scholarly journals The legacy of maternal SARS-CoV-2 infection on the immunology of the neonate

2021 ◽  
Author(s):  
Sarah Gee ◽  
Manju Chandiramani ◽  
Jeffrey Seow ◽  
Carlotta Modestini ◽  
Abhishek Das ◽  
...  
Keyword(s):  
In Utero ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Maternal Infection ◽  
Increased Risk ◽  
Specific Igg ◽  
Potential Impact ◽  
Effector Response ◽  
Ongoing Infection ◽  
Pro Inflammatory Cytokines

Despite extensive and ongoing studies of SARS-CoV-2 and evidence that pregnant women are at increased risk of severe COVID-19, the effect of maternal infection on the developing infant remains unclear. To determine the potential impact of exposure to SARS-CoV-2 in utero on the neonate, we have assessed the immunological status of infants born to mothers with confirmed SARS-CoV-2 infection during gestation. No evidence of vertical transmission of SARS-CoV-2 was observed, but transfer of maternal SARS-CoV-2 specific IgG to infants was apparent, although to a lesser extent in cases of active or recent maternal infection. Infants born to mothers with recent/ongoing infection had elevated circulating pro-inflammatory cytokines and enhanced percentages of innate immune cells compared to that seen in infants born to uninfected mothers. In tandem, higher frequencies of FOXP3+ regulatory T cells and circulating IL-10 demonstrated a further nuance to the neonatal effector response. Interestingly, cytokine functionality was enhanced in infants born to mothers exposed to SARS-CoV-2 at any time during pregnancy. This indicates that maternal SARS-CoV-2 infection influences in utero priming of the fetal immune system.

scholarly journals Macrophages and Dendritic Cells Are Not the Major Source of Pro-Inflammatory Cytokines Upon SARS-CoV-2 Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Marc A. Niles ◽  
Patricia Gogesch ◽  
Stefanie Kronhart ◽  
Samira Ortega Iannazzo ◽  
Georg Kochs ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Influenza A ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
M2 Macrophages ◽  
Myeloid Dendritic Cells ◽  
M1 And M2 Macrophages ◽  
Pro Inflammatory Cytokines

The exact role of innate immune cells upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and their contribution to the formation of the corona virus-induced disease (COVID)-19 associated cytokine storm is not yet fully understood. We show that human in vitro differentiated myeloid dendritic cells (mDC) as well as M1 and M2 macrophages are susceptible to infection with SARS-CoV-2 but are not productively infected. Furthermore, infected mDC, M1-, and M2 macrophages show only slight changes in their activation status. Surprisingly, none of the infected innate immune cells produced the pro-inflammatory cytokines interleukin (IL)−6, tumor necrosis factor (TNF)-α, or interferon (IFN)−α. Moreover, even in co-infection experiments using different stimuli, as well as non-influenza (non-flu) or influenza A (flu) viruses, only very minor IL-6 production was induced. In summary, we conclude that mDC and macrophages are unlikely the source of the first wave of cytokines upon infection with SARS-CoV-2.

scholarly journals Effect of vitamin D on immune response of respiratory system against influenzas and COVID-19: A review

2020 ◽  
Vol 3 (6) ◽  
pp. 100
Author(s):  
Payam Hashemi ◽  
Hossein Mirmiranpour ◽  
Shaghayegh Pezeshki
Keyword(s):  
Vitamin D ◽  
Immune Cells ◽  
Viral Infections ◽  
Severe Pneumonia ◽  
Innate Immune ◽  
System Response ◽  
Innate Immune Cells ◽  
Immune System Response ◽  
Tract Infections ◽  
Pro Inflammatory Cytokines

Vitamin D could decrease the risk of viral infections with regulation of the immune system response against viral activity. Proper level of 25(OH)D decreases the risk of chronic respiratory tract infections (RTIs), malignancies, hypertension, cardiovascular disease, and diabetes mellitus. Vitamin D can decrease risk of RTIs through some mechanisms. Adequate levels of vitamin D can decrease the level of pro-inflammatory cytokines which predominantly release from innate immune cells. It also can preserve tight junctions in the base membrane. Vitamin D may eliminate enveloped viruses by activating cathelicidin (a protein in the membrane of neutrophils, macrophages, and epithelial cells). These processes can reduce the risk of a cytokine storm and severe pneumonia. Clinical trials have shown the beneficial influences of vitamin D in decreasing the risk of viral pneumonia, dengue fever, hepatitis B, hepatitis C, and herpes infections.Keywords: Vitamin D, influenza, covid-19, innate immune cells, infections

scholarly journals Immunohistochemical Study of ASC Expression and Distribution in the Hippocampus of an Aged Murine Model of Alzheimer’s Disease

