Acute and potentially persistent effects of scuba diving on the blood transcriptome of experienced divers

During scuba diving, the circulatory system is stressed by an elevated partial pressure of oxygen while the diver is submerged and by decompression-induced gas bubbles on ascent to the surface. This diving-induced stress may trigger decompression illness, but the majority of dives are asymptomatic. In this study we have mapped divers' blood transcriptomes with the aim of identifying genes, biological pathways, and cell types perturbed by the physiological stress in asymptomatic scuba diving. Ten experienced divers abstained from diving for >2 wk before performing a 3-day series of daily dives to 18 m depth for 47 min while breathing compressed air. Blood for microarray analysis was collected before and immediately after the first and last dives, and 10 matched nondivers provided controls for predive stationary transcriptomes. MetaCore GeneGo analysis of the predive samples identified stationary upregulation of genes associated with apoptosis, inflammation, and innate immune responses in the divers, most significantly involving genes in the TNFR1 pathway of caspase-dependent apoptosis, HSP60/HSP70 signaling via TLR4, and NF-κB-mediated transcription. Diving caused pronounced shifts in transcription patterns characteristic of specific leukocytes, with downregulation of genes expressed by CD8+ T lymphocytes and NK cells and upregulation of genes expressed by neutrophils, monocytes, and macrophages. Antioxidant genes were upregulated. Similar transient responses were observed after the first and last dive. The results indicate that sublethal oxidative stress elicits the myeloid innate immune system in scuba diving and that extensive diving may cause persistent change in pathways controlling apoptosis, inflammation, and innate immune responses.

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Inflammation and the Gut-Liver Axis in the Pathophysiology of Cholangiopathies

International Journal of Molecular Sciences ◽

10.3390/ijms19103003 ◽

2018 ◽

Vol 19 (10) ◽

pp. 3003 ◽

Cited By ~ 11

Author(s):

Debora Giordano ◽

Claudio Pinto ◽

Luca Maroni ◽

Antonio Benedetti ◽

Marco Marzioni

Keyword(s):

Immune Responses ◽

Inflammatory Responses ◽

Enterohepatic Circulation ◽

Intestinal Barrier ◽

Cell Types ◽

Innate Immune ◽

Primary Biliary Cholangitis ◽

Innate Immune Responses ◽

Adaptive Immune Cells ◽

Bacterial Products

Cholangiocytes, the epithelial cells lining the bile ducts, represent the unique target of a group of progressive diseases known as cholangiopathies whose pathogenesis remain largely unknown. In normal conditions, cholangiocytes are quiescent and participate to the final bile volume and composition. Following exogenous or endogenous stimuli, cholangiocytes undergo extensive modifications of their phenotype. Reactive cholangiocytes actively proliferate and release a set of proinflammatory molecules, which act in autocrine/paracrine manner mediating the cross-talk with other liver cell types and innate and adaptive immune cells. Cholangiocytes themselves activate innate immune responses against gut-derived microorganisms or bacterial products that reach the liver via enterohepatic circulation. Gut microbiota has been implicated in the development and progression of the two most common cholangiopathies, i.e., primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC), which have distinctive microbiota composition compared to healthy individuals. The impairment of intestinal barrier functions or gut dysbiosis expose cholangiocytes to an increasing amount of microorganisms and may exacerbate inflammatory responses thus leading to fibrotic remodeling of the organ. The present review focuses on the complex interactions between the activation of innate immune responses in reactive cholangiocytes, dysbiosis, and gut permeability to bacterial products in the pathogenesis of PSC and PBC.

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The innate immune system

Oxford Textbook of Medicine ◽

10.1093/med/9780198746690.003.0038 ◽

2020 ◽

pp. 307-314

Author(s):

Paul Bowness

Keyword(s):

Immune System ◽

Immune Responses ◽

Innate Immune System ◽

Cell Types ◽

Innate Immune ◽

Microbial Pathogens ◽

Innate Immune Responses ◽

Adaptive Immune ◽

System P ◽

Different Cell Types

The innate immune system comprises evolutionarily ancient mechanisms that mediate first-line responses against microbial pathogens, and are also important in priming and execution of adaptive immune responses, and in defence against tumours. These responses, which recognize microbial non-self, damaged self, and absent self, are characterized by rapidity of action and they involve various different cell types, cell-associated receptors, and soluble factors. Previously thought to lack plasticity or memory, certain innate immune responses have recently been shown to be capable of ‘learning’ or ‘training’. Most cells of the innate immune system are derived from the myeloid precursors in the bone marrow. These include monocytes and their derivatives—macrophages and dendritic cells, blood granulocytes (neutrophils, basophils, and eosinophils), and tissue mast cells.

