Pentastomids and the tetrapod lung

Parasitology ◽  
1999 ◽  
Vol 119 (S1) ◽  
pp. S89-S105 ◽  
Author(s):  
J. Riley ◽  
R. J. Henderson
Keyword(s):  
Pulmonary Surfactant ◽  
Evolutionary History ◽  
Inflammatory Responses ◽  
Neutral Lipids ◽  
Critical Role ◽  
Immune Surveillance ◽  
Complex Mixture ◽  
Intermediate Hosts ◽  
Efferent Ducts

SUMMARYPentastomids comprise a highly specialized taxon of arthropod-like parasites that probably became adapted to the lungs of amphibians and reptiles early in their long evolutionary history. Few other macroparasites exploit this particular niche. Pentastomids are often large, long-lived and yet they cause little observable pathology in lungs, despite being haematophagous. The lungs of all tetrapods are lined with pulmonary surfactant, a remarkable biological material consisting of a complex mixture of phospholipids, neutral lipids and proteins that has the unique ability to disperse over the air-liquid lining of the lung. In the lower tetrapods it acts as an anti-glue preventing adhesion of respiratory surfaces when lungs collapse during swallowing prey or upon expiration. In mammals, pulmonary surfactant also plays a critical role regulating the activity of alveolar macrophages, the predominant phagocytes of the lower airways and alveoli. This review outlines the evidence suggesting that lung-dwelling pentastomids, and also nymphs encysted in the tissues of mammalian intermediate hosts, evade immune surveillance and reduce inflammation by coating the chitinous cuticle with a their own stage-specific surfactant. The lipid composition of surfactant derived from lung instars of the pentastomid Porocephalus crotali cultured in vitro is very similar to that recovered from the lung of its snake host. Pentastomid surfactant, visualised as lamellate droplets within sub-parietal cells, is delivered to the cuticle via chitin-lined efferent ducts that erupt at a surface density of < 400 mm-2. The fidelity of the system, which ensures that every part of the cuticle surface is membrane-coated, testifies to its strategic importance. Two other extensive glands discharge membrane-associated (hydrophobic ?) proteins onto the hooks and head; some have been purified and partly characterized but their role in minimising inflammatory responses is, as yet, undetermined.

scholarly journals The Inflammatory Role of Pro-Resolving Mediators in Endometriosis: An Integrative Review

2021 ◽  
Vol 22 (9) ◽  
pp. 4370
Author(s):  
Cássia de Fáveri ◽  
Paula M. Poeta Fermino ◽  
Anna P. Piovezan ◽  
Lia K. Volpato
Keyword(s):  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Critical Role ◽  
Integrative Review ◽  
Inflammatory Factors ◽  
Resolvin D1 ◽  
Endogenous Factors

The pathogenesis of endometriosis is still controversial, although it is known that the inflammatory immune response plays a critical role in this process. The resolution of inflammation is an active process where the activation of endogenous factors allows the host tissue to maintain homeostasis. The mechanisms by which pro-resolving mediators (PRM) act in endometriosis are still little explored. Thus, this integrative review aims to synthesize the available content regarding the role of PRM in endometriosis. Experimental and in vitro studies with Lipoxin A4 demonstrate a potential inhibitory effect on endometrial lesions’ progression, attenuating pro-inflammatory and angiogenic signals, inhibiting proliferative and invasive action suppressing intracellular signaling induced by cytokines and estradiol, mainly through the FPR2/ALX. Investigations with Resolvin D1 demonstrated the inhibition of endometrial lesions and decreased pro-inflammatory factors. Annexin A1 is expressed in the endometrium and is specifically present in women with endometriosis, although the available studies are still inconsistent. Thus, we believe there is a gap in knowledge regarding the PRM pathways in patients with endometriosis. It is important to note that these substances’ therapeutic potential is evident since the immune and abnormal inflammatory responses play an essential role in endometriosis development and progression.