2021 ◽  
Vol 22 (16) ◽  
pp. 8697
Author(s):  
Diana Reimers ◽  
Manuela Vallejo-Muñoz ◽  
María José Casarejos ◽  
Adriano Jimenez-Escrig ◽  
Rafael Gonzalo-Gobernado ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Immune Cells ◽  
Immunohistochemical Study ◽  
Transgenic Mouse Model ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Danger Signals ◽  
Model Of Alzheimer’S Disease ◽  
Pro Inflammatory Cytokines

Neuroinflammation is involved in the pathogenesis of neurodegenerative diseases such as Alzheimer’s disease (AD), and is notably dependent on age. One important inflammatory pathway exerted by innate immune cells of the nervous system in response to danger signals is mediated by inflammasomes (IF) and leads to the generation of potent pro-inflammatory cytokines. The protein “apoptosis-associated speck-like protein containing a caspase recruitment domain” (ASC) modulates IF activation but has also other functions which are crucial in AD. We intended to characterize immunohistochemically ASC and pattern recognition receptors (PRR) of IF in the hippocampus (HP) of the transgenic mouse model Tg2576 (APP), in which amyloid-beta (Aβ) pathology is directly dependent on age. We show in old-aged APP a significant amount of ASC in microglia and astrocytes associated withAβ plaques, in the absence of PRR described by others in glial cells. In addition, APP developed foci with clusters of extracellular ASC granules not spatiallyrelated to Aβ plaques, which density correlated with the advanced age of mice and AD development. Clusters were associated withspecific astrocytes characterized by their enlarged ring-shaped process terminals, ASC content, and frequent perivascular location. Their possible implication in ASC clearance and propagation of inflammation is discussed.

Cytokine networking of innate immunity cells: a potential target of therapy

2014 ◽  
Vol 126 (9) ◽  
pp. 593-612 ◽  
Author(s):  
Ilja Striz ◽  
Eva Brabcova ◽  
Libor Kolesar ◽  
Alena Sekerkova
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Regulatory T Cells ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Innate Immune ◽  
Lymphoid Cells ◽  
Extracellular Matrix Protein ◽  
Innate Immune Cells ◽  
Pro Inflammatory Cytokines

Innate immune cells, particularly macrophages and epithelial cells, play a key role in multiple layers of immune responses. Alarmins and pro-inflammatory cytokines from the IL (interleukin)-1 and TNF (tumour necrosis factor) families initiate the cascade of events by inducing chemokine release from bystander cells and by the up-regulation of adhesion molecules required for transendothelial trafficking of immune cells. Furthermore, innate cytokines produced by dendritic cells, macrophages, epithelial cells and innate lymphoid cells seem to play a critical role in polarization of helper T-cell cytokine profiles into specific subsets of Th1/Th2/Th17 effector cells or regulatory T-cells. Lastly, the innate immune system down-regulates effector mechanisms and restores homoeostasis in injured tissue via cytokines from the IL-10 and TGF (transforming growth factor) families mainly released from macrophages, preferentially the M2 subset, which have a capacity to induce regulatory T-cells, inhibit the production of pro-inflammatory cytokines and induce healing of the tissue by regulating extracellular matrix protein deposition and angiogenesis. Cytokines produced by innate immune cells represent an attractive target for therapeutic intervention, and multiple molecules are currently being tested clinically in patients with inflammatory bowel disease, rheumatoid arthritis, systemic diseases, autoinflammatory syndromes, fibrosing processes or malignancies. In addition to the already widely used blockers of TNFα and the tested inhibitors of IL-1 and IL-6, multiple therapeutic molecules are currently in clinical trials targeting TNF-related molecules [APRIL (a proliferation-inducing ligand) and BAFF (B-cell-activating factor belonging to the TNF family)], chemokine receptors, IL-17, TGFβ and other cytokines.

scholarly journals Cellular Interplay as a Consequence of Inflammatory Signals Leading to Liver Fibrosis Development

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 461 ◽  
Author(s):  
Simona-Rebeca Ignat ◽  
Sorina Dinescu ◽  
Anca Hermenean ◽  
Marieta Costache
Keyword(s):  
Cell Death ◽  
Liver Fibrosis ◽  
Molecular Mechanisms ◽  
Stellate Cells ◽  
Innate Immune ◽  
Sterile Inflammation ◽  
Innate Immune Cells ◽  
Inflammatory Signals ◽  
Molecular Patterns ◽  
Pro Inflammatory Cytokines

