The lung collectins, SP-A and SP-D, modulate pulmonary innate immunity

Sano, Hitomi; Kuroki, Yoshio

doi:10.1016/j.molimm.2004.07.014

Cited by 181 publications

(157 citation statements)

References 73 publications

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“…Collectins are thought to bind carbohydrate residues present on influenza hemagglutinin and neuraminidase, thereby aggregating viral particles and preventing invasion of host cells (Reading et al, 2007). In addition, a highly reduced clearance of influenza virus was observed in mice lacking either surfactant protein A or surfactant protein D, implicating the importance of these mammalian collectins in defense against influenza virus inoculations in vivo (Sano and Kuroki, 2005). In chicken, five collectins have been described thus far, which are mannan binding lectin (Laursen et al, 1998), surfactant Mammalian collectins have been found to play an important role in the defense against influenza A virus H9N2 inoculation, but for chicken collectins this has not yet been clarified.…”

Section: Introductionmentioning

confidence: 99%

Transcriptional expression levels of chicken collectins are affected by avian influenza A virus inoculation

Reemers

Veldhuizen

Fleming

et al. 2010

Veterinary Microbiology

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Section: Introductionmentioning

confidence: 99%

Transcriptional expression levels of chicken collectins are affected by avian influenza A virus inoculation

Reemers

Veldhuizen

Fleming

et al. 2010

Veterinary Microbiology

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“…Surfactant is a mixture of phospholipids which primarily functions to prevent alveolar collapse during end-expiration (Ochs, 2006). However, in addition to this physiological function, surfactant has been found to have potent antimicrobial properties which are largely attributed to the hydrophilic, collectin-like surfactant protein A and D (Crouch et al, 2000;Grubor et al, 2006;Kingma and Whitsett, 2006;Kishore et al, 2006;LeVine and Whitsett, 2001;Sano and Kuroki, 2005). The secretion of SP-A and SP-D is regulated by developmental stage King et al, 1975;Mescher et al, 1975), hormones and potentially, by environmental factors such as alcohol consumption.…”

Section: Introductionmentioning

confidence: 99%

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Lazic¹,

Wyatt²,

Matić³

et al. 2007

Alcohol

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In addition to neurodevelopmental effects, alcohol consumption at high levels during pregnancy is associated with immunomodulation and premature birth. Premature birth, in turn, is associated with increased susceptibility to various infectious agents such as Respiratory Syncytial Virus (RSV). The initial line of pulmonary innate defense includes the mucociliary apparatus, which expels microorganisms trapped within the airway secretions. Surfactant proteins A and D (SP-A and SP-D, respectively) are additional components of pulmonary innate immunity and have an important role in pulmonary defense against inhaled pathogens. The purpose of this study was to determine if chronic alcohol consumption during the third trimester of pregnancy alters the function of the mucociliary apparatus and expression of SP-A and SP-D of fetal lung epithelia. Sixteen, date-mated ewes were assigned to two different groups; an ethanol exposed group in which ewes received ethanol through surgically implanted intra-abomasal cannula during the third trimester of pregnancy, and a control group in which ewes received the equivalent amount of water instead of ethanol. Within these two groups, ewes were further randomly assigned to a full-term group in which the lambs were naturally delivered, and a pre-term group in which the lambs were delivered prematurely via an abdominal incision and uterotomy. Ethanol was administered 5 times a week as a 40% solution at 1gr/kg of body weight. The mean maternal serum alcohol concentration (SAC) measured 6 hr post administration was 16.3 +/− 4.36 mg/dL. Tracheas from 6 full-term lambs were collected to assess ciliary beat frequency (CBF). The lung tissue from all (24) lambs was collected for immunohistochemistry (IHC) analysis of SP-A and SP-D protein production and fluorogenic realtime quantitative polymerase chain reaction analysis (qPCR) of SP-A and SP-D mRNA levels. Exposure to ethanol during pregnancy significantly blocked stimulated increase in CBF though ethanol-mediated desensitization of cAMP-dependant protein kinase (PKA). In addition, pre-term born/ethanol-exposed lambs showed significantly decreased SP-A m-RNA expression when compared to the pre-term born/control group (p=0.004); no significant changes were seen with SP-D. The full-term/ethanol exposed lambs had no significant alterations in mRNA levels, but had significantly less detectable SP-A protein when compared to the full-term/control lambs (p=0.02).Corresponding author: Tatjana Lazic, DVM, MS, 2740 Veterinary Medicine, Department of Veterinary Pathology, Iowa State University, Ames, Iowa 50011-1250, 515-294-6688, FAX 515-294-5423, tlazic@iastate.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process error...

