scholarly journals Inflammation as an Animal Development Phenomenon

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Gustavo Campos Ramos
Keyword(s):  
Developmental Biology ◽  
Tissue Damage ◽  
Defense Mechanism ◽  
Clinical Symptoms ◽  
Disease Mechanism ◽  
Animal Development ◽  
Scientific Questions

Inflammation is a term that has been used throughout history in different contexts; it may represent a simple collection of clinical symptoms for which drugs are developed, a disease mechanism, or even a defense mechanism against microbes validating Pasteur's studies on bacteriology and Darwin's proposed struggle for survival. Thus, an explanation of this term must also consider the scientific questions addressed. In this study, I propose that several of the inflammatory events typically described in immunological, pathological, and pharmacological contexts can also be perceived as mechanisms of animal development. Thus, by recognizing that the generation of an animal form, its conservation, and its regeneration after tissue damage are phenomena of the same nature, inflammation can be addressed through the approach of developmental biology, thereby acquiring a much neglected physiological counterpart.

Role of Histamine and Leucotaxin in Function of Cellular Defense Mechanism

1956 ◽  
Vol 184 (2) ◽  
pp. 296-300 ◽  
Author(s):  
László Kátó ◽  
Béla Gözsy
Keyword(s):  
Fluid Flow ◽  
Tissue Damage ◽  
Inflammatory Process ◽  
Defense Mechanism ◽  
Volatile Oils ◽  
Time Intervals ◽  
Cellular Defense ◽  
Intradermal Administration ◽  
Flow Through

Experiments are presented to the effect that in an inflammatory process histamine and leucotaxin appear successively at different and orderly time intervals, thus assuring an increased fluid flow through the capillary wall. Histamine is released not only in the inflammatory process but also by intradermal administration of such substances (volatile oils or their components) which induce neither the triple response of Th. Lewis nor any tissue damage. This could be explained by the fact that in the tissues histamine is ‘present’ but leucotaxin is ‘formed.’

scholarly journals The IL-33-ILC2 pathway protects from amebic colitis

2021 ◽  
Author(s):  
Md Jashim Uddin ◽  
Jhansi L. Leslie ◽  
Stacey L. Burgess ◽  
Noah Oakland ◽  
Brandon Thompson ◽  
...  
Keyword(s):  
Tissue Damage ◽  
Cell Injury ◽  
Defense Mechanism ◽  
Protozoan Parasite ◽  
Lymphoid Cells ◽  
Amebic Colitis ◽  
Host Defense Mechanism ◽  
Important Host ◽  
Murine Colon

AbstractEntamoeba histolytica is a pathogenic protozoan parasite that causes intestinal colitis, diarrhea, and in some cases, liver abscess. Through transcriptomics analysis, we observed that E. histolytica infection was associated with increased expression of IL-33 mRNA in both the human and murine colon. IL-33, the IL-1 family cytokine, is released after cell injury to alert the immune system of tissue damage. Treatment with recombinant IL-33 protected mice from amebic infection and intestinal tissue damage; moreover, blocking IL-33 signaling made mice more susceptible to amebiasis. IL-33 limited the recruitment of inflammatory immune cells and decreased the pro-inflammatory cytokine IL-6 in the cecum. Type 2 immune responses were upregulated by IL-33 treatment during amebic infection. Interestingly, administration of IL-33 protected RAG2–/– mice but not RAG2−/−γc−/− mice, demonstrating that IL-33-mediated protection required the presence of innate lymphoid cells (ILCs). IL-33 induced recruitment of ILC2 but not ILC1 and ILC3 in RAG2−/− mice. At baseline and after amebic infection, there was a significantly higher IL13+ILC2s in C57BL/J mice, which are naturally resistant to amebiasis, than CBA/J mice. Adoptive transfer of ILC2s to RAG2−/−γc−/− mice restored IL-33-mediated protection. These data reveal that the IL-33-ILC2 pathway is an important host defense mechanism against amebic colitis.

Serum-derived bovine immunoglobulin in the alleviation of irinotecan-induced mucositis.

