Aim: To investigate the innate immune components surfactant protein A (SP-A) and D (SP-D) in victims of sudden infant death syndrome (SIDS).
Methods: Ten common single nucleotide polymorphisms (SNPs) in the exons of SP-A1, SP-A2 and SP-D genes were analysed in 42 cases of SIDS and 46 explained sudden infant deaths. SP-A and SP-D protein expression in tissue from the aerodigestive tract was semi-quantitatively evaluated by immunohistochemistry.
Results: SP-D immunoreactivity was found in lungs and tissue from submandibular gland, palatine tonsils and duodenum. Positive SP-A immune staining was found exclusively in lung tissue. Neither the allele nor the haplotype distribution of the SP-A and SP-D genes was significantly different in SIDS compared to explained deaths. The most common SP-A haplotype, 6A2/1A0, tended to be overrepresented in the cases with low immunohistochemical SP-A expression (61%) compared to cases with high expression (49%), p = 0.08. The SP-D expression was not influenced by the 11 C/T or 160 A/G polymorphisms.
Conclusion: No significant association between the common genetic variants of SP-A and SP-D and SIDS is disclosed by the present study. However, low SP-A protein expression may possibly be determined by the 6A2/1A0 SP-A haplotype, this should be subject for further investigation.
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http://dx.doi.org/10.1111/j.1651-2227.2008.01090.x | DOI Listing |
Nanotoxicology
January 2025
Infection, Inflammation and Repair, Faculty of Medicine, University of Southampton, Southampton, UK.
The role of surfactant proteins A and D (SP-A and SP-D) in lung clearance and translocation to secondary organs of inhaled nanoparticles was investigated by exposing SP-A and SP-D knockout (AKO and DKO) and wild type (WT) mice nose-only for 3 hours to an aerosol of 20 nm gold nanoparticles (AuNPs). Animals were euthanised at 0-, 1-, 7- and 28-days post-exposure. Analysis by inductively coupled plasma mass spectrometry (ICP-MS) of the liver and kidneys showed that extrapulmonary translocation was below the limits of detection.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Department of Pediatrics, The Pennsylvania State College of Medicine, Hershey, PA, USA.
Since its outbreak, the novel coronavirus (COVID-19) has significantly impacted the pediatric population. Pulmonary surfactant dysfunction has been linked to other respiratory diseases in children and COVID-19 in adults, but its role in COVID-19 severity remains unclear. We hypothesized that elevated surfactant protein (SP) levels and single nucleotide polymorphisms (SNPs) of SP genes are associated with severe COVID-19 in children.
View Article and Find Full Text PDFFront Immunol
January 2025
Department Integrative Agriculture, College of Agriculture and Veterinary Medicine, United Arab Emirates University, Al Ain, United Arab Emirates.
Surfactant protein D (SP-D) is a C-type lectin that was originally discovered as a lung surfactant associated phospholipid recognising protein. It was originally shown to be of great importance in surfactant turnover and homeostasis in conjunction with another hydrophilic surfactant protein i.e.
View Article and Find Full Text PDFPol J Vet Sci
September 2024
Department of Companion Animals and Horses, University Equine Hospital, Vetmeduni Vienna, Vienna, Austria.
Rhodococcus equi (R. equi) is a primary cause of pyogranulomatous pneumonia of foals between three weeks and five months of age. Early diagnosis of rhodococcal pneumonia has always been considered a preferable approach as it can lead to more successful treatment and better outcomes.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Targeted Lung Immunotherapy Group, Neonatology Department, Elizabeth Garrett Anderson Institute for Women's Health, University College London, London, United Kingdom.
The vast majority of early-life hospital admissions globally highlight respiratory syncytial virus (RSV), the leading cause of neonatal lower respiratory tract infections, as the major culprit behind the poor neonatal outcomes following respiratory infections. Unlike those of older children and adults, the immune system of neonates looks rather unique, therefore mostly counting on the innate immune system and antibodies of maternal origins. The collaborations between cells and immune compartments during infancy inclines bias toward a T-helper 2 (Th2) immune profile and thereby away from a T-helper 1 (Th1) immune response.
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