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20S-dihydroprotopanaxadiol, a ginsenoside derivative, boosts innate immune responses of monocytes and macrophages

Journal of Ginseng Research ◽

10.5142/jgr.2013.37.293 ◽

2013 ◽

Vol 37 (3) ◽

pp. 293-299 ◽

Cited By ~ 33

Author(s):

Mi-Yeon Kim ◽

Jae Youl Cho

Keyword(s):

Immune Responses ◽

Innate Immune ◽

Innate Immune Responses ◽

Monocytes And Macrophages

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Stem Cell and Macrophage Roles in Skeletal Muscle Regenerative Medicine

International Journal of Molecular Sciences ◽

10.3390/ijms221910867 ◽

2021 ◽

Vol 22 (19) ◽

pp. 10867

Author(s):

Pasqualina Scala ◽

Laura Rehak ◽

Valentina Giudice ◽

Elena Ciaglia ◽

Annibale Alessandro Puca ◽

...

Keyword(s):

Skeletal Muscle ◽

Stem Cells ◽

Immune Responses ◽

Muscle Tissue ◽

Peripheral Blood ◽

Cell Types ◽

Innate Immune ◽

Muscle Repair ◽

Innate Immune Responses ◽

Peripheral Cell

In severe muscle injury, skeletal muscle tissue structure and functionality can be repaired through the involvement of several cell types, such as muscle stem cells, and innate immune responses. However, the exact mechanisms behind muscle tissue regeneration, homeostasis, and plasticity are still under investigation, and the discovery of pathways and cell types involved in muscle repair can open the way for novel therapeutic approaches, such as cell-based therapies involving stem cells and peripheral blood mononucleate cells. Indeed, peripheral cell infusions are a new therapy for muscle healing, likely because autologous peripheral blood infusion at the site of injury might enhance innate immune responses, especially those driven by macrophages. In this review, we summarize current knowledge on functions of stem cells and macrophages in skeletal muscle repairs and their roles as components of a promising cell-based therapies for muscle repair and regeneration.

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Differential Expression of Genes Related to Innate Immune Responses in Ex Vivo Spinal Cord and Cerebellar Slice Cultures Infected with West Nile Virus

Brain Sciences ◽

10.3390/brainsci9010001 ◽

2018 ◽

Vol 9 (1) ◽

pp. 1 ◽

Cited By ~ 2

Author(s):

Parminder Vig ◽

Deyin Lu ◽

Amber Paul ◽

Ram Kuwar ◽

Maria Lopez ◽

...

Keyword(s):

Spinal Cord ◽

West Nile Virus ◽

Immune Responses ◽

Ex Vivo ◽

Expression Patterns ◽

Cell Types ◽

Innate Immune ◽

Slice Culture ◽

Innate Immune Responses ◽

West Nile

West Nile virus (WNV) infection results in a spectrum of neurological symptoms, ranging from a benign fever to severe WNV neuroinvasive disease with high mortality. Many who recover from WNV neuroinvasive infection present with long-term deficits, including weakness, fatigue, and cognitive problems. While neurons are a main target of WNV, other cell types, especially astrocytes, play an important role in promoting WNV-mediated central nervous system (CNS) damage. Conversely, it has been shown that cultured primary astrocytes secrete high levels of interferons (IFNs) immediately after WNV exposure to protect neighboring astrocytes, as well as neurons. However, how intrinsic responses to WNV in specific cell types and different regions of the brain modify immune protection is not fully understood. Here, we used a mouse ex vivo spinal cord slice culture (SCSC) and cerebellar slice culture (CSC) models to determine the innate immune responses specific to the CNS during WNV infection. Slices were prepared from the spinal cord and cerebellar tissue of 7–9-day-old mouse pups. Four-day-old SCSC or CSC were infected with 1 × 103 or 1 × 105 PFU of WNV, respectively. After 12 h exposure to WNV and 3 days post-infection in normal growth media, the pooled slice cultures were processed for total RNA extraction and for gene expression patterns using mouse Affymetrix arrays. The expression patterns of a number of genes were significantly altered between the mock- and WNV-treated groups, both in the CSCs and SCSCs. However, distinct differences were observed when CSC data were compared with SCSC. CSCs showed robust induction of interferons (IFNs), IFN-stimulated genes (ISGs), and regulatory factors. Some of the antiviral genes related to IFN were upregulated more than 25-fold in CSCs as compared to mock or SCSC. Though SCSCs had twice the number of dysregulated genes, as compared CSCs, they exhibited a much subdued IFN response. In addition, SCSCs showed astrogliosis and upregulation of astrocytic marker genes. In sum, our results suggest that early anti-inflammatory response to WNV infection in CSCs may be due to large population of distinct astrocytic cell types, and lack of those specialized astrocytes in SCSC may make spinal cord cells more susceptible to WNV damage. Further, the understanding of early intrinsic immune response events in WNV-infected ex vivo culture models could help develop potential therapies against WNV.

