Acquired resistance in rainbow trout against Gyrodactylus derjavini

2000 ◽  
Vol 74 (2) ◽  
pp. 155-160 ◽  
Author(s):  
T. Lindenstrøm ◽  
K. Buchmann
Keyword(s):  
Rainbow Trout ◽  
Host Response ◽  
Acquired Resistance ◽  
Mucous Cell ◽  
Passive Immunization ◽  
Host Responses ◽  
Cell Hyperplasia ◽  
Infection Pressure ◽  
High Infection ◽  
Parasite Populations

AbstractInvestigations were conducted on the host response in rainbow trout and the associated changes in mucous cell density during infection with the skin monogenean Gyrodactylus derjavini. Parasite populations increased on all naive hosts and peaked 4–5 weeks p.i. after which infection levels decreased. Introduction of naive fish into responding host populations resulted in heavy infections of the naive fish, whereas parasite expulsion continued in the responding host groups showing an acquired, non-sterile immunity. This non-sterile immunity lasted at least a month as these hosts were refractory to reinfection despite being exposed to a high infection pressure. Mucous cell hyperplasia was seen in some groups during the intermediary phase of infection, but at the termination of the study a significant depletion was evident. Passive immunization of naive host (with sera from immune hosts) did not confer protection. This indicates differences between host responses to G. derjavini compared to responses against other pathogens where such a passive immunity has been described.

scholarly journals Aggregation of Argulus coregoni (Crustacea: Branchiura) on rainbow trout (Oncorhynchus mykiss): a consequence of host susceptibility or exposure?

Parasitology ◽  
2004 ◽  
Vol 130 (2) ◽  
pp. 169-176 ◽  
Author(s):  
M. BANDILLA ◽  
T. HAKALAHTI ◽  
P. J. HUDSON ◽  
E. T. VALTONEN
Keyword(s):  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Acquired Resistance ◽  
Infection Intensity ◽  
Similar Rate ◽  
Resistance Mechanisms ◽  
Host Population ◽  
Host Susceptibility ◽  
Relative Significance ◽  
Argulus Coregoni

By sampling individual rainbow trout, Oncorhynchus mykiss, at a fish farm we showed that Argulus coregoni were aggregated within their host population. The relative significance of susceptibility and exposure generating the observed pattern was tested using experimental infections. We examined, whether rainbow trout developed protective resistance mechanisms against the louse following a challenge infection and if there was variation between individual trout in their susceptibility to A. coregoni metanauplii. Fish were exposed to 20 A. coregoni for 5, 25, 50, 85 or 120 min and the numbers attaching recorded. Three weeks later, developing argulids were removed and the experiment repeated with a standardized exposure of 20 metanauplii. Prior exposure of fish with A. coregoni did not reduce the total infection intensity compared to naïve fish, but fish gained infection more rapidly. We suggest that there is no protective acquired resistance of pre-exposed rainbow trout to subsequent Argulus exposure. The possibility that an immunosuppressive mechanism by argulids was acting enabling the higher attachment rate could be refuted since control individuals, not previously exposed to lice, gained the infection at a similar rate as the fish challenged twice. Our results do not indicate clear differences in susceptibility among individual fish but the transmission of metanauplii on fish seemed to be opportunistic and non-selective. Our results support the view that variation in exposure time, rather than differences in susceptibility of individual hosts, might be the key factor in generating the aggregated distribution of Argulus on their hosts.

Population dynamics in echinococcosis and cysticercosis: regulation ofTaenia hydatigenaandT. ovisin lambs through passively transferred immunity

Parasitology ◽  
1990 ◽  
Vol 101 (1) ◽  
pp. 145-151 ◽  
Author(s):  
M. A. Gemmell ◽  
J. R. Lawson ◽  
M. G. Roberts ◽  
J. F. T. Griffin
Keyword(s):  
Population Dynamics ◽  
Natural Environment ◽  
Population Regulation ◽  
Acquired Immunity ◽  
Taenia Hydatigena ◽  
Density Dependent ◽  
Active Immunity ◽  
Infection Pressure ◽  
High Infection

