Probiotics and Reduction of the Inflammatory Response for Prevention of Preeclampsia

Introduction: In the field of medicine and obstetrics, the most common hypertensive disorders are preeclampsia and it constitutes a great question that has not yet been completely resolved. Objective: To identify the effectiveness of the use of probiotics and the reduction of the inflammatory response in the prevention of pre-eclampsia. Method: This search took place in large databases both globally and locally, being Elsevier, La Reference, Scielo, Pubmed, Google Scholar, Redalyc, Scopus, among others, where probiotic and pre‐eclampsia terms were found. Results: 37 articles were found which were preselected, after correct appreciation 32 articles were selected and 5 articles were discarded, the selected ones met the inclusion and exclusion criteria, therefore they are related to the topic and objective of the present study review. Discussion: The epithelial cells of the intestine produce TNF‐α, once mixtures of different strains of probiotics are made, causing the immune response to be generated, especially if consumed before pregnancy or in early pregnancy and continued throughout of the same. the administration is safe and has a protective role in pre-eclampsia, gestational diabetes, vaginal infections, maternal, infant, and subsequent weight gain. Conclusion: The preventive effect occurs as long as probiotics are administered mainly in the second and third trimesters of pregnancy, although the consumption of probiotics before these results in a much greater benefit, and is even more potent if probiotic mixtures are made. Keywords: probiotics, preeclampsia, hypertensive disorder. RESUMEN Introducción: En el campo de la medicina y obstetricia, los trastornos hipertensivos más comunes son preeclampsia y compone una gran interrogante que aún no está resuelta completamente. Objetivo: Identificar la efectividad del uso de probióticos y la reducción de la respuesta inflamatoria en la prevención de la preeclampsia. Método: Esta búsqueda tuvo lugar en grandes bases de datos tanto a nivel mundial como local, siendo Elsevier, La Referencia, Scielo, Pubmed, Google Académico, Redalyc, Scopus, entre otras, donde se encontraron términos de probióticos y preeclampsia. Resultados: Se encontró 37 artículos los cuales fueron preseleccionados, luego de la correcta apreciación se seleccionaron 32 artículos y se descartaron 5 artículos, los seleccionados cumplían con los criterios inclusión y de exclusión por lo tanto van en relación con el tema y objetivo del presente estudio de revisión. Discusión: Las células epiteliales del intestino producen TNF‐α, una vez que se realicen mezclas de distintas cepas de probióticos, haciendo que se genere la respuesta inmunitaria, en especial si se consume antes del embarazo o en el embarazo temprano y continua a lo largo del mismo. La administración es segura y tiene un papel protector en la preeclampsia, diabetes gestacional, infecciones vaginales, aumento de peso materno, infantil, y posteriores. Conclusión: El efecto preventivo se da siempre y cuando se administre probióticos principalmente en el segundo y tercer trimestre de embarazo, aunque el consumo de probióticos con anterioridad a estos resulta de mucho mayor beneficio, y se potencia aún más si se realizan mezclas de probióticos. Palabas clave: probióticos, preeclampsia, trastorno hipertensivo.

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β-Sitosterol Alters the Inflammatory Response in CLP Rat Model of Sepsis by Modulation of NFκB Signaling

BioMed Research International ◽

10.1155/2021/5535562 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Sara Kasirzadeh ◽

Mohammad Hossein Ghahremani ◽

Neda Setayesh ◽

Fereshteh Jeivad ◽

Amir Shadboorestan ◽

...

Keyword(s):

Inflammatory Response ◽

Bacterial Infections ◽

Sham Group ◽

Cecal Ligation ◽

Serum Levels ◽

Protective Role ◽

Mrna Levels ◽

Tnf Α ◽

Male Wistar Rats ◽

Host Inflammatory Response

Purpose. Sepsis originates from the host inflammatory response, especially to bacterial infections, and is considered one of the main causes of death in intensive care units. Various agents have been developed to inhibit mediators of the inflammatory response; one prospective agent is β-sitosterol (βS), a phytosterol with a structure similar to cholesterol. This study is aimed at evaluating the effects of βS on the biomarkers of inflammation and liver function in cecal ligation and puncture- (CLP-) induced septic rats. Methods. Thirty male Wistar rats were divided equally into six groups as follows: sham, CLP, CLP+dexamethasone (DX, 0.2 mg/kg), CLP+βS (1 mg/kg), CLP+imipenem (IMI, 20 mg/kg), and CLP+IMI (20 mg/kg)+βS (1 mg/kg). Serum levels of IL-1β, IL-6, IL-10, AST, ALT, and liver glutathione (GSH) were assessed by ELISA. Liver expression levels of TNF-α and NF-κBi mRNAs were evaluated by RT-qPCR. Results. Serum concentrations of IL-1β, IL-6, IL-10, ALT, and AST and mRNA levels of TNF-α and NF-κBi were all significantly higher in septic rats than in normal rats ( p < 0.05 ). Liver GSH content was markedly lower in the CLP group than that in the sham group. βS-treated rats had remarkably lower levels of IL-1β, IL-6, IL-10, TNF-α, NF-κBi, AST, and ALT (51.79%, 62.63%, 41.46%, 54.35%, 94.37%, 95.30%, 34.87%, and 46.53% lower, respectively) and greater liver GSH content (35.71% greater) compared to the CLP group ( p < 0.05 ). Conclusion. βS may play a protective role in the septic process by mitigating inflammation. This effect is at least partly mediated by inhibition of the NF-κB signaling pathway. Thus, βS can be considered as a supplementary treatment in septic patients.

