scholarly journals Membrane glycoconjugates expressed on sheep airway epithelium.

1994 ◽  
Vol 42 (10) ◽  
pp. 1341-1347 ◽  
Author(s):  
K Abdi ◽  
L Kobzik ◽  
X Li ◽  
S J Mentzer
Keyword(s):  
Western Blotting ◽  
Airway Epithelium ◽  
Viral Infections ◽  
Transplant Rejection ◽  
Histochemical Staining ◽  
Inflammatory Reactions ◽  
Peripheral Airways ◽  
Trichosanthes Kirilowii ◽  
Mammalian Lung ◽  
Selective Reactivity

In mammalian lung, selective airway inflammatory reactions have been associated with viral infections, transplant rejection, and autoimmune diseases. Although the molecular basis for this selective reactivity is unknown, the importance of carbohydrates in immunologic processes suggests a potential role for membrane glycoconjugates in tissue-specific inflammatory reactions. In the present work we examined a panel of 39 lectins for their pattern of reactivity in the peripheral airways of the sheep lung. The size of the panel facilitated a comprehensive description of the glycoconjugate localization on the airway epithelium. Four lectins (agglutinins for Helix aspersa, Psophocarpus tetragonolobus, Trichosanthes kirilowii, and Griffonia simplifolia II) revealed selective reactivity with the small airway epithelium. On lectin Western blotting, these four lectins demonstrated a common low molecular weight banding profile that was distinct from control lectins. The histochemical staining patterns and Western blotting profiles provided evidence for the selective expression of membrane glycoconjugates in the peripheral airways of the sheep lung.

scholarly journals C-type lectins and extracellular vesicles in virus-induced NETosis

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Pei-Shan Sung ◽  
Shie-Liang Hsieh
Keyword(s):  
Extracellular Vesicles ◽  
Viral Infections ◽  
Multiple Organ ◽  
Intercellular Adhesion Molecule ◽  
Inflammatory Reactions ◽  
Intravascular Coagulopathy ◽  
Encephalomyelitis Virus ◽  
Toll Like Receptor 2 ◽  
Lectin Family ◽  
Virus Spreading

AbstractDysregulated formation of neutrophil extracellular traps (NETs) is observed in acute viral infections. Moreover, NETs contribute to the pathogenesis of acute viral infections, including those caused by the dengue virus (DV) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Furthermore, excessive NET formation (NETosis) is associated with disease severity in patients suffering from SARS-CoV-2-induced multiple organ injuries. Dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) and other members of C-type lectin family (L-SIGN, LSECtin, CLEC10A) have been reported to interact with viral glycans to facilitate virus spreading and exacerbates inflammatory reactions. Moreover, spleen tyrosine kinase (Syk)-coupled C-type lectin member 5A (CLEC5A) has been shown as the pattern recognition receptor for members of flaviviruses, and is responsible for DV-induced cytokine storm and Japanese encephalomyelitis virus (JEV)-induced neuronal inflammation. Moreover, DV activates platelets via CLEC2 to release extracellular vesicles (EVs), including microvesicles (MVs) and exosomes (EXOs). The DV-activated EXOs (DV-EXOs) and MVs (DV-MVs) stimulate CLEC5A and Toll-like receptor 2 (TLR2), respectively, to enhance NET formation and inflammatory reactions. Thus, EVs from virus-activated platelets (PLT-EVs) are potent endogenous danger signals, and blockade of C-type lectins is a promising strategy to attenuate virus-induced NETosis and intravascular coagulopathy.

scholarly journals Monocytes in Neonatal Bacterial Sepsis: Think Tank or Workhorse?