SUMMARYA comparison has been made of the interactions between passively transferred and actively acquired immunity in regulating populations ofTaenia hydatigenaandT. ovis.When ewes were grazed prior to parturition under a high infection pressure, immunity was transferred to their offspring for up to 8 weeks. A qualititative difference between the species was the destruction of larvalT. ovisprior to their establishment (‘pre-encystment immunity’) and that ofT. hydatigenaafter they had become established (‘post-encystment immunity’) in the challenged lambs. The major difference in terms of population regulation between the two parasites was that infection occurred withT. hydatigenabut not withT. ovisin those lambs reared from birth for 16 weeks under high infection pressure. Passive, like active immunity, is a density-dependent constraint. It plays an important role in the population regulation ofT. ovis, but not ofT. hydatigena. This is discussed in terms of transmission in the natural environment, an hypothesis on humoral protection and the need to elucidate pathways of protection when immunization schedules are being evaluated for controlling the taeniid zoonoses.

scholarly journals Transcriptional and proteomic insights into the host response in fatal COVID-19 cases

2020 ◽  
Vol 117 (45) ◽  
pp. 28336-28343 ◽  
Author(s):  
Meng Wu ◽  
Yaobing Chen ◽  
Han Xia ◽  
Changli Wang ◽  
Chin Yee Tan ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Host Response ◽  
Drug Targets ◽  
Potential Role ◽  
Host Responses ◽  
Human Lung Tissue ◽  
Proteomics Analysis ◽  
Global Pandemic ◽  
A Site ◽  
Potential Drug Targets

Coronavirus disease 2019 (COVID-19), the global pandemic caused by SARS-CoV-2, has resulted thus far in greater than 933,000 deaths worldwide; yet disease pathogenesis remains unclear. Clinical and immunological features of patients with COVID-19 have highlighted a potential role for changes in immune activity in regulating disease severity. However, little is known about the responses in human lung tissue, the primary site of infection. Here we show that pathways related to neutrophil activation and pulmonary fibrosis are among the major up-regulated transcriptional signatures in lung tissue obtained from patients who died of COVID-19 in Wuhan, China. Strikingly, the viral burden was low in all samples, which suggests that the patient deaths may be related to the host response rather than an active fulminant infection. Examination of the colonic transcriptome of these patients suggested that SARS-CoV-2 impacted host responses even at a site with no obvious pathogenesis. Further proteomics analysis validated our transcriptome findings and identified several key proteins, such as the SARS-CoV-2 entry-associated protease cathepsins B and L and the inflammatory response modulator S100A8/A9, that are highly expressed in fatal cases, revealing potential drug targets for COVID-19.

scholarly journals Wild salmonids are running the gauntlet of pathogens and climate as fish farms expand northwards

2020 ◽  
Author(s):  
Knut Wiik Vollset ◽  
Robert J Lennox ◽  
Jan Grimsrud Davidsen ◽  
Sindre Håvarstein Eldøy ◽  
Trond E Isaksen ◽  
...  
Keyword(s):  
Cold Water ◽  
Arctic Charr ◽  
Fish Farming ◽  
Fish Farms ◽  
The North ◽  
Arctic Regions ◽  
Northern Areas ◽  
Infection Pressure ◽  
High Infection ◽  
Research Questions

Abstract Salmon farming has multiplied from a side business of coastal farmers to one of the world's major aquaculture species. This has dramatically altered the disease dynamics between farmed and wild salmonids. As salmon fish farming has increased, new restrictions have been enforced to combat emerging density-dependent impacts of pathogen spillover. In most northern and arctic regions, the effects of pathogens from fish farms on wild salmonids have been minimal for two key reasons: (i) relative low density of fish farms in the north and (ii) cold water temperatures. However, both factors are set to change dramatically. On one side, there is an increasing interest in utilizing northern areas for fish farming due to limited capacity for expansion in mid-latitude regions. On the other side, climate change is rapidly changing these northern ecosystems. High-latitude regions inhabit some of the largest remaining wild Atlantic salmon populations in the world along with sea trout and Arctic charr. Wild salmonids in the north have most likely seldom been exposed to high infection pressure, and we question how these populations will cope with changes that are coming. We identify 12 research questions emerging from these imminent changes and discuss methodologies for addressing them. We conclude that policies related to fish farming must consider uncertainties with respect to pathogen dynamics in the north until these research questions are fully addressed.