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Endogenous and Exogenous Glucocorticoids in Experimental Enterococcal Infection

Clinical and Vaccine Immunology ◽

10.1128/cvi.13.3.349-355.2006 ◽

2006 ◽

Vol 13 (3) ◽

pp. 349-355 ◽

Cited By ~ 4

Author(s):

Christopher J. Papasian ◽

Nilofer Qureshi ◽

David C. Morrison

Keyword(s):

Lethal Dose ◽

Lavage Fluid ◽

Protective Role ◽

Necrosis Factor Alpha ◽

Enterococcal Infection ◽

Peritoneal Tumor ◽

Glucocorticoid Response ◽

Tnf Α ◽

Different Strains ◽

Adrenal Glucocorticoid

ABSTRACT The potentially protective role of the host adrenal-glucocorticoid response to enterococcal infection was evaluated in an experimental model in which mice were infected intraperitoneally with two distinct Enterococcus faecalis strains (K9 and CP-1). We demonstrated that corticosterone levels in serum and peritoneal-lavage fluid were elevated within 1 hour of infection with either E. faecalis strain. We also demonstrated that adrenalectomized mice generated a more robust localized peritoneal tumor necrosis factor alpha (TNF-α) response to both E. faecalis strains than did sham-adrenalectomized mice but that neither E. faecalis strain induced a systemic TNF-α response. Further, peritoneal TNF-α production in adrenalectomized mice infected with either E. faecalis K9 or CP-1 was suppressed by prior treatment with an exogenous glucocorticoid (dexamethasone). The potential clinical significance of these results was suggested by our findings that adrenalectomy markedly increased susceptibility (a >100-fold decrease in the 50% lethal dose) to lethal infections with E. faecalis CP-1 and that prior dexamethasone treatment partially compensated for adrenalectomy. In marked contrast to these findings, however, adrenalectomy did not substantially increase susceptibility to lethal E. faecalis K9 infection. Further, preinfection with E. faecalis CP-1 1 hour before infection with E. faecalis K9 did not protect mice from lethal E. faecalis K9 infections. Collectively, these studies indicate that the host can generate a glucocorticoid response to E. faecalis infection that suppresses TNF-α production. Further, this glucocorticoid response can protect the host from potentially lethal E. faecalis infections, but different strains show heterogeneity with respect to the extent of protection afforded by the adrenal-glucocorticoid response.

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Bifidobacterium plays a protective role in TNF-α-induced inflammatory response in Caco-2 cell through NF-κB and p38MAPK pathways

Molecular and Cellular Biochemistry ◽

10.1007/s11010-019-03651-3 ◽

2019 ◽

Vol 464 (1-2) ◽

pp. 83-91 ◽

Cited By ~ 4

Author(s):

Nana Nie ◽

Cui Bai ◽

Shanai Song ◽

Yanyan Zhang ◽

Benzhen Wang ◽

...

Keyword(s):

Inflammatory Response ◽

Protective Role ◽

Tnf Α

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Danshensu inhibits the IL-1β-induced inflammatory response in chondrocytes and osteoarthritis possibly via suppressing NF-κB signaling pathway

Molecular Medicine ◽

10.1186/s10020-021-00329-9 ◽

2021 ◽

Vol 27 (1) ◽

Author(s):

Zhixian Xu ◽

Tie Ke ◽

Yongfa Zhang ◽

Licheng Guo ◽

Feng Chen ◽

...

Keyword(s):