Disruption of endothelial Pfkfb3 ameliorates diet-induced murine insulin resistance

2021 ◽  
Author(s):  
Qiuhua Yang ◽  
Jiean Xu ◽  
Qian Ma ◽  
Zhiping Liu ◽  
Yaqi Zhou ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cells ◽  
High Fat Diet ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Endothelial Inflammation ◽  
Glucose Clearance ◽  
Deficient Mice

Overnutrition-induced endothelial inflammation plays a crucial role in high fat diet (HFD)-induced insulin resistance in animals. Endothelial glycolysis plays a critical role in endothelial inflammation and proliferation, but its role in diet-induced endothelial inflammation and subsequent insulin resistance has not been elucidated. PFKFB3 is a critical glycolytic regulator, and its increased expression has been observed in adipose vascular endothelium of C57BL/6J mice fed with HFD in vivo, and in palmitate (PA)-treated primary human adipose microvascular endothelial cells (HAMECs) in vitro. We generated mice with Pfkfb3 deficiency selective for endothelial cells to examine the effect of endothelial Pfkfb3 in endothelial inflammation in metabolic organs and in the development of HFD-induced insulin resistance. EC Pfkfb3-deficient mice exhibited mitigated HFD-induced insulin resistance, including decreased body weight and fat mass, improved glucose clearance and insulin sensitivity, and alleviated adiposity and hepatic steatosis. Mechanistically, cultured PFKFB3 knockdown HAMECs showed decreased NF-κB activation induced by PA, and consequent suppressed adhesion molecule expression and monocyte adhesion. Taken together, these results demonstrate that increased endothelial PFKFB3 expression promotes diet-induced inflammatory responses and subsequent insulin resistance, suggesting that endothelial metabolic alteration plays an important role in the development of insulin resistance.

Trematodes and snails: an intimate association

2004 ◽  
Vol 82 (2) ◽  
pp. 251-269 ◽  
Author(s):  
Anne E Lockyer ◽  
Catherine S Jones ◽  
Leslie R Noble ◽  
David Rollinson
Keyword(s):  
Evolutionary History ◽  
Intermediate Hosts ◽  
Molecular Approaches ◽  
Complex Interactions ◽  
Intimate Association ◽  
In Vitro Cell Cultures ◽  
Medical Burden ◽  
Insight Into ◽  
Trematode Parasites

Trematode parasites share an intimate relationship with their gastropod intermediate hosts, which act as the vehicle for their development and transmission. They represent an enormous economic and medical burden in developing countries, stimulating much study of snail–trematode interactions. Laboratory-maintained snail–trematode systems and in vitro cell cultures are being used to investigate the molecular dialogue between host and parasite. These dynamic and finely balanced antagonistic relationships, in which parasites strongly influence the physiology of the host, are highly specific and may occasionally demonstrate co-speciation. We consider the mechanisms and responses deployed by trematodes and snails that result in compatibility or rejection of the parasite, and the macroevolutionary implications that they may effect. Although for gastropods the fossil record gives some insight into evolutionary history, elucidation of trematode evolution must rely largely upon molecular approaches, and for both, such techniques have provided fresh and often surprising evidence of their origins and dispersal over time. Co-evolution of snails and trematodes is becoming increasingly apparent at both cellular and population levels; the implications of which are only beginning to be understood for disease control. Untangling the complex interactions of trematodes and snails promise fresh opportunities for intervention to relieve the burden of parasitic disease.

scholarly journals Immunization with 3-oxododecanoyl-l-homoserine lactone–protein conjugate protects mice from lethal Pseudomonas aeruginosa lung infection

2006 ◽  
Vol 55 (10) ◽  
pp. 1381-1387 ◽  
Author(s):  
Shinichi Miyairi ◽  
Kazuhiro Tateda ◽  
Etsu T. Fuse ◽  
Chihiro Ueda ◽  
Hiroaki Saito ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Specific Antibody ◽  
Bacterial Infections ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Lung Infection ◽  
Homoserine Lactone ◽  
Vaccine Strategy ◽  
Protein Conjugate

