Allergen‐induced bronchial inflammation is associated with decreased levels of surfactant proteins A and D in a murine model of asthma

Wang, Jiu-Yao; Shieh, Chi‐Chang; Yu, Chih-Sheng; Lei, H. Y.

doi:10.1046/j.1365-2222.2001.01031.x

Cited by 62 publications

(52 citation statements)

References 35 publications

(34 reference statements)

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“…Despite some reported increases in SP-A and SP-D levels 24 h after allergen challenge, which may well represent an innate immune defense mechanism (11,12,15,59), given our findings, we believe that as well as very short-term exposure, which has been discussed above, long-term exposure to HDM allergens would disrupt the physiological levels and functions of SP-D in the lungs, and this could have profound consequences. Consistent with this, decreased levels of SP-A and SP-D in BALF are seen in the chronic phase of allergen exposure in murine models of allergic hypersensitivity to HDM allergens (58).…”

Section: Discussionsupporting

confidence: 65%

Major House Dust Mite Allergens Dermatophagoides pteronyssinus 1 and Dermatophagoides farinae 1 Degrade and Inactivate Lung Surfactant Proteins A and D

Deb

Shakib

Reid

et al. 2007

Journal of Biological Chemistry

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Section: Discussionsupporting

confidence: 65%

Major House Dust Mite Allergens Dermatophagoides pteronyssinus 1 and Dermatophagoides farinae 1 Degrade and Inactivate Lung Surfactant Proteins A and D

Deb

Shakib

Reid

et al. 2007

Journal of Biological Chemistry

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“…Based on studies in murine models of allergic inflammation and in studies of patients with asthma, it has become increasingly evident that SP-A and SP-D play important regulatory roles in allergic airways diseases. Mice challenged with OVA, house dust mite (HDM), or fungi have alterations in SP-A/-D levels at the height of eosinophilia (58)(59)(60). An increase in SP-A/-D during eosinophilic inflammation is likely a key defense mechanism for eosinophil regulation: SP-D inhibits eosinophil chemotaxis, SP-A and SP-D bind eosinophils and attenuate degranulation, and SP-A suppresses IL-8 production from eosinophils (61)(62)(63).…”

Section: Asthmamentioning

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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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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“…A number of studies have used animal models to address the mechanistic issues that underlie the inverse relationship between the epidemiologies of helminth infection and allergic disease in human populations (5,61,64,65) and the immunological observations that preexisting helminth infection alters the magnitude and character of the immune responses to subsequent pathogen or antigen challenges (7,12,45). Results from studies where infection with the nematode N. brasiliensis, H. polygyrus, or Strongyloides stercoralis was superimposed upon the ovalbumin allergy model demonstrated that reductions in the responses to allergen challenge were characterized by downregulation of eotaxin production, a commensurate decrease in eosinophil infiltration, and a decrease in lung-associated IgE levels (60,64,65).…”

Section: Vol 76 2008 Nippostrongylus-induced Pulmonary Changes 3519mentioning

confidence: 99%

Hookworm-Induced Persistent Changes to the Immunological Environment of the Lung

et al. 2008

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A number of important helminth parasites of humans have incorporated short-term residence in the lungs as an obligate phase of their life cycles. The significance of this transient pulmonary exposure to the infection and immunity is not clear. Employing a rodent model of infection with hookworm (Nippostrongylus brasiliensis), we characterized the long-term changes in the immunological status of the lungs induced by parasite infection. At 36 days after infection, alterations included a sustained increase in the transcription of both Th2 and Th1 cytokines as well as a significant increase in the number and frequency of alveolar macrophages displaying an alternatively activated phenotype. While N. brasiliensis did not induce alternate activation of lung macrophages in STAT6؊/؊ animals, the parasite did induce a robust Th17 response in the pulmonary environment, suggesting that STAT6 signaling plays a role in modulating Th17 immunity and pathology in the lungs. In the context of the cellular and molecular changes induced by N. brasiliensis infection, there was a significant reduction in overall airway responsiveness and lung inflammation in response to allergen. In addition, the N. brasiliensis-altered pulmonary environment showed dramatic alterations in the nature and number of genes that were up-and downregulated in the lung in response to allergen challenge. The results demonstrate that even a transient exposure to a helminth parasite can effect significant and protracted changes in the immunological environment of the lung and that these complex molecular and cellular changes are likely to play a role in modulating a subsequent allergen-induced inflammatory response.Historically, an infection with one or multiple helminth parasites has been essentially universal for human populations. It is estimated that a majority of living humans have a history of or are currently infected with a helminth parasite, with the highest prevalence of exposure in developing areas (11). A number of important helminth parasites such as hookworm, Ascaris, and Schistosoma have incorporated a short-term residence in the lungs as an obligate phase of their life cycle. The significance of the lung phase to the developmental biology of these parasites has not been clearly defined. Equally unclear is the impact that the pulmonary phase has on the immunobiology and pathogenesis of infection and the nature and extent to which the immunological environment of the lung is altered by these transient exposures. If significant changes to the pulmonary environment do ensue, to what extent do they influence the level and nature of the responses to subsequent challenges from bacteria, fungi, viruses, and allergens?In recent decades, the incidence and prevalence of allergy and asthma have increased dramatically in industrialized nations, with no comparable increase in developing regions of the world (3, 9, 10, 39). Although a number of factors have been proposed to explain this difference in disease prevalence in developed and developing regions, incl...

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Allergen‐induced bronchial inflammation is associated with decreased levels of surfactant proteins A and D in a murine model of asthma

Abstract: These results indicated the involvement of pulmonary surfactant proteins in the allergic bronchial inflammation of sensitized mice.

Cited by 62 publications

References 35 publications

Major House Dust Mite Allergens Dermatophagoides pteronyssinus 1 and Dermatophagoides farinae 1 Degrade and Inactivate Lung Surfactant Proteins A and D

Major House Dust Mite Allergens Dermatophagoides pteronyssinus 1 and Dermatophagoides farinae 1 Degrade and Inactivate Lung Surfactant Proteins A and D

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

Hookworm-Induced Persistent Changes to the Immunological Environment of the Lung

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