2014 ◽  
Vol 32 (31_suppl) ◽  
pp. 166-166
Author(s):  
Emma Hazel Bateman ◽  
Eric Weaver ◽  
Gerald Klein ◽  
Erin Plews ◽  
Anthony Wignall ◽  
...  
Keyword(s):  
Tissue Damage ◽  
Inflammatory Cell ◽  
Clinical Symptoms ◽  
Intraperitoneal Administration ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Histological Damage ◽  
Surgical Recovery ◽  
Bovine Immunoglobulin ◽  
Induced Changes

166 Background: Gastrointestinal (GI) mucositis is associated with diarrhoea and intestinal barrier dysfunction caused by apoptosis, immune dysfunction, and microbiome alterations. Serum-derived bovine immunoglobulin (SBI) has been shown to ameliorate inflammation in colitis models, has been shown to improve HIV-induced enteropathy and nutritional status, and is being investigated in post-surgical recovery in oncology patients. We investigated in a rat model whether SBI was effective in alleviating symptoms of GI mucositis. Methods: Animals were gavaged with 250 or 500mg/kg of SBI twice daily, before intraperitoneal administration of 200mg/kg irinotecan on day 4, and for 6 days post-irinotecan. Animals were monitored for bodyweight and diarrhoea. Tissues were collected at necropsy 6, 48, 96 and 144 hours post-irinotecan. H&E-stained colon and jejunum were analysed for histological damage. Results: The overall incidence, severity and duration of diarrhoea, and clinical symptoms of mucositis, were decreased in irinotecan-treated animals that had received SBI. Animals receiving 500 mg SBI/kg also tended to lose less bodyweight than animals treated only with irinotecan (P>0.10). Animals receiving SBI had less pronounced irinotecan-induced changes in neutrophil levels (P≈0.02), and lower tissue damage scores than those receiving irinotecan alone (P<0.0001). Conclusions: Twice-daily oral gavage of SBI was well-tolerated, and reduced the incidence, severity and duration of irinotecan-induced mucositis. SBI was associated with less pronounced changes in inflammatory cell levels and intestinal tissue damage. Ongoing experiments aim to explore the mechanisms of SBI-associated gastrointestinal protection.

Chronic hyperbaric exposure activates proinflammatory mediators in humans

2002 ◽  
Vol 92 (6) ◽  
pp. 2375-2380 ◽  
Author(s):  
Anders Ersson ◽  
Maria Walles ◽  
Kjell Ohlsson ◽  
Anders Ekholm
Keyword(s):  
Defense Mechanism ◽  
Clinical Symptoms ◽  
Ambient Pressure ◽  
Proinflammatory Mediators ◽  
Mechanical Explanation ◽  
Inflammatory Mechanism ◽  
Before And After ◽  
Hyperbaric Exposure ◽  
Neutrophil Gelatinase ◽  
Inflammatory System

Decompression illness (DCI) is an illness affecting divers subjected to reductions in ambient pressure. Besides a mechanical explanation to DCI, an inflammatory mechanism has been suggested. In this study, levels of interleukin (IL)-8, IL-6, IL-1 receptor antagonist (IL-1ra), secretory leukocyte protease inhibitor (SLPI), and neutrophil gelatinase-associated lipocalcin (NGAL) were measured in divers before and after a 2-mo period of daily diving. The divers were military conscripts and completed their diving period with no clinical symptoms of DCI. We found no change in IL-6 and IL1-ra but did find an increase in IL-8 and NGAL together with a decrease in SLPI levels. The findings suggest an inflammatory activation. This activation is not severe because no changes in IL-6 or IL-1ra were found. The increase in NGAL and IL-8 levels were interpreted as a sign of leukocyte activation. The decreased SLPI levels suggest an influence on the inflammatory defense mechanism. All in all, the findings of this study show a compensated activation of the inflammatory defense mechanism without loss of homeostasis of the inflammatory system.