BioChem ◽  
2022 ◽  
Vol 2 (1) ◽  
pp. 27-43
Author(s):  
Caitlin Doughty ◽  
Louise Oppermann ◽  
Niels-Ulrik Hartmann ◽  
Stephan Dreschers ◽  
Christian Gille ◽  
...  
Keyword(s):  
T Cell Activation ◽  
Bacterial Infections ◽  
Cell Activation ◽  
Viral Infections ◽  
Organ Damage ◽  
Host Responses ◽  
Critical Event ◽  
Think Tank ◽  
Inflammatory Reactions ◽  
Inflammatory Conditions

Infection and sepsis remain among the leading causes of neonatal mortality. The susceptibility of newborns to infection can be attributed to their immature immune system. Regarding immune response, monocytes represent a numerically minor population of leukocytes. However, they contribute to a variety of immunological demands, such as continuous replenishment of resident macrophages under non-infectious conditions and migration to inflamed sites where they neutralize pathogens and secrete cytokines. Further functions include the presentation of antigens and T-cell activation. Cytokines coordinate host responses to bacterial and viral infections and orchestrate ongoing physiological signaling between cells of non-immune tissues. A critical event is the skewing of the cytokine repertoire to achieve a resolution of infection. In this regard, monocytes may hold a key position as deciders in addition to their phagocytic activity, securing the extinction of pathogens to prevent broader organ damage by toxins and pro-inflammatory reactions. Neonatal monocytes undergo various regulatory and metabolic changes. Thus, they are thought to be vulnerable in anticipating pro-inflammatory conditions and cause severe progressions which increase the risk of developing sepsis. Furthermore, clinical studies have shown that exposure to inflammation puts neonates at a high risk for adverse pulmonary, immunological and other organ developments, which may result in multiorgan disease. This review discusses significant functions and impairments of neonatal monocytes that are decisive for the outcome of bacterial infections.

Rapid increase in mast cell numbers in canine central and peripheral airways

1988 ◽  
Vol 65 (1) ◽  
pp. 445-451 ◽  
Author(s):  
C. R. Turner ◽  
J. Kolbe ◽  
E. W. Spannhake
Keyword(s):  
Mast Cell ◽  
Airway Epithelium ◽  
Time Course ◽  
Isotonic Saline ◽  
Cell Movement ◽  
Cell Number ◽  
Small Airways ◽  
Cell Numbers ◽  
Peripheral Airways ◽  
Cell Counts

In preliminary studies of antigen-induced airway inflammation, we noted an apparent increase in peribronchiolar mast cell number. Experiments were thus undertaken to investigate the nature of this migration of mast cells into the central and peripheral airway epithelium and to determine its time course. The tracheae and small airways of 10 anesthetized mongrel dogs were exposed via a bronchoscope to Ascaris suum antigen (Ag), fMet-Leu-Phe (fMLP), ovalbumin (OVA), and isotonic saline (SAL). In the central airways, all stimuli provoked a significant increase (P less than 0.05) in mast cell numbers at the base of the airway epithelium within 3 h. In the peripheral airways, only Ag aerosol stimulated a significant mast cell increase compared with unexposed tissue. In a second series of experiments, the trachea of seven dogs were exposed to 0.026, 0.26, and 2.6 micrograms of Ag. The tissue was collected at 1, 3, 6, and 10 h after exposure. In these experiments, there was a significant mast cell increase seen within 1 h but it was not dose dependent. By 6-10 h after exposure, mast cell counts were not significantly different from the unexposed condition, which is consistent with the idea that some of the cells either degranulated or migrated into the airway lumen. We conclude that mast cell migration is an acute response that can be demonstrated within 1 h of stimulation with Ag. The observation that nonimmunological stimuli may, in some cases, also stimulate mast cell movement affords the possibility that this process represents a generalized response to airway irritation.

