been shown to modulate eosinophil chemotaxis, inhibit eosinophil mediator release, and mediate macrophage clearance of apoptotic eosinophils. Dysregulation of SP-A/-D function in eosinophil-dominated diseases is also not uncommon. Alterations in serum SP-A/-D levels are associated with disease severity in allergic rhinitis and chronic obstructive pulmonary disease. Furthermore, oligimerization of SP-A/-D, necessary for their proper function, can be perturbed by reactive nitrogen species, which are increased in eosinophilic disease. In this review, we highlight the associations of eosinophilic lung diseases with SP-A and SP-D levels and functions.

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Section: Roles Of Sp-a/-d In Cell-mediated Immunitysupporting

confidence: 76%

Section: Alterations Of Sp-a/-d In Eosinophil-predominant Diseasesmentioning

confidence: 99%

Eosinophil-Associated Lung Diseases. A Cry for Surfactant Proteins A and D Help?

Ledford

Addison

Foster

et al. 2014

Am J Respir Cell Mol Biol

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“…Eosinophils were associated with a lack of protection against C. neoformans in pulmonary infection model in which their presence was associated with excessive lung inflammation [91]. C57BL/6 mice develop eosinophilic pneumonia in response to pulmonary cryptococcal infection [92] and eosinophilia has also been observed in human cryptococcosis [93].…”

Section: Innate Immune and Cellular Responses To C Neoformansmentioning

confidence: 99%

Host Immunity to Cryptococcus Neoformans

2015

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Cryptococcosis is caused by the fungal genus Cryptococcus. Cryptococcosis, predominantly meningoencephalitis, emerged with the HIV pandemic, primarily afflicting HIV-infected patients with profound T-cell deficiency. Where in use, combination antiretroviral therapy has markedly reduced the incidence of and risk for disease, but cryptococcosis continues to afflict those without access to therapy, particularly in sub-Saharan Africa and Asia. However, cryptococcosis also occurs in solid organ transplant recipients and patients with other immunodeficiencies as well as those with no known immunodeficiency. This article reviews innate and adaptive immune responses to C. neoformans, with an emphasis on recent studies on the role of B cells, natural IgM and Fc gamma receptor polymorphisms in resistance to cryptococcosis.

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“…Additionally, a recent study reported that SP‐D is responsible for IL‐5‐induced eosinophilic inflammation in Cryptococcus ‐infected mice (Holmer et al. ). Although the model is different to our allergic model, it partly explains decreased IL‐5 production and airway eosinophilia in SP‐D deficiency.…”

Section: Discussionmentioning

confidence: 99%

Frequency-dependent airway hyperresponsiveness in a mouse model of emphysema and allergic inflammation

et al. 2018

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Asthma and chronic obstructive pulmonary disease (COPD), chronic airway inflammatory diseases characterized by airflow limitation, have different etiologies and pathophysiologies. Asthma–COPD Overlap (ACO) has recently been used for patients with mixed asthma and COPD. The pathophysiological mechanisms of ACO have not been clearly understood due to the lack of an appropriate murine model. To investigate its pathophysiology, we examined a murine model by allergen challenge in surfactant protein‐D (SP‐D)‐deficient mice that spontaneously developed pulmonary emphysema. SP‐D‐deficient mice were sensitized and challenged by ovalbumin (OVA). Lungs and bronchoalveolar lavage fluid (BALF) were collected for analysis, and static lung compliance and airway hyperresponsiveness (AHR) were measured 48 h after the last OVA challenge. In SP‐D‐deficient, naïve, or OVA‐challenged mice, the mean linear intercept and static lung compliance were increased compared with wild‐type (WT) mice. There was no significant difference in goblet cell hyperplasia and the gene expression of Mucin 5AC (MUC5AC) between SP‐D‐deficient and WT OVA‐challenged mice. In SP‐D‐deficient OVA‐challenged mice, airway hyperresponsiveness was significantly enhanced despite the lower eosinophil count and the concentration of interleukin (IL)‐5 and IL‐13 in BALF compared with WT OVA‐challenged mice at 120 ventilations per minute. When mice were ventilated at a lower ventilation frequency of 100 ventilations per minute, elevated airway hyperresponsiveness in SP‐D‐deficient OVA‐challenged mice was diminished. This model of emphysematous change with allergic airway inflammation raises the possibility that frequency‐dependent airway hyperresponsiveness may be involved in the pathophysiology of ACO.

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Impact of Surfactant Protein D, Interleukin-5, and Eosinophilia on Cryptococcosis

Abstract: Cryptococcus neoformans is an opportunistic fungal pathogen that initiates infection following inhalation. As a result, the pulmonary immune response provides a first line of defense against C. neoformans.

Cited by 33 publications

References 49 publications

Eosinophil-Associated Lung Diseases. A Cry for Surfactant Proteins A and D Help?

Eosinophil-Associated Lung Diseases. A Cry for Surfactant Proteins A and D Help?

Host Immunity to Cryptococcus Neoformans

Frequency-dependent airway hyperresponsiveness in a mouse model of emphysema and allergic inflammation

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