Bronchial epithelial cells (BEC) play a crucial role in innate immunity against inhaled fungi. Indeed, in response to microorganisms, BEC synthesize proinflammatory cytokines involved in the recruitment of neutrophils. We have recently shown that BEC exert antifungal activity against by inhibiting filament growth. In the present study, we first analyzed the inflammatory and antifungal responses of BEC infected by several fungal species such as spp., and , which are frequently isolated from the sputum of people with chronic pulmonary diseases. The airways of these patients, such as people with cystic fibrosis (pwCF), are mainly colonized by and secondary by fungal pathogens. We have previously demonstrated that BEC are capable of innate immune memory, allowing them to increase their inflammatory response against following a previous contact with flagellin. To identify the impact of bacteria exposure on BEC responses to other fungal infections, we extended the analysis of BEC innate immune memory to spp., and infection. Our results show that BEC are able to recognize and respond to spp., and infection and that the modulation of BEC responses by pre-exposure to flagellin varies according to the fungal species encountered. Deepening our knowledge of the innate immune memory of BEC should open new therapeutic avenues to modulate the inflammatory response against polymicrobial infections observed in chronic pulmonary diseases such as CF.
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http://dx.doi.org/10.3390/jof8121268 | DOI Listing |
J Immunother Cancer
January 2025
Department of Oncology, Taipei Veterans General Hospital, Taipei, Taiwan
Background: Cholangiocarcinoma is a challenging malignancy with limited responses to conventional therapies, particularly immune checkpoint inhibitor therapy. Tumor-infiltrating lymphocytes (TILs) and tertiary lymphoid structures (TLSs) are key components of the tumor microenvironment (TME) and have been implicated in the immune response to cancer. However, the role and difference of TLSs and TILs in patients with cholangiocarcinoma remains unclear.
View Article and Find Full Text PDFMethods Enzymol
January 2025
Department of Chemistry, Washington University in St. Louis, MO, United States. Electronic address:
Adenosine-to-inosine (A-to-I) editing, catalyzed by adenosine deaminases acting on RNA (ADARs), is a prevalent post-transcriptional modification that is vital for numerous biological functions. Given that this modification impacts global gene expression, RNA localization, and innate cellular immunity, dysregulation of A-to-I editing has unsurprisingly been linked to a variety of cancers and other diseases. However, our current understanding of the underpinning mechanisms that connect dysregulated A-to-I editing and disease processes remains limited.
View Article and Find Full Text PDFMethods Enzymol
January 2025
Department of Chemistry, University of California, Davis, CA, United States; Department of Molecular and Cellular Biology, University of California, Davis, CA, United States. Electronic address:
Adenosine deaminases acting on RNAs (ADARs) are a class of RNA editing enzymes found in metazoa that catalyze the hydrolytic deamination of adenosine to inosine in duplexed RNA. Inosine is a nucleotide that can base pair with cytidine, therefore, inosine is interpreted by cellular processes as guanosine. ADARs are functionally important in RNA recoding events, RNA structure modulation, innate immunity, and can be harnessed for therapeutically-driven base editing to treat genetic disorders.
View Article and Find Full Text PDFMethods Enzymol
January 2025
St.Vincent's Institute of Medical Research, Fitzroy, Victoria, Australia; Department of Medicine, St. Vincent's Hospital, Melbourne Medical School, University of Melbourne, Fitzroy, Victoria, Australia; Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, Victoria, Australia; Department of Molecular and Translational Science, Monash University, Clayton, Victoria, Australia. Electronic address:
Adenosine-to-inosine (A-to-I) editing, is a highly prevalent posttranscriptional modification of RNA, mediated by the adenosine deaminases acting on RNA (ADAR) proteins. Mammalian transcriptomes contain tens of thousands to millions of A-to-I editing events. Mutations in ADAR can result in rare autoinflammatory disorders such as Aicardi-Goutières syndrome (AGS) through to irreversible conditions such as motor neuron disease, amyotrophic lateral sclerosis (ALS).
View Article and Find Full Text PDFMicrob Pathog
January 2025
College of Animal Science and Technology, Shandong Agricultural University, 61 Daizong Street, Tai'an, Shandong Province, 271018, China; Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Tai'an, Shandong, 271018, China; Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Tai'an, Shandong, 271018, China. Electronic address:
Pigeon adenovirus type 1 predominantly infects pigeons under 12 months of age (mainly 3-5 months old), causing major clinical symptoms such as vomiting, dehydration, and discharge of thin yellow feces. In February 2023, an outbreak of a pathogen with symptoms similar to pigeon adenovirus infections occurred on a pigeon farm in Shandong Province, which was eventually identified as pigeon adenovirus type 1. In this study, a strain of PiAdV-1 was isolated from naturally infected pigeons and named pigeon-adenovirus-1-isolate-CH-SD-2023, and the hexon gene sequence as amplified and analyzed using polymerase chain reaction (PCR).
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