P0647ACUTE KIDNEY INJURY SECONDARY TO SUCROSE CONTAING INTAVENOUS IMMUNOGLOBULIN

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sadiq Al Lawati ◽  
Issa Al Salmi ◽  
SUAD Hannawi
Keyword(s):  
Acute Kidney Injury ◽  
Serum Level ◽  
Kidney Function ◽  
Viral Infections ◽  
Kidney Transplant Recipient ◽  
Transplant Rejection ◽  
Organ Transplant ◽  
Vital Signs ◽  
Kidney Injury ◽  
Kaposi Sarcoma

Abstract Background and Aims Intravenous immunoglobulins (IVIG) are pooled polyvalent IgG antibodies extracted from the human plasma. While the initial indications were mainly immune deficiency states and some autoimmune diseases, the usage has been widened to include several immune mediated diseases, viral infections, and organ transplant rejection. Stabilizers in IVIG may include sugars, such as sucrose, glucose, or maltose. Sucrose in IVIG preparations may cause acute kidney injury. We report the case of a renal transplant patient who developed acute kidney injury due to sucrose nephropathy following the administration of sucrose containing IVIG. Method Four months after transplantation he was referred to our Hospital for deterioration of kidney function with eGFR (by MDRD formula) of 27ml/min. Cytomegalovirus virus (CMV) PCR turned positive (3300 copies/ml). Cyclosporine levels were high (C2: 2937 ng/ml) and hence, cyclosporine dose was adjusted. Induction therapy with Injection Ganciclovir for 2 weeks, followed by therapeutic dose of oral Valganciclovir was administered for the treatment of CMV infection. Skin examination revealed annular purple patches, suspicious of Kaposi Sarcoma, on the upper limbs. Skin biopsy confirmed the diagnosis. It was planned to give total IVIG of 2 gm/ kg in four daily divided doses. After completion of the second dose, serum creatinine increased to 370 µmol/L. He was clinically asymptomatic, euvolumic, vital signs were stable, and his urine output remained normal and his urinalysis was inactive. Results The ultrasound of the transplant kidney was normal with normal resistivity index. IVIG was stopped. He was well hydrated and underwent ultrasound guided biopsy. The graft biopsy showed acute tubular injury with flattening and vacuolation of tubular epithelial cells. Mitosis indicating tubular regeneration was seen. There was mild focal interstitial inflammation (20%) with mild lymphocytic tubulitis not amounting to graft rejection. Immunohistochemistry for C4d and polyomavirus (BKV) were both negative. The features were most consistent with sucrose induced nephropathy (Figure 1). Subsequent visits showed a decrease in BKV-PCR serum level and eventually undetected serum level of BKV-PCR at follow up about a month later. Conclusion In this paper, we presented a case of a living unrelated kidney transplant recipient who developed BKV nephropathy and developed impaired kidney function. The patient also had new onset diabetes mellitus after kidney transplantation (NODAT) but was otherwise in good general health. Treatment included sucrose containing IVIG. The patient subsequently developed acute kidney injury. The outcome was favorable with recovery of filtration rate to the baseline within 21 days without the need for dialysis. We conclude that the administration of sucrose containing IVIG may lead to acute kidney injury. We recommend the use of sucrose-free IVIG whenever possible. In all cases, caution is required when administrating IVIG.

Latent Viral Infections in Airway Epithelium

CHEST Journal ◽  
1992 ◽  
Vol 101 (3) ◽  
pp. 80S-82S ◽  
Author(s):  
James C. Hogg
Keyword(s):  
Airway Epithelium ◽  
Viral Infections

scholarly journals Infection with human coronavirus NL63 enhances streptococcal adherence to epithelial cells

2011 ◽  
Vol 92 (6) ◽  
pp. 1358-1368 ◽  
Author(s):  
Anna Golda ◽  
Natalia Malek ◽  
Bartosz Dudek ◽  
Slawomir Zeglen ◽  
Jacek Wojarski ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Airway Epithelium ◽  
Viral Infections ◽  
Platelet Activating Factor ◽  
Virus Infected Cell ◽  
Human Coronavirus ◽  
Bacterial Pathogenicity ◽  
Human Airway Epithelium ◽  
Detailed Evaluation ◽  
Respiratory Tract Illnesses

Understanding the mechanisms of augmented bacterial pathogenicity in post-viral infections is the first step in the development of an effective therapy. This study assessed the effect of human coronavirus NL63 (HCoV-NL63) on the adherence of bacterial pathogens associated with respiratory tract illnesses. It was shown that HCoV-NL63 infection resulted in an increased adherence of Streptococcus pneumoniae to virus-infected cell lines and fully differentiated primary human airway epithelium cultures. The enhanced binding of bacteria correlated with an increased expression level of the platelet-activating factor receptor (PAF-R), but detailed evaluation of the bacterium–PAF-R interaction revealed a limited relevance of this process.

