scholarly journals Effects of mannose-binding lectin on pulmonary gene expression and innate immune inflammatory response to ozone

2016 ◽  
Vol 311 (2) ◽  
pp. L280-L291 ◽  
Author(s):  
Jonathan M. Ciencewicki ◽  
Kirsten C. Verhein ◽  
Kevin Gerrish ◽  
Zachary R. McCaw ◽  
Jianying Li ◽  
...  
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Innate Immune System ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Innate Immune ◽  
Gene Sets ◽  
Mannose Binding ◽  
Gene Transcripts ◽  
Binding Lectin

Ozone is a common, potent oxidant pollutant in industrialized nations. Ozone exposure causes airway hyperreactivity, lung hyperpermeability, inflammation, and cell damage in humans and laboratory animals, and exposure to ozone has been associated with exacerbation of asthma, altered lung function, and mortality. The mechanisms of ozone-induced lung injury and differential susceptibility are not fully understood. Ozone-induced lung inflammation is mediated, in part, by the innate immune system. We hypothesized that mannose-binding lectin (MBL), an innate immunity serum protein, contributes to the proinflammatory events caused by ozone-mediated activation of the innate immune system. Wild-type ( Mbl+/+) and MBL-deficient ( Mbl−/−) mice were exposed to ozone (0.3 ppm) for up to 72 h, and bronchoalveolar lavage fluid was examined for inflammatory markers. Mean numbers of eosinophils and neutrophils and levels of the neutrophil attractants C-X-C motif chemokines 2 [ Cxcl2 (major intrinsic protein 2)] and 5 [ Cxcl5 (limb expression, LIX)] in the bronchoalveolar lavage fluid were significantly lower in Mbl−/− than Mbl+/+ mice exposed to ozone. Using genome-wide mRNA microarray analyses, we identified significant differences in transcript response profiles and networks at baseline [e.g., nuclear factor erythroid-related factor 2 (NRF2)-mediated oxidative stress response] and after exposure (e.g., humoral immune response) between Mbl+/+ and Mbl−/− mice. The microarray data were further analyzed to discover several informative differential response patterns and subsequent gene sets, including the antimicrobial response and the inflammatory response. We also used the lists of gene transcripts to search the LINCS L1000CDS2 data sets to identify agents that are predicted to perturb ozone-induced changes in gene transcripts and inflammation. These novel findings demonstrate that targeted deletion of Mbl caused differential levels of inflammation-related gene sets at baseline and after exposure to ozone and significantly reduced pulmonary inflammation, thus indicating an important innate immunomodulatory role of the gene in this model.

scholarly journals ORIGINAL ARTICLE: A Role for Mannose-Binding Lectin, a Component of the Innate Immune System in Pre-Eclampsia

2008 ◽  
Vol 60 (4) ◽  
pp. 333-345 ◽  
Author(s):  
Nandor Gabor Than ◽  
Roberto Romero ◽  
Offer Erez ◽  
Juan Pedro Kusanovic ◽  
Adi L. Tarca ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Mannose Binding Lectin ◽  
Innate Immune ◽  
Mannose Binding ◽  
Binding Lectin

scholarly journals Activity of Mannose-Binding Lectin on Bacterial-Infected Chickens—A Review

Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 787
Author(s):  
Peter A. Idowu ◽  
Adeola P. Idowu ◽  
Oliver T. Zishiri ◽  
Takalani J. Mpofu ◽  
Edwin J. A. Veldhuizen ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Pathogenic Bacteria ◽  
Mannose Binding Lectin ◽  
Innate Immune ◽  
Lectin Pathway ◽  
Enzyme Linked Immunosorbent Assay ◽  
Bacterial Strains ◽  
Mannose Binding ◽  
Binding Lectin