Quorum-sensing systems have been reported to play a critical role in the pathogenesis of several bacterial infections. Recent data have demonstrated that Pseudomonas N-3-oxododecanoyl-l-homoserine lactone (3-oxo-C12-homoserine lactone, 3-oxo-C12-HSL), but not N-butanoyl-l-homoserine lactone (C4-HSL), induces apoptosis in macrophages and neutrophils. In the present study, the effects of active immunization with 3-oxo-C12-HSL–carrier protein conjugate on acute P. aeruginosa lung infection in mice were investigated. Immunization with 3-oxo-C12-HSL–BSA conjugate (subcutaneous, four times, at 2-week intervals) elaborated significant amounts of specific antibody in serum. Control and immunized mice were intranasally challenged with approximately 3×106 c.f.u. P. aeruginosa PAO1, and survival was then compared. All control mice died by day 2 post bacterial challenge, while 36 % of immunized mice survived to day 4 (P<0.05). Interestingly, bacterial numbers in the lungs did not differ between control and immunized groups, whereas the levels of pulmonary tumour necrosis factor (TNF)-α in the immunized mice were significantly lower than those of control mice (P<0.05). Furthermore, the extractable 3-oxo-C12-HSL levels in serum and lung homogenate were also significantly diminished in the immunized mice. Immune serum completely rescued reduction of cell viability by 3-oxo-C12-HSL-mediated apoptosis in macrophages in vitro. These results demonstrated that specific antibody to 3-oxo-C12-HSL plays a protective role in acute P. aeruginosa infection, probably through blocking of host inflammatory responses, without altering lung bacterial burden. The present data identify a promising potential vaccine strategy targeting bacterial quorum-sensing molecules, including autoinducers.

scholarly journals TLR4 Signaling in MPP+-Induced Activation of BV-2 Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Peng Zhou ◽  
Ruihui Weng ◽  
Zhaoyu Chen ◽  
Rui Wang ◽  
Jing Zou ◽  
...  
Keyword(s):  
Western Blot ◽  
Mtt Assay ◽  
Inflammatory Responses ◽  
Cell Model ◽  
Critical Role ◽  
Control Group ◽  
Immunofluorescence Technique ◽  
Rt Pcr ◽  
Sirna Interference

Aims.This work was conducted to establish anin vitroParkinson’s disease (PD) model by exposing BV-2 cells to 1-methyl-4-phenylpyridinium (MPP+) and exploring the roles of TLR2/TLR4/TLR9 in inflammatory responses to MPP+.Methods/Results.MTT assay showed that cell viability of BV-2 cells was 84.78 ± 0.86% and 81.18 ± 0.99% of the control after incubation with 0.1 mM MPP+for 12 hours and 24 hours, respectively. Viability was not significantly different from the control group. With immunofluorescence technique, we found that MPP+incubation at 0.1 mM for 12 hours was the best condition to activate BV-2 cells. In this condition, the levels of TNF-α, IL-1β, and iNOS protein were statistically increased compared to the control according to ELISA tests. Real time RT-PCR and western blot measurements showed thatTLR4was statistically increased after 0.1 mM MPP+incubation for 12 hours. Furthermore, after siRNA interference ofTLR4mRNA, NF-κB activation and the levels of TNF-α, IL-1β, and iNOS were all statistically decreased in this cell model.Conclusion.MPP+incubation at the concentration of 0.1 mM for 12 hours is the best condition to activate BV-2 cells for mimicking PD inflammation in BV-2 cells. TLR4 signalling plays a critical role in the activation of BV-2 cells and the induction of inflammation in this cell model.

Diesel exhaust particulate-induced activation of Stat3 requires activities of EGFR and Src in airway epithelial cells

2007 ◽  
Vol 292 (2) ◽  
pp. L422-L429 ◽  
Author(s):  
Dongsun Cao ◽  
Tamara L. Tal ◽  
Lee M. Graves ◽  
Ian Gilmour ◽  
William Linak ◽  
...  
Keyword(s):  
Growth Factor ◽  
Diesel Exhaust ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Airway Epithelial Cells ◽  
Diesel Exhaust Particles ◽  
Diesel Exhaust Particulate ◽  
Stat3 Phosphorylation

In vivo exposure to diesel exhaust particles (DEP) elicits acute inflammatory responses in the lung characterized by inflammatory cell influx and elevated expression of mediators such as cytokines and chemokines. Signal transducers and activators of transcription (STAT) proteins are a family of cytoplasmic transcription factors that are key transducers of signaling in response to cytokine and growth factor stimulation. One member of the STAT family, Stat3, has been implicated as a regulator of inflammation but has not been studied in regard to DEP exposure. The results of this study show that DEP induces Stat3 phosphorylation as early as 1 h following stimulation and that phosphorylated Stat3 translocates into the nucleus. Inhibition of epidermal growth factor receptor (EGFR) and Src activities by the inhibitors PD-153035 and PP2, respectively, abolished the activation of Stat3 by DEP, suggesting that Stat3 activation by DEP requires EGFR and Src kinase activation. The present study suggests that oxidative stress induced by DEP may play a critical role in activating EGFR signaling, as evidenced by the fact that pretreatment with antioxidant prevented the activation of EGFR and Stat3. These findings demonstrate that DEP inhalation can activate proinflammatory Stat3 signaling in vitro.

