Evidence for the absence of visceral pain in C57BL6/N mice subjected to therapeutically relevant O3/O2-pneumoperitoneum

2016 ◽  
Vol 51 (1) ◽  
pp. 17-23
Author(s):  
Michael Bette ◽  
Volker Springmann ◽  
Annette Rossmann ◽  
Eberhard Weihe ◽  
Burkhard Schütz
Keyword(s):  
Immune Responses ◽  
Peritoneal Cavity ◽  
Visceral Pain ◽  
Acute Effects ◽  
Inflammatory Reactions ◽  
Individual Effects ◽  
Ozonized Oxygen ◽  
Abdominal Constriction ◽  
Mrna Expression Levels ◽  
Pro Inflammatory Cytokines

Each different gas that is used to induce a pneumoperitoneum (PP) exhibits individual effects within the peritoneal cavity. This might include adverse effects such as pain and/or inflammatory reactions. The acute effects of ozonized oxygen (O3/O2), a highly oxidative gas mixture, after being insufflated into the peritoneal cavity are analysed in this study. Using the abdominal constriction response (‘writhing’) assay of chemical nociception in C57BL6/N mice, O3/O2-PP was found not to be associated with visible pain responses and did not alter the c-fos expression in the spinal cord. In addition, mRNA expression levels of the pro-inflammatory cytokines, interleukin (IL)-1β and IL-6, were found unaltered in the spleen 2 h after insufflation. In conclusion, O3/O2-PP is free of adverse pain and does not trigger inflammatory immune responses.

COVID-19 and nutritional deficiency: a review of existing knowledge

2021 ◽  
Vol 42 (1) ◽  
pp. 77-85
Author(s):  
Meghana Muthuvattur Pallath ◽  
Ashok Kumar Ahirwar ◽  
Satyendra Chandra Tripathi ◽  
Priyanka Asia ◽  
Apurva Sakarde ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infection ◽  
Close Contact ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Antibody Affinity ◽  
Global Pandemic ◽  
Underlying Diseases ◽  
Pro Inflammatory Cytokines

Abstract COVID-19 has resulted in an ongoing global pandemic, which spread largely among people who have had close contact with the infected person. The immunopathology of the SARS-CoV-2 virus includes the production of an excess amount of pro-inflammatory cytokines “a cytokine-storm”. The respiratory system (main), cardiovascular system and the gastrointestinal tract are the most affected body systems during viral infection. It has been found that most of the patients who require admission to hospital are elderly or have chronic underlying diseases. Higher cases of malnutrition and co-morbidities like diabetes mellitus and cardiovascular diseases are reported in elderly patients due to which, the immune system weakens and hence, the response to the virus is diminished in magnitude. A deficiency of micronutrients results in impaired immune responses leading to improper secretion of cytokines, alterations in secretory antibody response and antibody affinity which increases susceptibility to viral infection. The deficiency of various micronutrients in COVID-19 patient can be treated by appropriate nutritional supplements, prescribed after evaluating the patients’ nutritional status. Here we aim to highlight the role of a few particular nutrients namely Vitamin D, Vitamin C, Omega-3 fatty acids, Zinc and Magnesium along with the synergistic roles they play in enhancing immunity and thus, maintaining homeostasis.

scholarly journals The tolerogenic interplay(s) among HLA-G, myeloid APCs, and regulatory cells

Blood ◽  
2011 ◽  
Vol 118 (25) ◽  
pp. 6499-6505 ◽  
Author(s):  
Edgardo D. Carosella ◽  
Silvia Gregori ◽  
Joel LeMaoult
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Immune Responses ◽  
Recent Work ◽  
Large Body ◽  
Regulatory Cells ◽  
Individual Effects ◽  
The Individual ◽  
Key Aspects ◽  
Antigen Presenting

Abstract Myeloid antigen-presenting cells (APCs), regulatory cells, and the HLA-G molecule are involved in modulating immune responses and promoting tolerance. APCs are known to induce regulatory cells and to express HLA-G as well as 2 of its receptors; regulatory T cells can express and act through HLA-G; and HLA-G has been directly involved in the generation of regulatory cells. Thus, interplay(s) among HLA-G, APCs, and regulatory cells can be easily envisaged. However, despite a large body of evidence on the tolerogenic properties of HLA-G, APCs, and regulatory cells, little is known on how these tolerogenic players cooperate. In this review, we first focus on key aspects of the individual relationships between HLA-G, myeloid APCs, and regulatory cells. In its second part, we highlight recent work that gathers individual effects and demonstrates how intertwined the HLA-G/myeloid APCs/regulatory cell relationship is.