In recent years, diseases caused by pathogenic bacteria have profoundly impacted chicken production by causing economic loss in chicken products and by-product revenues. MBL (mannose-binding lectin) is part of the innate immune system (IIS), which is the host’s first line defense against pathogens. The IIS functions centrally by identifying pathogen-specific microorganism-associated molecular patterns (MAMPs) with the help of pattern recognition receptors (PRRs). Studies have classified mannose-binding lectin (MBL) as one of the PRR molecules which belong to the C-type lectin family. The protective role of MBL lies in its ability to activate the complement system via the lectin pathway and there seems to be a direct link between the chicken’s health status and the MBL concentration in the serum. Several methods have been used to detect the presence, the level and the structure of MBL in chickens such as Enzyme-linked immunosorbent assay (ELISA), Polymerase Chain Reaction (PCR) among others. The concentration of MBL in the chicken ranges from 0.4 to 35 µg/mL and can be at peak levels at three to nine days at entry of pathogens. The variations observed are known to depend on the bacterial strains, breed and age of the chicken and possibly the feed manipulation strategies. However, when chicken MBL (cMBL) becomes deficient, it can result in malfunctioning of the innate immune system, which can predispose chickens to diseases. This article aimed to discuss the importance and components of mannose-binding lectin (MBL) in chickens, its mode of actions, and the different methods used to detect MBL. Therefore, more studies are recommended to explore the causes for low and high cMBL production in chicken breeds and the possible effect of feed manipulation strategies in enhancing cMBL production.

477: A role for mannose-binding lectin, a component of the innate immune system in preeclampsia nandor

2007 ◽  
Vol 197 (6) ◽  
pp. S139
Author(s):  
Gabor Than ◽  
Roberto Romero ◽  
Offer Erez ◽  
Juan Pedro Kusanovic ◽  
Adi L. Tarca ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Mannose Binding Lectin ◽  
Innate Immune ◽  
Mannose Binding ◽  
Binding Lectin

scholarly journals The Autumn Low Milk Yield Syndrome in High Genetic Merit Dairy Cattle: The Possible Role of a Dysregulated Innate Immune Response

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 388
Author(s):  
Massimo Amadori ◽  
Chiara Spelta
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Dairy Cattle ◽  
Memory Effect ◽  
Milk Yield ◽  
Innate Immune System ◽  
Innate Immune ◽  
Effective Control ◽  
Dry Period ◽  
Genetic Merit

The analysis of milk yield data shows that high genetic merit dairy cows do not express their full production potential in autumn. Therefore, we focused on metabolic stress and inflammatory response in the dry and peripartum periods as possible causes thereof. It was our understanding that some cows could not cope with the stress imposed by their physiological and productive status by means of adequate adaptation strategies. Accordingly, this study highlights the noxious factors with a potential to affect cows in the above transition period: hot summer climate, adverse genetic traits, poor coping with unfavorable environmental conditions, outright production diseases and consequences thereof. In particular, the detrimental effects in the dry period of overcrowding, photoperiod change and heat stress on mammary gland development and milk production are highlighted in the context of the autumn low milk yield syndrome. The latter could be largely accounted for by a “memory” effect on the innate immune system induced in summer by diverse stressors after dry-off, according to strong circumstantial and indirect experimental evidence. The “memory” effect is based on distinct epigenetic changes of innate immunity genes, as already shown in cases of bovine mastitis. Following a primary stimulation, the innate immune system would be able to achieve a state known as “trained immunity”, a sort of “education” which modifies the response to the same or similar stressors upon a subsequent exposure. In our scenario, the “education” of the innate immune system would induce a major shift in the metabolism of inflammatory cells following their reprogramming. This would entail a higher basal consumption of glucose, in competition with the need for the synthesis of milk. Also, there is strong evidence that the inflammatory response generated in the dry period leads to a notable reduction of dry matter intake after calving, and to a reduced efficiency of oxidative phosphorylation in mitochondria. On the whole, an effective control of the stressors in the dry period is badly needed for better disease control and optimal production levels in dairy cattle.

scholarly journals Inhibition of Toll-like Receptor and Cytokine Signaling—A Unifying Theme in Ischemic Tolerance

2004 ◽  
Vol 24 (11) ◽  
pp. 1288-1304 ◽  
Author(s):  
Katalin Karikó ◽  
Drew Weissman ◽  
Frank A. Welsh
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Lipid Rafts ◽  
Inflammatory Cytokines ◽  
Innate Immune System ◽  
Endotoxin Tolerance ◽  
Ischemic Tolerance ◽  
Innate Immune ◽  
Cytokine Signaling ◽  
The Brain