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“…In human pulmonary surfactant, POPG is the most abundant molecular species present within the PG class of phospholipid. Recent findings now indicate that selected surfactant lipids and proteins may complement each other in the homeostatic suppression of inflammation in the lung (17,21,22).We have undertaken a comprehensive examination of the role of POPG in regulating multiple aspects of innate immunity. As part of this endeavor we focused upon the interrelationships between CD14, POPG, and RSV.…”

mentioning

confidence: 99%

Pulmonary surfactant phosphatidylglycerol inhibits respiratory syncytial virus–induced inflammation and infection

Numata

Chu

Dakhama

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

158

244

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Respiratory syncytial virus (RSV) is the most common cause of hospitalization for respiratory tract infection in young children. It is also a significant cause of morbidity and mortality in elderly individuals and in persons with asthma and chronic obstructive pulmonary disease. Currently, no reliable vaccine or simple RSV antiviral therapy is available. Recently, we determined that the minor pulmonary surfactant phospholipid, palmitoyl-oleoyl-phosphatidylglycerol (POPG), could markedly attenuate inflammatory responses induced by lipopolysaccharide through direct interactions with the Toll-like receptor 4 (TLR4) interacting proteins CD14 and MD-2. CD14 and TLR4 have been implicated in the host response to RSV. Treatment of bronchial epithelial cells with POPG significantly inhibited interleukin-6 and -8 production, as well as the cytopathic effects induced by RSV. The phospholipid bound RSV with high affinity and inhibited viral attachment to HEp2 cells. POPG blocked viral plaque formation in vitro by 4 log units, and markedly suppressed the expansion of plaques from cells preinfected with the virus. Administration of POPG to mice, concomitant with viral infection, almost completely eliminated the recovery of virus from the lungs at 3 and 5 days after infection, and abrogated IFN-γ (IFN-γ) production and the enhanced expression of surfactant protein D (SP-D). These findings demonstrate an important approach to prevention and treatment of RSV infections using exogenous administration of a specific surfactant phospholipid.antiviral | innate immunity | respiratory epithelium R espiratory syncytial virus (RSV) is an important pathogen that infects 98% of children within the first 2 years of life, and also causes serious disease in elderly individuals and persons with chronic lung disease. In the 1980s, an estimated 100,000 children were hospitalized annually with RSV infection in the United States (1). Although RSV is commonly considered a pediatric disease, it is also highlighted as an opportunistic pathogen (2), with infections producing a mortality rate of 30-100% in immunosuppressed individuals (1). There is growing appreciation that RSV is an important pathogen in elderly and high-risk patients, and a cause of acute exacerbations of asthma (3, 4) and chronic obstructive pulmonary disease (COPD) (5). Over the period 1999-2003, RSV was responsible for hospitalization rates of 10.6% for pneumonia, 11.4% for COPD, 5.4% for congestive heart failure, and 7.2% for asthma (6).No vaccine is currently available for prevention of RSV infection. Several vaccine candidates have not only proved to be ineffective, but have also been shown to lead to vaccine-enhanced disease (7,8). Inhibitors directed against the RSV fusion protein (F protein) were abandoned partly because of the frequency of resistant mutations mapping to the F gene (9). A monoclonal antibody against F protein, Palivizumab, has restricted application and it is recommended for prophylactic use during the RSV season, for high-risk infants (1). Currently the onl...

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The lung collectins, SP-A and SP-D, modulate pulmonary innate immunity

Cited by 181 publications

References 73 publications

Transcriptional expression levels of chicken collectins are affected by avian influenza A virus inoculation

Transcriptional expression levels of chicken collectins are affected by avian influenza A virus inoculation

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Pulmonary surfactant phosphatidylglycerol inhibits respiratory syncytial virus–induced inflammation and infection

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