Bcl-2 in LPS- and allergen-induced hyperplastic mucous cells in airway epithelia of Brown Norway rats

2000 ◽  
Vol 279 (6) ◽  
pp. L1210-L1217 ◽  
Author(s):  
Yohannes Tesfaigzi ◽  
Mark J. Fischer ◽  
Andrea J. Martin ◽  
Jeanclare Seagrave
Keyword(s):  
Inflammatory Response ◽  
Mucous Cell ◽  
Cell Number ◽  
Environmental Toxins ◽  
Brown Norway ◽  
Mucous Cells ◽  
Cell Hyperplasia ◽  
Airway Epithelia ◽  
Cell Numbers ◽  
Norway Rats

Environmental toxins, infection, and allergens lead to a transient mucous cell hyperplasia (MCH) in airway epithelia; however, the mechanisms for reducing mucous cell numbers during recovery are largely unknown. This study investigated Bcl-2 expression in mucous cells induced by a neutrophilic or eosinophilic inflammatory response. Brown Norway rats intratracheally instilled with lipopolysaccharide (LPS) showed an inflammatory response characterized primarily by neutrophils. Secreted mucin was increased fourfold at 1 day, and the number of mucous cells was increased fivefold 2, 3, and 4 days post-LPS instillation compared with those in noninstilled rats. None of the mucous cells in non- or saline-instilled control animals expressed Bcl-2, whereas 20–30% of mucous cells were Bcl-2 positive 1 and 2 days post-LPS instillation. Brown Norway rats immunized and challenged with ovalbumin (OVA) for 2, 4, and 6 days showed an inflammatory response characterized primarily by eosinophils. Secreted mucin increased fivefold, and mucous cell number increased fivefold after 4 and 6 days of OVA exposure compared with water-immunized control rats challenged with OVA aerosols. Approximately 10–25% of mucous cells were Bcl-2 positive in OVA-immunized and -challenged rats. These data demonstrate Bcl-2 expression in hyperplastic mucous cells of Brown Norway rats regardless of the type of inflammatory response and indicate that apoptotic mechanisms may be involved in the resolution of MCHs.

Host–parasite interactions in rodent nematode infections

2003 ◽  
Vol 77 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Y.R. Mahida
Keyword(s):  
Neutralizing Antibodies ◽  
Host Response ◽  
Trichinella Spiralis ◽  
Host Responses ◽  
Nippostrongylus Brasiliensis ◽  
Trichuris Muris ◽  
Epithelial Phenotype ◽  
Worm Expulsion ◽  
Genetically Manipulated ◽  
Host Parasite

AbstractIn rodents,Trichinella spiralisandNippostrongylus brasiliensisinfect the small intestine andTrichuris murisresides in the colon. The intestinal host response in these animals is characterized by changes in mucosal architecture and inflammation and is associated with worm expulsion. The requirement of T cell-mediated host response in worm expulsion has been demonstrated over many years. Subsequent studies have shown that Th2-type, but not Th1-type, responses mediate resistance to the nematodes. Investigations using neutralizing antibodies and genetically manipulated mice have characterized the contribution of individual Th2-type cytokines in not only worm expulsion, but also specific cellular changes that occur in the mucosa, such as alterations in epithelial phenotype and smooth muscle. There is also increasing appreciation of the contribution of non-bone marrow-derived cells in innate and adaptive host responses in these models.

scholarly journals Viral RNA load in plasma is associated with critical illness and a dysregulated host response in COVID-19

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Jesús F. Bermejo-Martin ◽  
Milagros González-Rivera ◽  
Raquel Almansa ◽  
Dariela Micheloud ◽  
Ana P. Tedim ◽  
...  
Keyword(s):  
Critical Illness ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Host Response ◽  
Correlation Coefficients ◽  
Digital Pcr ◽  
Viral Rna ◽  
Host Responses ◽  
Nucleoprotein Gene ◽  
Pcr Targeting