Inflammation has been known to be an important driver of fibrogenesis in the liver and onset of hepatic fibrosis. It starts off as a process meant to protect the liver from further damage, but it can become the main promoter of liver fibrosis. There are many inflammation-related pathways activated during liver fibrosis that lead to hepatic stellate cells (HSCs) activation and collagen-deposition in the liver. Such events are mostly modulated upstream of HSCs and involve signals from hepatocytes and innate immune cells. One particular event is represented by cell death during liver injury that generates multiple inflammatory signals that further trigger sterile inflammation and enhancement of inflammatory response. The assembly of inflammasome that responds to danger-associated molecular patterns (DAMPs) stimulates the release of pro-inflammatory cytokines and at the same time, initiates programmed cell death called pyroptosis. This review focuses on cellular and molecular mechanisms responsible for initiation and progress of inflammation in the liver.

scholarly journals The Contribution of Allergen-Specific IgG to the Development of Th2-Mediated Airway Inflammation

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Jesse W. Williams ◽  
Melissa Y. Tjota ◽  
Anne I. Sperling
Keyword(s):  
Airway Inflammation ◽  
Immune Cells ◽  
Allergic Inflammation ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Fc Gamma Receptor ◽  
Allergic Lung Disease ◽  
Gamma Receptor ◽  
Specific Igg ◽  
Antigen Presenting

In both human asthmatics and animal models of allergy, allergen-specific IgG can contribute to Th2-mediated allergic inflammation. Mouse models have elucidated an important role for IgG and Fc-gamma receptor (FcγR) signaling on antigen presenting cells (APC) for the induction of airway inflammation. These studies suggest a positive feedback loop between IgG produced by the adaptive B cell response and FcγR signaling on innate immune cells. Studies of IgG and FcγRs in humans with asthma or allergic lung disease have been more controversial. Some reports have identified associations between allergen-specific IgG and severity of allergic responses, while other studies have found associations of IgG subclass IgG4 with allergic tolerance. In this paper, we review the literature to help define the nature of IgG and FcγR signaling on innate immune cells and how it contributes to the development of allergic immune responses.

In utero exposure to low doses of genistein and di‐(2‐ethylhexyl) phthalate (DEHP) alters innate immune cells in neonatal and adult rat testes

Andrology ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 943-964
Author(s):  
Casandra Walker ◽  
Shahrzad Ghazisaeidi ◽  
Berenice Collet ◽  
Annie Boisvert ◽  
Martine Culty
Keyword(s):  
Immune Cells ◽  
In Utero ◽  
Innate Immune ◽  
In Utero Exposure ◽  
Innate Immune Cells ◽  
Low Doses ◽  
Adult Rat ◽  
Ethylhexyl Phthalate

scholarly journals Immunoporosis: Role of Innate Immune Cells in Osteoporosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yogesh Saxena ◽  
Sanjeev Routh ◽  
Arunika Mukhopadhaya
Keyword(s):  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Inflammatory Mediators ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Myeloid Lineage ◽  
Molecular Patterns ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Osteoporosis or porous bone disorder is the result of an imbalance in an otherwise highly balanced physiological process known as ‘bone remodeling’. The immune system is intricately involved in bone physiology as well as pathologies. Inflammatory diseases are often correlated with osteoporosis. Inflammatory mediators such as reactive oxygen species (ROS), and pro-inflammatory cytokines and chemokines directly or indirectly act on the bone cells and play a role in the pathogenesis of osteoporosis. Recently, Srivastava et al. (Srivastava RK, Dar HY, Mishra PK. Immunoporosis: Immunology of Osteoporosis-Role of T Cells. Frontiers in immunology. 2018;9:657) have coined the term “immunoporosis” to emphasize the role of immune cells in the pathology of osteoporosis. Accumulated pieces of evidence suggest both innate and adaptive immune cells contribute to osteoporosis. However, innate cells are the major effectors of inflammation. They sense various triggers to inflammation such as pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), cellular stress, etc., thus producing pro-inflammatory mediators that play a critical role in the pathogenesis of osteoporosis. In this review, we have discussed the role of the innate immune cells in great detail and divided these cells into different sections in a systemic manner. In the beginning, we talked about cells of the myeloid lineage, including macrophages, monocytes, and dendritic cells. This group of cells explicitly influences the skeletal system by the action of production of pro-inflammatory cytokines and can transdifferentiate into osteoclast. Other cells of the myeloid lineage, such as neutrophils, eosinophils, and mast cells, largely impact osteoporosis via the production of pro-inflammatory cytokines. Further, we talked about the cells of the lymphoid lineage, including natural killer cells and innate lymphoid cells, which share innate-like properties and play a role in osteoporosis. In addition to various innate immune cells, we also discussed the impact of classical pro-inflammatory cytokines on osteoporosis. We also highlighted the studies regarding the impact of physiological and metabolic changes in the body, which results in chronic inflammatory conditions such as ageing, ultimately triggering osteoporosis.