scholarly journals The Role of PPAR Alpha in the Modulation of Innate Immunity

2021 ◽  
Vol 22 (19) ◽  
pp. 10545
Author(s):  
Maja Grabacka ◽  
Małgorzata Pierzchalska ◽  
Przemysław M. Płonka ◽  
Piotr Pierzchalski
Keyword(s):  
Innate Immunity ◽  
Energy Homeostasis ◽  
Viral Infections ◽  
Endocannabinoid System ◽  
Lymphoid Cells ◽  
Peroxisome Proliferator ◽  
Ppar Alpha ◽  
Peroxisome Proliferator Activated Receptor ◽  
Inflammatory Reactions ◽  
Transcription Factor Signaling

Peroxisome proliferator-activated receptor α is a potent regulator of systemic and cellular metabolism and energy homeostasis, but it also suppresses various inflammatory reactions. In this review, we focus on its role in the regulation of innate immunity; in particular, we discuss the PPARα interplay with inflammatory transcription factor signaling, pattern-recognition receptor signaling, and the endocannabinoid system. We also present examples of the PPARα-specific immunomodulatory functions during parasitic, bacterial, and viral infections, as well as approach several issues associated with innate immunity processes, such as the production of reactive nitrogen and oxygen species, phagocytosis, and the effector functions of macrophages, innate lymphoid cells, and mast cells. The described phenomena encourage the application of endogenous and pharmacological PPARα agonists to alleviate the disorders of immunological background and the development of new solutions that engage PPARα activation or suppression.

scholarly journals Airway hyperresponsiveness; smooth muscle as the principal actor

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 306 ◽  
Author(s):  
Anne-Marie Lauzon ◽  
James G. Martin
Keyword(s):  
Smooth Muscle ◽  
Airway Epithelium ◽  
Airway Hyperresponsiveness ◽  
Healthy Subjects ◽  
Tumor Necrosis ◽  
Airway Narrowing ◽  
Peripheral Airways ◽  
The Matrix ◽  
Factor Α ◽  
Necrosis Factor

Airway hyperresponsiveness (AHR) is a defining characteristic of asthma that refers to the capacity of the airways to undergo exaggerated narrowing in response to stimuli that do not result in comparable degrees of airway narrowing in healthy subjects. Airway smooth muscle (ASM) contraction mediates airway narrowing, but it remains uncertain as to whether the smooth muscle is intrinsically altered in asthmatic subjects or is responding abnormally as a result of the milieu in which it sits. ASM in the trachea or major bronchi does not differ in its contractile characteristics in asthmatics, but the more pertinent peripheral airways await complete exploration. The mass of ASM is increased in many but not all asthmatics and therefore cannot be a unifying hypothesis for AHR, although when increased in mass it may contribute to AHR. The inability of a deep breath to reverse or prevent bronchial narrowing in asthma may reflect an intrinsic difference in the mechanisms that lead to softening of contracted ASM when subjected to stretch. Cytokines such as interleukin-13 and tumor necrosis factor-α promote a more contractile ASM phenotype. The composition and increased stiffness of the matrix in which ASM is embedded promotes a more proliferative and pro-inflammatory ASM phenotype, but the expected dedifferentiation and loss of contractility have not been shown. Airway epithelium may drive ASM proliferation and/or molecular remodeling in ways that may lead to AHR. In conclusion, AHR is likely multifactorial in origin, reflecting the plasticity of ASM properties in the inflammatory environment of the asthmatic airway.

scholarly journals Identification of the Molecular Mechanism by which TLR Ligation and IFN-γ Synergize to Induce Mig