Abstract Background COVID-19 can course with respiratory and extrapulmonary disease. SARS-CoV-2 RNA is detected in respiratory samples but also in blood, stool and urine. Severe COVID-19 is characterized by a dysregulated host response to this virus. We studied whether viral RNAemia or viral RNA load in plasma is associated with severe COVID-19 and also to this dysregulated response. Methods A total of 250 patients with COVID-19 were recruited (50 outpatients, 100 hospitalized ward patients and 100 critically ill). Viral RNA detection and quantification in plasma was performed using droplet digital PCR, targeting the N1 and N2 regions of the SARS-CoV-2 nucleoprotein gene. The association between SARS-CoV-2 RNAemia and viral RNA load in plasma with severity was evaluated by multivariate logistic regression. Correlations between viral RNA load and biomarkers evidencing dysregulation of host response were evaluated by calculating the Spearman correlation coefficients. Results The frequency of viral RNAemia was higher in the critically ill patients (78%) compared to ward patients (27%) and outpatients (2%) (p < 0.001). Critical patients had higher viral RNA loads in plasma than non-critically ill patients, with non-survivors showing the highest values. When outpatients and ward patients were compared, viral RNAemia did not show significant associations in the multivariate analysis. In contrast, when ward patients were compared with ICU patients, both viral RNAemia and viral RNA load in plasma were associated with critical illness (OR [CI 95%], p): RNAemia (3.92 [1.183–12.968], 0.025), viral RNA load (N1) (1.962 [1.244–3.096], 0.004); viral RNA load (N2) (2.229 [1.382–3.595], 0.001). Viral RNA load in plasma correlated with higher levels of chemokines (CXCL10, CCL2), biomarkers indicative of a systemic inflammatory response (IL-6, CRP, ferritin), activation of NK cells (IL-15), endothelial dysfunction (VCAM-1, angiopoietin-2, ICAM-1), coagulation activation (D-Dimer and INR), tissue damage (LDH, GPT), neutrophil response (neutrophils counts, myeloperoxidase, GM-CSF) and immunodepression (PD-L1, IL-10, lymphopenia and monocytopenia). Conclusions SARS-CoV-2 RNAemia and viral RNA load in plasma are associated with critical illness in COVID-19. Viral RNA load in plasma correlates with key signatures of dysregulated host responses, suggesting a major role of uncontrolled viral replication in the pathogenesis of this disease.

scholarly journals 3055 Reconstruction of Patient-specific Distal Airway Regeneration Patterns in COPD

2019 ◽  
Vol 3 (s1) ◽  
pp. 154-154
Author(s):  
Seyed Babak Mahjour ◽  
Kazunori Gomi ◽  
Samir Rustam ◽  
Phurbu Dolma ◽  
Jamuna Krishnan ◽  
...  
Keyword(s):  
Single Cell ◽  
Stromal Cells ◽  
Airway Remodeling ◽  
Expression Patterns ◽  
Mucous Cell ◽  
Patient Specific ◽  
Mucin 1 ◽  
Cell Hyperplasia ◽  
Chronic Lung Diseases ◽  
Distal Airway

OBJECTIVES/SPECIFIC AIMS: The objective of this study was to reconstruct patient-specific distal airway patterns at the tissue- and single-cell resolution and develop personalized distal airway models based on utilization of patient-derived DABCs and autologous region-specific stromal cells. METHODS/STUDY POPULATION: Patient-specific distal airway units, containing parental small bronchiole (<2 mm in diameter, >12th generation) and daughter airway branches, including pre-terminal/terminal bronchioles, leading to alveoli (3-7 units/lung), were dissected. Epithelial and stromal cells were isolated from these units and processed for ddSeq single-cell RNA-sequencing (n=6 samples). Autologous DABCs and stromal cells were isolated, propagated, biobanked, and used for establishment of patient-specific distal airway models (3D-organoids and air-liquid interface-based airway wall model; n=10 samples). Region-specific tissue patterns were evaluated using immunofluorescence and laser-capture microdissection (LCM; n=6 samples). RESULTS/ANTICIPATED RESULTS: Single-cell-based human distal airway transcriptome map (constructed based on the analysis of >6,500 distal airway cells obtained from 6 subjects) identified physiological and COPD-relevant distal airway differentiation patterns, including distal airway-specific secretory phenotype (DASP) characterized with high expression of secretoglobins 3A2 and 3A1, surfactant proteins SFTPB and SFTPA2, and mucin 1, unique signatures of DABCs, and stromal (fibroblasts, smooth muscle, endothelial cell subpopulations) and immune (macrophage, T cells, B cell, mast cells). Immunofluorescence analysis and LCM confirmed distribution of cell type-specific markers with differential expression patterns of DABC and DASP signatures. Patient-derived DABC-stromal co-culture models reproduced 3 regenerative patterns: 1) physiological (high DABC-clonogenic potency, establishment of polarized differentiated organoids and DASP-expressing epithelia); 2) hypo-regenerative (failure of DABCs to form clones, spheres and mechanically stable differentiated epithelial barrier); and 3) hyperplastic (generation of DABC hyperplasia accompanied in some COPD samples by mucous-cell hyperplasia mimicking in vivo remodeling patterns). DISCUSSION/SIGNIFICANCE OF IMPACT: Patient-specific maps and models of distal airway regeneration patterns have been established in this study, which can be used to identify candidate pathways that mediate disease-relevant airway remodeling and potentially utilized as pre-clinical platforms for developing personalized therapeutic approaches to suppress the progression of distal airway remodeling in chronic lung diseases, including COPD.

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