ArticleRespiratory research2004
Coccidioides posadasii infection alters the expression of pulmonary surfactant proteins (SP)-A and SP-D.
Article in Respiratory research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 34 citations in OpenAlex.
- Single-cell analysis of human airway epithelium identifies cell-type-specific responses tomBio · 2025Article
- The Host Response to Coccidioidomycosis.Journal of fungi (Basel, Switzerland) · 2024Review
- Host Response toFrontiers in cellular and infection microbiology · 2020Review
- Surfactant Protein D Recognizes Multiple Fungal Ligands: A Key Step to Initiate and Intensify the Anti-fungal Host Defense.Frontiers in cellular and infection microbiology · 2020Review
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Early Events in Coccidioidomycosis.Clinical microbiology reviews · 2019Review
- Article
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- Surfactant proteins, SP-A and SP-D, in respiratory fungal infections: their role in the inflammatory response.Respiratory research · 2016Review
- Toll-like receptor 4-interacting SPA4 peptide suppresses the NLRP3 inflammasome in response to LPS and ATP stimuli.Journal of leukocyte biology · 2015Article
- The Role of Surfactant in Lung Disease and Host Defense against Pulmonary Infections.Annals of the American Thoracic Society · 2015Review
- A TLR4-interacting peptide inhibits lipopolysaccharide-stimulated inflammatory responses, migration and invasion of colon cancer SW480 cells.Oncoimmunology · 2012Article
- An Insight into the Diverse Roles of Surfactant Proteins, SP-A and SP-D in Innate and Adaptive Immunity.Frontiers in immunology · 2012Article
- A toll-like receptor-4-interacting surfactant protein-A-derived peptide suppresses tumor necrosis factor-α release from mouse JAWS II dendritic cells.The Journal of pharmacology and experimental therapeutics · 2011Article
- Cryptococcus neoformans is resistant to surfactant protein A mediated host defense mechanisms.PloS one · 2007Article
- Animal models: an important tool in mycology.Medical mycology · 2007Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCoccidioidomycosis or Valley Fever is caused by Coccidioides in Southwest US and Central America. Primary pulmonary infection is initiated by inhalation of air-borne arthroconidia. Since, lung is the first organ that encounters arthroconidia, different components of the pulmonary innate immune system may be involved in the regulation of host defense. Pulmonary surfactant proteins (SP)-A and SP-D have been recognized to play an important role in binding and phagocytosis of various microorganisms, but their roles in Coccidioides infection are not known.
methodsIn this study, we studied the changes in amounts of pulmonary SP-A, SP-D and phospholipid in murine model of Coccidioides posadasii infection, and binding of SP-A and SP-D to Coccidioidal antigens. Mice were challenged intranasally with a lethal dose of C. posadasii (n = 30 arthroconidia) and bronchoalveolar lavage fluid (BALF) samples were collected on day 10, post infection. In another group of animals, mice were immunized with protective formalin killed spherule (FKS) vaccine prior to infection. The concentrations of BALF SP-A, SP-D, total phospholipid were measured using enzyme linked immunosorbent assay and biochemical assays.
resultsWe found that in lavage fluid samples of C. posadasii infected mice, the concentrations of total phospholipid, SP-A and SP-D were 17 % (SEM 3.5, p < 0.001), 38 % (SEM 5.8, p < 0.001) and 4 % (SEM 1.3, p < 0.001) of those in lavage fluid samples of non-infected control mice, respectively. However, the concentrations of SP-A and SP-D remained unchanged in BALF samples of C. posadasii protected mice after immunization with FKS vaccine. Also, we found that both SP-A and SP-D bind to Coccidiodal antigens.
conclusionOur results suggest that the C. posadasii infection perturbs the pulmonary SP-A, SP-D, and phospholipids, potentially enabling the disease progression and promoting fungal dissemination.
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