Cerebral ischemia triggers acute inflammation, which exacerbates primary brain damage. Activation of the innate immune system is an important component of this inflammatory response. Inflammation occurs through the action of proinflammatory cytokines, such as TNF, IL-1β and IL-6, that alter blood flow and increase vascular permeability, thus leading to secondary ischemia and accumulation of immune cells in the brain. Production of these cytokines is initiated by signaling through Toll-like receptors (TLRs) that recognize host-derived molecules released from injured tissues and cells. Recently, great strides have been made in understanding the regulation of the innate immune system, particularly the signaling mechanisms of TLRs. Negative feedback inhibitors of TLRs and inflammatory cytokines have now been identified and characterized. It is also evident that lipid rafts exist in membranes and play a role in receptor-mediated inflammatory signaling events. In the present review, using this newly available large body of knowledge, we take a fresh look at studies of ischemic tolerance. Based on this analysis, we recognize a striking similarity between ischemic tolerance and endotoxin tolerance, an immune suppressive state characterized by hyporesponsiveness to lipopolysaccharide (LPS). In view of this analogy, and considering recent discoveries related to molecular mechanisms of endotoxin tolerance, we postulate that inhibition of TLR and proinflammatory cytokine signaling contributes critically to ischemic tolerance in the brain and other organs. Ischemic tolerance is a protective mechanism induced by a variety of preconditioning stimuli. Tolerance can be established with two temporal profiles: (i) a rapid form in which the trigger induces tolerance to ischemia within minutes and (ii) a delayed form in which development of protection takes several hours or days and requires de-novo protein synthesis. The rapid form of tolerance is achieved by direct interference with membrane fluidity, causing disruption of lipid rafts leading to inhibition of TLR/cytokine signaling pathways. In the delayed form of tolerance, the preconditioning stimulus first triggers the TLR/cytokine inflammatory pathways, leading not only to inflammation but also to simultaneous upregulation of feedback inhibitors of inflammation. These inhibitors, which include signaling inhibitors, decoy receptors, and anti-inflammatory cytokines, reduce the inflammatory response to a subsequent episode of ischemia. This novel interpretation of the molecular mechanism of ischemic tolerance highlights new avenues for future investigation into the prevention and treatment of stroke and related diseases.

Recognition of Plasmodium falciparum proteins by mannan-binding lectin, a component of the human innate immune system

2002 ◽  
Vol 88 (2) ◽  
pp. 113-117 ◽  
Author(s):  
Jens Klabunde ◽  
Anne-Catrin Uhlemann ◽  
Anne E. Tebo ◽  
Jürgen Kimmel ◽  
Ralph T. Schwarz ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Immune System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Mannan Binding Lectin ◽  
Binding Lectin

scholarly journals Receptor Mincle promotes skin allergies and is capable of recognizing cholesterol sulfate

2017 ◽  
Vol 114 (13) ◽  
pp. E2758-E2765 ◽  
Author(s):  
Alexey V. Kostarnoy ◽  
Petya G. Gancheva ◽  
Bernd Lepenies ◽  
Amir I. Tukhvatulin ◽  
Alina S. Dzharullaeva ◽  
...  
Keyword(s):  
Immune System ◽  
Inflammatory Response ◽  
Innate Immune System ◽  
Molecular Mechanisms ◽  
Tissue Injury ◽  
Innate Immune ◽  
Sterile Inflammation ◽  
Skin Damage ◽  
Cholesterol Sulfate ◽  
Local Inflammatory Response

Sterile (noninfected) inflammation underlies the pathogenesis of many widespread diseases, such as allergies and autoimmune diseases. The evolutionarily conserved innate immune system is considered to play a key role in tissue injury recognition and the subsequent development of sterile inflammation; however, the underlying molecular mechanisms are not yet completely understood. Here, we show that cholesterol sulfate, a molecule present in relatively high concentrations in the epithelial layer of barrier tissues, is selectively recognized by Mincle (Clec4e), a C-type lectin receptor of the innate immune system that is strongly up-regulated in response to skin damage. Mincle activation by cholesterol sulfate causes the secretion of a range of proinflammatory mediators, and s.c. injection of cholesterol sulfate results in a Mincle-mediated induction of a severe local inflammatory response. In addition, our study reveals a role of Mincle as a driving component in the pathogenesis of allergic skin inflammation. In a well-established model of allergic contact dermatitis, the absence of Mincle leads to a significant suppression of the magnitude of the skin inflammatory response as assessed by changes in ear thickness, myeloid cell infiltration, and cytokine and chemokine secretion. Taken together, our results provide a deeper understanding of the fundamental mechanisms underlying sterile inflammation.

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