scholarly journals Unlocking the Potential of Vaccines Built on Messenger RNA

2021 ◽  
pp. 160-197
Author(s):  
Elena Locci ◽  
Silvia Raymond
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Side Effects ◽  
Immune Responses ◽  
Messenger Rna ◽  
Healthy Tissue ◽  
Therapeutic Approaches ◽  
Inflammatory Reactions ◽  
Discontinuation Of Treatment ◽  
Keywords Cancer

In recent years, immunotherapy has revolutionized the treatment of cancer; however, inflammatory reactions in healthy tissues often have side effects that can be serious and lead to permanent discontinuation of treatment. This toxicity is not yet well understood and is a major obstacle to the use of immunotherapy. When the immune system is so severely activated, the resulting inflammatory reaction can have detrimental effects and sometimes serious damage to healthy tissue. We wanted to know if there was a difference between an optimal immune response that aims to kill cancer and an unwanted response that could affect healthy tissue. Identifying the distinctive elements between these two immune responses allows the development of new, more effective and less toxic therapeutic approaches. Keywords: Cancer; Cells; Tissues, Tumors; Prevention, Prognosis; Diagnosis; Imaging; Screening; Treatment; Management

scholarly journals Host F-box protein 22 enhances the uptake of Brucella by macrophages and drives a sustained release of pro-inflammatory cytokines through degradation of the anti-inflammatory effector proteins of Brucella.

2021 ◽  
Author(s):  
Girish Radhakrishnan ◽  
Varadendra Mazumdar ◽  
Kiranmai Joshi ◽  
Binita Roy Nandi ◽  
Swapna Namani ◽  
...  
Keyword(s):  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Effector Proteins ◽  
Host Protein ◽  
Limited Information ◽  
Phagocytic Cells ◽  
Scf Complex ◽  
Enhanced Production ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Brucella species are intracellular bacterial pathogens, causing the world-wide zoonotic disease, brucellosis.  Brucella invade professional and non-professional phagocytic cells, followed by resisting intracellular killing and establishing a replication permissive niche. Brucella also modulate the innate and adaptive immune responses of the host for their chronic persistence. The complex intracellular cycle of Brucella majorly depends on multiple host factors but limited information is available on host and bacterial proteins that play essential role in the invasion, intracellular replication and modulation of host immune responses. By employing an siRNA screening, we identified a role for the host protein, FBXO22 in Brucella -macrophage interaction. FBXO22 is the key element in the SCF E3 ubiquitination complex where it determines the substrate specificity for ubiquitination and degradation of various host proteins.  Downregulation of FBXO22 by siRNA or CRISPR-Cas9 system, resulted diminished uptake of Brucella into macrophages, which was dependent on NF-κB-mediated regulation of phagocytic receptors. FBXO22 expression was upregulated in Brucella -infected macrophages that resulted induction of phagocytic receptors and enhanced production of pro-inflammatory cytokines through NF-κB. Furthermore, we found that FBXO22 recruits the effector proteins of Brucella , including the anti-inflammatory proteins, TcpB and OMP25 for degradation through the SCF complex. We did not observe any role for another F-box containing protein of SCF complex, β-TrCP in Brucella -macrophage interaction. Our findings unravel novel functions of FBXO22 in host-pathogen interaction and its contribution to pathogenesis of infectious diseases.

scholarly journals Peptidoglycan derived from Lactobacillus rhamnosus MLGA up-regulates the expression of chicken β-defensin 9 without triggering an inflammatory response

2020 ◽  
Vol 26 (8) ◽  
pp. 733-745
Author(s):  
Juan Huang ◽  
Junhui Li ◽  
Qiufen Li ◽  
Lin Li ◽  
Nianhua Zhu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Immune Responses ◽  
Mrna Expression ◽  
Salmonella Enteritidis ◽  
Lactobacillus Rhamnosus ◽  
Innate Immune ◽  
Induction Effect ◽  
Adaptive Immune ◽  
Critical Components ◽  
Pro Inflammatory Cytokines

