The human intestinal tract is inhabited by trillions of microorganisms and houses the largest pool of macrophages in the human body. Being a part of the innate immune system, the macrophages, the professional phagocytes, vigorously respond to the microbial and dietary antigens present in the intestine. Because such a robust immune response poses the danger to the survival of the non-harmful and beneficial gut microbiota, the macrophages developed mechanisms of recognition and hyposensitivity toward the non-harmful/beneficial inhabitants of the gut. We will discuss the evolution and identity of some of these mechanisms in the following chapter.
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http://dx.doi.org/10.1007/978-3-030-51849-3_23 | DOI Listing |
ACS Appl Mater Interfaces
January 2025
Department of Chemical Engineering, University of Massachusetts Amherst, Amherst, Massachusetts 01003, United States.
The innate immune system is tightly regulated by a complex network of chemical signals triggered by pathogens, cellular damage, and environmental stimuli. While it is well-established that changes in the extracellular environment can significantly influence the immune response to pathogens and damage-associated molecules, there remains a limited understanding of how changes in environmental stimuli specifically impact the activation of the NLRP3 inflammasome, a key component of innate immunity. Here, we demonstrated how shear stress can act as Signal 2 in the NLRP3 inflammasome activation pathway by treating LPS-primed immortalized bone marrow-derived macrophages (iBMDMs) with several physiologically relevant magnitudes of shear stress to induce inflammasome activation.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
January 2025
University of Groningen, University Medical Center Groningen, Department of Pulmonology and Pediatric Allergy, Beatrix Children's Hospital, Groningen, Netherlands.
Asthma is a genetically complex inflammatory airway disease associated with over 200 Single nucleotide polymorphisms (SNPs). However, the functional effects of many asthma-associated SNPs in lung and airway epithelial samples are unknown. Here, we aimed to conduct expression quantitative trait loci (eQTL) analysis using a meta-analysis of nasal and lung samples.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
January 2025
Division of Pulmonology, Asthma, Cystic Fibrosis, and Sleep, Emory University School of Medicine, Atlanta, GA, USA.
Secondhand smoke exposure (SHSe) is a public health threat for people with cystic fibrosis (CF) and other lung diseases. Primary smoking reduces CFTR channel function, the causative defect in CF. We reported that SHSe worsens respiratory and nutritional outcomes in CF by disrupting immune responses and metabolic signaling.
View Article and Find Full Text PDFClin Transl Med
January 2025
Vascular Research Laboratory, IIS-Fundación Jiménez Díaz, Madrid, Spain.
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids and leukocytes within the arterial wall. By studying the aortic transcriptome of atherosclerosis-prone apolipoprotein E (ApoE) mice, we aimed to identify novel players in the progression of atherosclerosis.
Methods: RNA-Seq analysis was performed on aortas from ApoE and wild-type mice.
ACS Nano
January 2025
Jiangsu Key Laboratory for Biomaterials and Devices, School of Biomedical Sciences and Medical Engineering, Southeast University, Nanjing 210096, P. R. China.
The blood flow, when restored clinically following a myocardial infarction (MI), disrupts the physiological and metabolic equilibrium of the ischemic myocardial area, resulting in secondary damage termed myocardial ischemia-reperfusion injury (MIRI). Reactive oxygen species (ROS) generation and inflammatory reactions stand as primary culprits behind MIRI. Current strategies focusing on ROS-scavenging and anti-inflammatory actions have limited remission of MIRI.
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