2004 ◽  
Vol 11 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Jonathan D. Powell ◽  
Sada Boodoo ◽  
Maureen R. Horton
Keyword(s):  
T Cell ◽  
Molecular Mechanisms ◽  
Viral Infections ◽  
Transplant Rejection ◽  
Potent Inducer ◽  
Cell Immunity ◽  
Tnf Α ◽  
Mouse Macrophages ◽  
Ifn Γ ◽  
Responsive Element

Monokine Induced by Interferon- (MIG), a CXC chemokine, is a potent inducer of T-cell chemotaxis and activation and has been implicated in the host response to viral infections and tumor immunity as well as in the pathogenesis of autoimmunity and transplant rejection. Although it is known that the Toll-Like Receptor-4 (TLR-4) ligand LPS synergizes with IFN-γ to induce MIG expression in macrophages, the molecular mechanisms responsible for the synergy have yet to be elucidated. We determined that the marked synergy between LPS and IFN-γ on MIG mRNA expression in mouse macrophages is a result of LPS-induced NF-κB and IFN-γ-induced STAT. The synergy was not dependent on new protein synthesis, was independent of TNF-α, and occurred at the level of gene transcription. We identified 2 NF-κB sites located at -154 and -129 of the MIG promoter proximal to the -responsive element that mediated this effect. Finally, we demonstrated that other TLR ligands (zymosan, double stranded RNA and CpG) synergized with IFN-γ to induce MIG in an NF-κB dependent fashion. These data emphasize the ability of bacterial and viral products to activate/modify immune responses and promote adaptive T cell immunity through the NF-κB pathway.

scholarly journals Biomolecular changes and cortical neurodegenerative lesions in Trichinella spiralis infected BALB/c mice: a preliminary study elucidating a potential relationship between systemic helminthic infections and idiopathic Parkinson’s

2018 ◽  
Vol 55 (4) ◽  
pp. 261-274 ◽  
Author(s):  
M. Hasby Saad ◽  
O. Safwat ◽  
D. El-Guindy ◽  
R. Raafat ◽  
D. Elgendy ◽  
...  
Keyword(s):  
Viral Infections ◽  
Trichinella Spiralis ◽  
Histopathological Examination ◽  
Parasitic Infection ◽  
Brain Homogenate ◽  
Dopamine Level ◽  
Inflammatory Reactions ◽  
Oxidative Stresses ◽  
Helminthic Infections ◽  
The Brain

Abstract Idiopathic Parkinson’s (IP) is a neurodegenerative disease that is suspected to be due to exposure to infections during early life. Toxoplasmosishas been the only suspected parasitic infection in IP (Celik et al., 2010). Recently, some non-central nervous system bacterial and viral infections have been incriminated in IP (Çamcı & Oğuz, 2016). So in the current study, we tried to explore if the systemic infl ammatory reactions triggered by some helminths like Trichinella spiralis can induce Parkinsonian lesions in the brain, especially that the cerebral complications have been reported in 10-20% of Trichinella spiralis infected patients . An experimental study was designed to assess the neurodegenerative and biomolecular changes that may occur in Trichinella spiralis infected BALB/C mice in comparison to rotenone induced PD model and apparently healthy ones. The motor affection was significantly lesser in the Trichinella infected mice than the Parkinson’s model, but when the catalepsy score was calculated (through the grid and bar tests) it was found to be significantly higher in the infected mice than in the healthy ones. A significant increase in the blood advanced oxidative protein products (AOPP), IFN-γ, TGF-β, and brain DNA fragmentation was also detected in the Trichinella spiralis infected mice. After histopathological examination, a significant increase in the cortical apoptotic neurons and Lewy’s body were observed in the Trichinella infected and the rotenone induced Parkinson’s model sections. A significant decrease in the immunohistochemical expression of the tyrosine hydroxylase expression in the brain sections and the ELISA measured dopamine level in the brain homogenate was also reported in the infected mice group. This study findings may collectively suggest that the systemic inflammatory reactions and the oxidative stresses associated with some systemic helminthic infections like trichinellosis are possible to precipitate neurodegenerative lesions and biomolecular changes in the brain , and manifest with IPD later in life.

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