scholarly journals Malaria Modifies Neonatal and Early-Life Toll-Like Receptor Cytokine Responses

2013 ◽  
Vol 81 (8) ◽  
pp. 2686-2696 ◽  
Author(s):  
Komi Gbédandé ◽  
Stefania Varani ◽  
Samad Ibitokou ◽  
Parfait Houngbegnon ◽  
Sophie Borgella ◽  
...  
Keyword(s):  
Immune Responses ◽  
Early Life ◽  
In Utero ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Content Type ◽  
Cytokine Responses ◽  
Increased Risk ◽  
Tnf Α

ABSTRACTProtection from infections in early life relies extensively on innate immunity, but it is unknown whether and how maternal infections modulate infants' innate immune responses, thereby altering susceptibility to infections.Plasmodium falciparumcauses pregnancy-associated malaria (PAM), and epidemiological studies have shown that PAM enhances infants' susceptibility to infection withP. falciparum. We investigated how PAM-mediated exposuresin uteroaffect innate immune responses and their relationship with infection in infancy. In a prospective study of mothers and their babies in Benin, we investigated changes in Toll-like receptor (TLR)-mediated cytokine responses related toP. falciparuminfections. Whole-blood samples from 134 infants at birth and at 3, 6, and 12 months of age were stimulated with agonists specific for TLR3, TLR4, TLR7/8, and TLR9. TLR-mediated interleukin 6 (IL-6) and IL-10 production was robust at birth and then stabilized, whereas tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ) responses were weak at birth and then increased. In multivariate analyses, maternalP. falciparuminfections at delivery were associated with significantly higher TLR3-mediated IL-6 and IL-10 responses in the first 3 months of life (P< 0.05) and with significantly higher TLR3-, TLR7/8-, and TLR9-mediated TNF-α responses between 6 and 12 months of age (P< 0.05). Prospective analyses showed that higher TLR3- and TLR7/8-mediated IL-10 responses at birth were associated with a significantly higher risk ofP. falciparuminfection in infancy (P< 0.05). Neonatal and infant intracellular TLR-mediated cytokine responses are conditioned byin uteroexposure through PAM late in pregnancy. Enhanced TLR-mediated IL-10 responses at birth are associated with an increased risk ofP. falciparuminfection, suggesting a compromised ability to combat infection in early life.

scholarly journals CFTR-mediated monocyte-macrophage dysfunction revealed by cystic fibrosis proband-parent comparisons

2021 ◽  
Author(s):  
Xi Zhang ◽  
Camille Moore ◽  
Laura Harmacek ◽  
Joanne Domenico ◽  
Vittobai Rangaraj ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Immune Cells ◽  
Molecular Mechanisms ◽  
Mononuclear Cells ◽  
Mononuclear Phagocyte ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Peripheral Blood Mononuclear ◽  
Increased Risk ◽  
Biallelic Mutations

Cystic fibrosis (CF) is an inherited disorder caused by biallelic mutations of the cystic fibrosis transmembrane conductance regulator gene (CFTR). Converging lines of evidence suggest that CF carriers with only one defective CFTR copy are at increased risk for CF-related conditions and pulmonary infections, but the molecular mechanisms underpinning this effect remain unknown. Here, we performed transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) of CF child-parent trios (proband, father, and mother) and healthy control PBMCs or THP-1 cells incubated with the plasma of these subjects. Transcriptomic analyses revealed suppression of cytokine-enriched immune-related genes (IL-1, CXCL8, CREM) implicating lipopolysaccharide tolerance in innate immune cells (monocytes) of CF probands and their parents and in the control innate immune cells incubated with proband or parent plasma. These data suggest that not only a homozygous but also a heterozygous CFTR mutation can modulate the immune/inflammatory system. This conclusion is further supported by the findings of lower numbers of circulating monocytes in CF probands and their parents compared to healthy controls, the abundance of mononuclear phagocyte subsets (macrophages, monocytes, and activated dendritic cells) which correlated with Pseudomonas aeruginosa infection, lung disease severity, and CF progression in the probands. This study provides insight into demonstrated CFTR-related innate immune dysfunction in individuals with CF and carriers of a CFTR mutation that may serve as a target for personalized therapy.

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