Isoprostanes in clinically isolated syndrome and early multiple sclerosis as biomarkers of tissue damage and predictors of clinical course

2012 ◽  
Vol 19 (4) ◽  
pp. 411-417 ◽  
Author(s):  
Emilia Sbardella ◽  
Anita Greco ◽  
Maria L Stromillo ◽  
Luca Prosperini ◽  
Maria Puopolo ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Tissue Damage ◽  
Roc Analysis ◽  
Brain Volume ◽  
Clinical Symptoms ◽  
Early Stage ◽  
Relapsing Remitting ◽  
Neurological Conditions ◽  
Magnetic Resonance Imaging Mri ◽  
Biomarkers Of Oxidative Stress

Background: Isoprostanes (IsoP) are sensitive biomarkers of oxidative stress. Their cerebrospinal-fluid (CSF) level is increased in several neurological conditions, including multiple sclerosis (MS). In particular, in relapsing–remitting MS, IsoP have been proposed as an index of neurodegenerative processes. The mechanisms leading to neuroaxonal damage in MS are not fully understood but oxidative mechanisms play a substantial role. Although axonal loss is present in MS patients since their first clinical symptoms, IsoP levels at this early stage have not been evaluated yet. Objectives: The objectives of this study were (a) to assess IsoP levels in CSF of patients with a first clinical attack suggestive of MS; (b) to correlate IsoP levels with magnetic resonance imaging (MRI) measures of brain damage and (c) to assess IsoP value in predicting disease clinical evolution. Methods: Thirty-nine patients with a first clinical attack suggestive of MS underwent neurological examination, lumbar puncture with IsoP levels quantification and conventional/spectroscopic-MRI. Patients were followed up for 24 months. Results: CSF IsoP levels were higher in patients than controls (mean±standard deviation (SD) 123.4±185.8 vs 4.5±2.9 pg/ml; p<0.0001) and inversely correlated to normalized brain volume ( p=0.04) and N-acetylaspartate/choline (NAA/Cho) ( p=0.01). The risk of experiencing clinical relapses differed according to IsoP level: subjects with levels higher than 95 pg/ml (a cut-off value resulting from ROC analysis) were more likely to relapse than patients with levels equal or lower than 95 pg/ml (59% vs 27% respectively; p=0.03). Conclusions: CSF IsoP might be useful biomarkers of tissue damage in MS with a predictive value of disease course.

scholarly journals Phenotypic PIA-Dependent Biofilm Production by Clinical Non-Typeable Staphylococcus aureus Is Not Associated with the Intensity of Inflammation in Mammary Gland: A Pilot Study Using Mouse Mastitis Model

Animals ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 3047
Author(s):  
Jully Gogoi-Tiwari ◽  
Dorji Dorji ◽  
Harish Kumar Tiwari ◽  
Gayatri Shirolkar ◽  
Joshua W. Aleri ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Mammary Gland ◽  
Tissue Damage ◽  
Clinical Symptoms ◽  
Mammary Glands ◽  
Aureus Strain ◽  
Mammary Tissue ◽  
Damage Level ◽  
Biofilm Production ◽  
The Impact

Non-typeable (NT) Staphylococcus aureus strains are associated with chronic bovine mastitis. This study investigates the impact of biofilm formation by clinical NT S. aureus on cytokine production and mammary tissue damage by using a mouse mastitis model. Mice infected with two different NT S. aureus strains with strong and weak biofilm forming potential demonstrated identical clinical symptoms (moderate), minimal inflammatory infiltrates, and tissue damage (level 1 histopathological changes) in the mammary glands. However, the S. aureus load in the mammary glands of mice and the level of pro-inflammatory cytokines (IL-1β, IL-6, IL-12, IL-17 and IFN-γ) in serum were significantly higher (p ≤ 0.05) in those infected with the strong biofilm forming NT S. aureus strain. The level of IL-6 in sera samples of these mice was extremely high (15,479.9 ± 532 Pg/mL. Furthermore, these mice died in 24h of post infection compared to 30 h in the weak biofilm forming NT S. aureus infected group. The study demonstrates no association between the strength of PIA (polysaccharide intercellular adhesion)-dependent biofilm production by clinical NT S. aureus and mammary gland pathology in a mouse mastitis model. However, the role of biofilm in the virulence of S. aureus advancing the time of mortality in mice warrants further investigation.

P121. Tissue damage by S-nitrosothiol formation: A disease mechanism in colitis and other chronic disease

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 57
Author(s):  
William Roediger ◽  
Ken Porter ◽  
Susan Millard ◽  
Wendy Babidge
Keyword(s):  
Chronic Disease ◽  
Tissue Damage ◽  
Disease Mechanism
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