Osteopontin, a key component of the hematopoietic stem cell niche and regulator of primitive hematopoietic progenitor cells

Blood ◽  
2005 ◽  
Vol 106 (4) ◽  
pp. 1232-1239 ◽  
Author(s):  
Susan K. Nilsson ◽  
Hayley M. Johnston ◽  
Genevieve A. Whitty ◽  
Brenda Williams ◽  
Ryan J. Webb ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Negative Regulator ◽  
Hematopoietic Stem ◽  
Hematopoietic Stem Cell Niche ◽  
Hsc Niche ◽  
Cell Niche

Abstract Although recent data suggests that osteoblasts play a key role within the hematopoietic stem cell (HSC) niche, the mechanisms underpinning this remain to be fully defined. The studies described herein examine the role in hematopoiesis of Osteopontin (Opn), a multidomain, phosphorylated glycoprotein, synthesized by osteoblasts, with well-described roles in cell adhesion, inflammatory responses, angiogenesis, and tumor metastasis. We demonstrate a previously unrecognized critical role for Opn in regulation of the physical location and proliferation of HSCs. Within marrow, Opn expression is restricted to the endosteal bone surface and contributes to HSC transmarrow migration toward the endosteal region, as demonstrated by the markedly aberrant distribution of HSCs in Opn–/– mice after transplantation. Primitive hematopoietic cells demonstrate specific adhesion to Opn in vitro via β1 integrin. Furthermore, exogenous Opn potently suppresses the proliferation of primitive HPCs in vitro, the physiologic relevance of which is demonstrated by the markedly enhanced cycling of HSC in Opn–/– mice. These data therefore provide strong evidence that Opn is an important component of the HSC niche which participates in HSC location and as a physiologic-negative regulator of HSC proliferation.

scholarly journals Digestive vacuole of Plasmodium falciparum released during erythrocyte rupture dually activates complement and coagulation

Blood ◽  
2012 ◽  
Vol 119 (18) ◽  
pp. 4301-4310 ◽  
Author(s):  
Prasad Dasari ◽  
Sophia D. Heber ◽  
Maike Beisele ◽  
Michael Torzewski ◽  
Kurt Reifenberg ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Inflammatory Responses ◽  
Alternative Pathway ◽  
Critical Role ◽  
Plasmodium Falciparum Malaria ◽  
Digestive Vacuole ◽  
Phagocytic Cells ◽  
Nociceptive Responses

Abstract Severe Plasmodium falciparum malaria evolves through the interplay among capillary sequestration of parasitized erythrocytes, deregulated inflammatory responses, and hemostasis dysfunction. After rupture, each parasitized erythrocyte releases not only infective merozoites, but also the digestive vacuole (DV), a membrane-bounded organelle containing the malaria pigment hemozoin. In the present study, we report that the intact organelle, but not isolated hemozoin, dually activates the alternative complement and the intrinsic clotting pathway. Procoagulant activity is destroyed by phospholipase C treatment, indicating a critical role of phospholipid head groups exposed at the DV surface. Intravenous injection of DVs caused alternative pathway complement consumption and provoked apathy and reduced nociceptive responses in rats. Ultrasonication destroyed complement-activating and procoagulant properties in vitro and rendered the DVs biologically inactive in vivo. Low-molecular-weight dextran sulfate blocked activation of both complement and coagulation and protected animals from the harmful effects of DV infusion. We surmise that in chronic malaria, complement activation by and opsonization of the DV may serve a useful function in directing hemozoin to phagocytic cells for safe disposal. However, when the waste disposal system of the host is overburdened, DVs may transform into a trigger of pathology and therefore represent a potential therapeutic target in severe malaria.

scholarly journals Critical Role of Zinc in a New Murine Model of EnterotoxigenicEscherichia coliDiarrhea