Defensins are critical components of the innate immune system and play an important role in the integration of innate and adaptive immune responses. Although information on the immunomodulatory properties of peptidoglycan from bacteria is abundant, little is known about the β-defensin induction effect of peptidoglycan from the probiotic Lactobacillus. This study investigated the effect of intact peptidoglycan from L. rhamnosus MLGA on the induction of avian β-defensin 9 in chicken immune cells and intestinal explants. Peptidoglycan from Lactobacillus rhamnosus MLGA dose dependently promoted avian β-defensin 9 mRNA expression in chicken PBMCs, splenocytes, thymocytes, hepatocytes, and chicken embryo jejunum, ileum, and cecum explants and increased the capacity of PBMC or splenocyte lysates to inhibit the growth of Salmonella Enteritidis. In contrast to the effect of L. rhamnosus MLGA-derived peptidoglycan, peptidoglycan derived from pathogenic Staphylococcus aureus reduced avian β-defensin 9 mRNA expression in chicken PBMCs and splenocytes. The inducible effect of peptidoglycan from L. rhamnosus MLGA on avian β-defensin 9 expression in PBMCs and splenocytes was observed without activation of the expression of associated pro-inflammatory cytokines IL-1β, IL-8, and IL-12p40, whereas these cytokine expressions were suppressed by peptidoglycan hydrolysate obtained by lysozyme digestion. The results of the present study show the capability of peptidoglycan derived from L. rhamnosus MLGA to induce the antimicrobial peptide defensin while simultaneously avoiding the deleterious risks of an inflammatory response.

The Wellcome Trust Lecture: Infection and disease in lymphatic filariasis: an immunological perspective

Parasitology ◽  
1992 ◽  
Vol 104 (S1) ◽  
pp. S71-S79 ◽  
Author(s):  
E. A. OtteSen
Keyword(s):  
Immune Responses ◽  
Lymphatic Filariasis ◽  
Clinical Manifestations ◽  
Genetic Determination ◽  
Inflammatory Reactions ◽  
Alternative Pathways ◽  
Immunodeficient Mice ◽  
Parasite Antigen ◽  
Immunological Responses ◽  
Asymptomatic Patients

SUMMARYThe basic tenet of the immunological perspective of fuiarial disease is that differential immune responsiveness among individuals exposed to infection results in the different clinical manifestations that develop. The mechanisms involved in this differential responsiveness appear to reflect different T-cell cytokine response patterns. Asymptomatic patients with the clinically silent presentation of ‘asymptomatic microfilaraemia’, who have been previously described as being ‘immunosuppressed’ with respect to their generating pro-inflammatory (Th1-type) immune responses to parasite antigen, are now recognized to be fully responsive to parasite antigen but to produce cytokines and mediators that have primarily anti-inflammatory (Th2-like) effects. Studies with immunodeficient mice have indicated the existence of two alternative pathways to the development of lymphatic pathology: one dependent on the induction of inflammatory reactions by the host immune response, the other entirely independent of the immune system and reflecting the direct actions of the parasite or its products on the lymphatics. As histopathology of affected human lymphatics is consistent with this hypothesis, it may be that the lymphatic pathology seen normally in the amicrofilaraemic, highly immunoresponsive infected patients derives from inflammation induced by immune responses to parasite antigen, whereas the lymphatic pathology sometimes seen coexisting with the ‘immunosuppressed’ state of asymptomatic microfilaraemia actually reflects lymphatic damage that is not immunologically mediated. Though little information exists about the ‘natural history’ of lymphatic filariasis, there is no evidence for an inevitable progression from one clinical form to another. Instead, there appears to be a definite plasticity in the response that depends on prior (? pre-natal) and current exposure to the parasite as well as on the immunomodulatory effects it induces. This plasticity does not appear to be complete, however, as there is no evidence that a chronically infected host who has developed strong pro-inflammatory immune responses can subsequently become sufficiently ‘down-regulated’ to support an asymptomatic microfilaraemia type of infection. Another possible constraint to the plasticity of the clinical and immunological responses may be the genetic determination of certain unusual syndromes, such as tropical pulmonary eosinophilia or TPE, though this hypothesis remains to be proven.

scholarly journals Cell Adhesion Molecules in Inflammation and Immunity: Relevance to Periodontal Diseases

1994 ◽  
Vol 5 (2) ◽  
pp. 91-123 ◽  
Author(s):  
John M. Crawford ◽  
Keiko Watanabe
Keyword(s):  
Cell Adhesion ◽  
Immune Responses ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Current Knowledge ◽  
Close Contact ◽  
Periodontal Diseases ◽  
Inflammatory Reactions ◽  
Adhesive Interactions

Inflammatory and immune responses involve close contact between different populations of cells. These adhesive interactions mediate migration of cells to sites of inflammation and the effector functions of cells within the lesions. Recently, there has been significant progress in understanding the molecular basis of these intercellular contacts. Blocking interactions between cell adhesion molecules and their ligands has successfully suppressed inflammatory reactions in a variety of animal models in vivo. The role of the host response in periodontal disease is receiving renewed attention, but little is known of the function of cell adhesion molecules in these diseases. In this review we summarize the structure, distribution, and function of cell adhesion molecules involved in inflammatory/immune responses. The current knowledge of the distribution of cell adhesion molecules is described and the potential for modulation of cell adhesion molecule function is discussed.