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Disparate Entry of Adenoviruses Dictates Differential Innate Immune Responses on the Ocular Surface

Microorganisms ◽

10.3390/microorganisms7090351 ◽

2019 ◽

Vol 7 (9) ◽

pp. 351 ◽

Cited By ~ 6

Author(s):

Matthew R. Pennington ◽

Amrita Saha ◽

David F. Painter ◽

Christina Gavazzi ◽

Ashrafali M. Ismail ◽

...

Keyword(s):

Immune Responses ◽

Ocular Surface ◽

Human Adenovirus ◽

Cell Types ◽

Specific Pattern ◽

Innate Immune ◽

Dependent Manner ◽

Innate Immune Responses ◽

Cell Type ◽

Corneal Infiltrates

Human adenovirus infection of the ocular surface is associated with severe keratoconjunctivitis and the formation of subepithelial corneal infiltrates, which may persist and impair vision for months to years following infection. Long term pathology persists well beyond the resolution of viral replication, indicating that the prolonged immune response is not virus-mediated. However, it is not clear how these responses are sustained or even initiated following infection. This review discusses recent work from our laboratory and others which demonstrates different entry pathways specific to both adenovirus and cell type. These findings suggest that adenoviruses may stimulate specific pattern recognition receptors in an entry/trafficking-dependent manner, leading to distinct immune responses dependent on the virus/cell type combination. Additional work is needed to understand the specific connections between adenoviral entry and the stimulation of innate immune responses by the various cell types present on the ocular surface.

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Innate immune responses of human tracheal epithelium toPseudomonas aeruginosaflagellin, TNF-α, and IL-1β

AJP Cell Physiology ◽

10.1152/ajpcell.00166.2005 ◽

2006 ◽

Vol 290 (3) ◽

pp. C678-C690 ◽

Cited By ~ 36

Author(s):

Jill Tseng ◽

Jiun Do ◽

Jonathan H. Widdicombe ◽

Terry E. Machen

Keyword(s):

Immune Responses ◽

Tight Junctions ◽

Inflammatory Responses ◽

Cell Types ◽

Innate Immune ◽

Apical Surface ◽

Basal Cells ◽

Innate Immune Responses ◽

Tnf Α ◽

Columnar Cells

We measured innate immune responses by primary human tracheal epithelial (HTE) cells grown as confluent, pseudostratified layers during exposure to inflammatory activators on apical vs. basolateral surfaces. Apical Pseudomonas aeruginosa strain PAK (but not flagellin mutant PAK·fliC), flagellin, and flagellin + PAK·fliC activated NF-κB and IL-8 expression and secretion. In contrast, HTE cells were insensitive to LPS compared to flagellin. Flagellin activated NF-κB in columnar but not basal cells. IL-1β + TNF-α elicited responses similar to those of flagellin. Basolateral flagellin or IL-1β + TNF-α caused 1.5- to 4-fold larger responses, consistent with the fact that NF-κB activation occurred in both columnar and basal cells. MyD88 (toll receptor-associated adapter), IL-1 receptor (IL1R)1, and TNF-α receptor (TNFR)1 were expressed in columnar and basal cells. ZO-1 was localized to tight junctions of columnar cells but not to basal cells. We infer the following. 1) Flagellin is necessary and sufficient to trigger inflammatory responses in columnar cells during accumulation of P. aeruginosa in the airway surface liquid (ASL); columnar cells express toll-like receptor 5 and MyD88, often associated with flagellin-activated cell signaling. 2) IL-1β + TNF-α in the ASL also activate columnar cells, and these cells also express IL1R1 and TNFR1. 3) Apical flagellin, IL-1β, and TNF-α do not activate basal cells because tight junctions between columnar cells prevent access from the apical surface to the basal cells. 4) Exposure of basolateral surfaces to inflammatory activators elicits larger responses because both columnar and basal cells are activated, likely because both cell types express receptors for flagellin, IL-1β, and TNF-α.

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Oral Immune Activation by Disgust and Disease-Related Pictures

Journal of Psychophysiology ◽

10.1027/0269-8803/a000143 ◽

2015 ◽

Vol 29 (3) ◽

pp. 119-129 ◽

Cited By ~ 4

Author(s):

Richard J. Stevenson ◽

Deborah Hodgson ◽

Megan J. Oaten ◽

Luba Sominsky ◽

Mehmet Mahmut ◽

...

Keyword(s):

Immune Response ◽

Immune Responses ◽

Innate Immune Response ◽

Negative Control ◽

Innate Immune ◽

Innate Immune Responses ◽

Immune Markers ◽

Before And After ◽

Secondary Analyses ◽

Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

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