2018 ◽  
Vol 86 (7) ◽  
pp. e00183-18 ◽  
Author(s):  
D. T. Bolick ◽  
P. H. Q. S. Medeiros ◽  
S. E. Ledwaba ◽  
A. A. M. Lima ◽  
J. P. Nataro ◽  
...  
Keyword(s):  
Murine Model ◽  
Intestinal Inflammation ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Disease Onset ◽  
Watery Diarrhea ◽  
Content Type ◽  
Heat Stable

ABSTRACTEnterotoxigenicEscherichia coli(ETEC) is a major cause of traveler's diarrhea as well as of endemic diarrhea and stunting in children in developing areas. However, a small-mammal model has been badly needed to better understand and assess mechanisms, vaccines, and interventions. We report a murine model of ETEC diarrhea, weight loss, and enteropathy and investigate the role of zinc in the outcomes. ETEC strains producing heat-labile toxins (LT) and heat-stable toxins (ST) that were given to weaned C57BL/6 mice after antibiotic disruption of normal microbiota caused growth impairment, watery diarrhea, heavy stool shedding, and mild to moderate intestinal inflammation, the latter being worse with zinc deficiency. Zinc treatment promoted growth in zinc-deficient infected mice, and subinhibitory levels of zinc reduced expression of ETEC virulence genescfa1,cexE,sta2, anddegPbut not ofeltA in vitro. Zinc supplementation increased shedding and the ileal burden of wild-type (WT) ETEC but decreased shedding and the tissue burden of LT knockout (LTKO) ETEC. LTKO ETEC-infected mice had delayed disease onset and also had less inflammation by fecal myeloperoxidase (MPO) assessment. These findings provide a new murine model of ETEC infection that can help elucidate mechanisms of growth, diarrhea, and inflammatory responses as well as potential vaccines and interventions.

scholarly journals Lung pericyte-like cells are functional interstitial immune sentinel cells

2017 ◽  
Vol 312 (4) ◽  
pp. L556-L567 ◽  
Author(s):  
Chi F. Hung ◽  
Kristen L. Mittelsteadt ◽  
Rena Brauer ◽  
Bonnie L. McKinney ◽  
Teal S. Hallstrand ◽  
...  
Keyword(s):  
Lung Injury ◽  
Inflammatory Responses ◽  
Immune Surveillance ◽  
Lavage Fluid ◽  
Microvascular Endothelium ◽  
Epithelial Injury ◽  
Chemokine Expression ◽  
Proinflammatory Molecules

Pericytes are perivascular PDGF receptor-β+ (PDGFRβ+) stromal cells required for vasculogenesis and maintenance of microvascular homeostasis in many organs. Because of their unique juxtaposition to microvascular endothelium, lung PDGFRβ+ cells are well situated to detect proinflammatory molecules released following epithelial injury and promote acute inflammatory responses. Thus we hypothesized that these cells represent an unrecognized immune surveillance or injury-sentinel interstitial cell. To evaluate this hypothesis, we isolated PDGFRβ+ cells from murine lung and demonstrated that they have characteristics consistent with a pericyte population (referred to as pericyte-like cells for simplicity hereafter). We showed that pericyte-like cells expressed functional Toll-like receptors and upregulated chemokine expression following exposure to bronchoalveolar lavage fluid (BALF) collected from mice with sterile lung injury. Interestingly, BALF from mice without lung injury also induced chemokine expression in pericyte-like cells, suggesting that pericyte-like cells are primed to sense epithelial injury (permeability changes). Following LPS-induced lung inflammation, increased numbers of pericyte-like cells expressed IL-6, chemokine (C-X-C motif) ligand-1, chemokine (C-C motif) ligand 2/ monocyte chemotactic protein-1, and ICAM-1 in vivo. Sterile lung injury in pericyte-ablated mice was associated with decreased inflammation compared with normal mice. In summary, we found that pericyte-like cells are immune responsive and express diverse chemokines in response to lung injury in vitro and in vivo. Furthermore, pericyte-like cell ablation attenuated inflammation in sterile lung injury, suggesting that these cells play an important functional role in mediating lung inflammatory responses. We propose a model in which pericyte-like cells function as interstitial immune sentinels, detecting proinflammatory molecules released following epithelial barrier damage and participating in recruitment of circulating leukocytes.

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