scholarly journals Polyamine Transport Protein PotD Protects Mice against Haemophilus parasuis and Elevates the Secretion of Pro-Inflammatory Cytokines of Macrophage via JNK–MAPK and NF–κB Signal Pathways through TLR4

Vaccines ◽  
2019 ◽  
Vol 7 (4) ◽  
pp. 216 ◽  
Author(s):  
Ke Dai ◽  
Xiaoyu Ma ◽  
Zhen Yang ◽  
Yung-Fu Chang ◽  
Sanjie Cao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Transport System ◽  
Signal Pathways ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Cellular Immune Responses ◽  
Polyamine Transport ◽  
Cellular Immune ◽  
Pro Inflammatory Cytokines

The potD gene, belonging to the well-conserved ABC (ATP-binding cassette) transport system potABCD, encodes the bacterial substrate-binding subunit of the polyamine transport system. In this study, we found PotD in Haemophilus (Glaesserella) parasuis could actively stimulate both humoral immune and cellular immune responses and elevate lymphocyte proliferation, thus eliciting a Th1-type immune response in a murine immunity and infection model. Stimulation of Raw 264.7 macrophages with PotD validated that Toll-like receptor 4, rather than 2, participated in the positive transcription and expression of pro-inflammatory cytokines IL–1β, IL–6, and TNF–α using qPCR and ELISA. Blocking signal-regulated JNK–MAPK and RelA(p65) pathways significantly decreased PotD-induced pro-inflammatory cytokine production. Overall, we conclude that vaccination of PotD could induce both humoral and cellular immune responses and provide immunoprotection against H. parasuis challenge. The data also suggest that Glaesserella PotD is a novel pro-inflammatory mediator and induces TLR4-dependent pro-inflammatory activity in Raw 264.7 macrophages through JNK–MAPK and RelA(p65) pathways.

scholarly journals Detection of the complement fragment C5a in inflammatory exudates from the rabbit peritoneal cavity using radioimmunoassay.

1983 ◽  
Vol 158 (6) ◽  
pp. 2177-2182 ◽  
Author(s):  
P J Jose ◽  
M J Forrest ◽  
T J Williams
Keyword(s):  
Peritoneal Cavity ◽  
Inflammatory Mediator ◽  
Microvascular Permeability ◽  
Oedema Formation ◽  
Inflammatory Reactions ◽  
Pmn Leukocytes ◽  
The Many

We describe a radioimmunoassay for rabbit C5a and its use to obtain evidence of extravascular C5a generation in two inflammatory reactions in the peritoneal cavity. These observations, together with the potent activity of C5a in inducing increased microvascular permeability involving circulating PMN leukocytes, strengthen the case for considering C5a an important inflammatory mediator. These findings offer an explanation for the many different experimental inflammatory reactions where oedema formation can be suppressed either by systemic depletion of complement or by depletion of circulating PMN leukocytes.

scholarly journals Migration matters: regulatory T-cell compartmentalization determines suppressive activity in vivo

Blood ◽  
2005 ◽  
Vol 106 (9) ◽  
pp. 3097-3104 ◽  
Author(s):  
Kerstin Siegmund ◽  
Markus Feuerer ◽  
Christiane Siewert ◽  
Saeed Ghani ◽  
Uta Haubold ◽  
...  
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Conclusive Evidence ◽  
Effector Memory ◽  
Induction Phase ◽  
Inflammatory Reactions ◽  
Selectin Ligands ◽  
Treg Subset ◽  
Cell Compartmentalization

AbstractRegulatory T cells (Tregs) play a fundamental role in the suppression of different immune responses; however, compartments at which they exert suppressive functions in vivo are unknown. Although many groups have described the presence of Tregs within inflammatory sites, it has not been shown that inflamed tissues are, indeed, the sites of active suppression of ongoing immune reactions. Here, by using αE+ effector/memory-like Tregs from fucosyltransferase VII-deficient animals, which lack E/P-selectin ligands and fail to migrate into inflamed sites, we analyzed the functional importance of appropriate Treg localization for in vivo suppressive capacity in an inflammation model. Lack of suppression by Tregs deficient in E/P-selectin ligands demonstrates that immigration into inflamed sites is a prerequisite for the resolution of inflammatory reactions in vivo because these selectin ligands merely regulate entry into inflamed tissues. In contrast, control of proliferation of naive CD4+ T cells during the induction phase of the immune response is more efficiently exerted by the naive-like αE–CD25+ Treg subset preferentially recirculating through lymph nodes when compared with its inflammation-seeking counterpart. Together, these findings provide the first conclusive evidence that appropriate localization is crucial for in vivo activity of Tregs and might have significant implications for anti-inflammatory therapies targeting recruitment mechanisms.

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