Inflammatory Response ◽

Signaling Pathway ◽

Protective Role ◽

Cell Counting ◽

Inos Mrna ◽

Mrna Levels ◽

Dependent Manner ◽

Tnf Α ◽

Cox 2

Abstract Purpose Osteoarthritis (OA) is the most common inflammatory disease associated with pain and cartilage destruction. Interleukin (IL)-1β is widely used to induce inflammatory response in OA models. This study aimed to explore the role of Danshensu (DSS) in IL-1β-induced inflammatory responses in OA. Methods IL-1β was used to induce chondrocyte inflammation. Cell viability was evaluated by Cell Counting Kit-8 (CCK-8) assay. IL-6, COX-2, TNF-α, and iNOS mRNA levels were detected by qRT-PCR. MMP3, MMP13, ADAMTS4, ADAMTS5, Aggrecan, Collagen, p-IκBα, and p-p65 protein levels were detected by Western blot. An OA mouse model was established by surgical destabilization of the medial meniscus (DMM), and the Osteoarthritis Research Society International (OARSI) score was evaluated by H&E staining. Results DSS did not affect the levels of inflammatory indicators including IL-6, COX-2, TNF-α, iNOS, PEG2, and NO but suppressed COX-2 and iNOS protein expression in IL-1β treated chondrocytes. In addition, DSS downregulated IL-1β-enhanced expression of MMP3, MMP13, ADAMTS4, and ADAMTS5 and upregulated aggrecan and collagen expression. Moreover, DSS significantly inhibited IL-1β-induced phosphorylation of p-IκBα and p-p65 in a dose-dependent manner in chondrocytes, suggesting it plays a role in the NF-κB signaling pathway. Furthermore, DSS significantly reduced DMM-induced cartilage OARSI score in mice, further demonstrating its protective role in OA progression in vivo. Conclusions Our study revealed the protective role of DSS in OA, suggesting that DSS might act as a potential treatment for OA.

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Sorghum Fermented by Aspergillus oryzae NK Enhances Inhibition of Vascular Inflammation in TNF-α-stimulated Human Aortic Smooth Muscle Cells

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000496 ◽

2018 ◽

Vol 88 (5-6) ◽

pp. 309-318

Author(s):

Hae Seong Song ◽

Jung-Eun Kwon ◽

Hyun Jin Baek ◽

Chang Won Kim ◽

Hyelin Jeon ◽

...

Keyword(s):

Smooth Muscle ◽

Inflammatory Response ◽

Smooth Muscle Cells ◽

Adhesion Molecule ◽

Vascular Inflammation ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle ◽

Tnf Α ◽

Cox 2

Abstract. Sorghum bicolor L. Moench is widely grown all over the world for food and feed. The effects of sorghum extracts on general inflammation have been previously studied, but its anti-vascular inflammatory effects are unknown. Therefore, this study investigated the anti-vascular inflammation effects of sorghum extract (SBE) and fermented extract of sorghum (fSBE) on human aortic smooth muscle cells (HASMCs). After the cytotoxicity test of the sorghum extract, a series of experiments were conducted. The inhibition effects of SBE and fSBE on the inflammatory response and adhesion molecule expression were measured using treatment with tumor necrosis factor-α (TNF-α), a crucial promoter for the development of atherosclerotic lesions, on HASMCs. After TNF-α (10 ng/mL) treatment for 2 h, then SBE and fSBE (100 and 200 μg/mL) were applied for 12h. Western blotting analysis showed that the expression of vascular cell adhesion molecule-1 (VCAM-1) (2.4-fold) and cyclooxygenase-2 (COX-2) (6.7-fold) decreased, and heme oxygenase-1 (HO-1) (3.5-fold) increased compared to the TNF-α control when treated with 200 μg/mL fSBE (P<0.05). In addition, the fSBE significantly increased the expression of HO-1 and significantly decreased the expression of VCAM-1 and COX-2 compared to the TNF-α control in mRNA level (P<0.05). These reasons of results might be due to the increased concentrations of procyanidin B1 (about 6-fold) and C1 (about 30-fold) produced through fermentation with Aspergillus oryzae NK for 48 h, at 37 °C. Overall, the results demonstrated that fSBE enhanced the inhibition of the inflammatory response and adherent molecule expression in HASMCs.

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4-(Phenylsulfanyl) Butan-2-One Attenuates the Inflammatory Response Induced by Amyloid-β Oligomers in Retinal Pigment Epithelium Cells

Marine Drugs ◽

10.3390/md19010001 ◽

2020 ◽

Vol 19 (1) ◽

pp. 1

Author(s):

Peeraporn Varinthra ◽

Shun-Ping Huang ◽

Supin Chompoopong ◽

Zhi-Hong Wen ◽

Ingrid Y. Liu

Keyword(s):

Retinal Pigment Epithelium ◽

Inflammatory Response ◽

Pigment Epithelium ◽

Retinal Pigment ◽

Amyloid Β ◽

Age Related Macular Degeneration ◽

Epithelial Cell Line ◽

Age Related ◽

Tnf Α ◽

Cox 2

Age-related macular degeneration (AMD) is a progressive eye disease that causes irreversible impairment of central vision, and effective treatment is not yet available. Extracellular accumulation of amyloid-beta (Aβ) in drusen that lie under the retinal pigment epithelium (RPE) has been reported as one of the early signs of AMD and was found in more than 60% of Alzheimer’s disease (AD) patients. Extracellular deposition of Aβ can induce the expression of inflammatory cytokines such as IL-1β, TNF-α, COX-2, and iNOS in RPE cells. Thus, finding a compound that can effectively reduce the inflammatory response may help the treatment of AMD. In this research, we investigated the anti-inflammatory effect of the coral-derived compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) on Aβ1-42 oligomer (oAβ1-42) added to the human adult retinal pigment epithelial cell line (ARPE-19). Our results demonstrated that 4-PSB-2 can decrease the elevated expressions of TNF-α, COX-2, and iNOS via NF-κB signaling in ARPE-19 cells treated with oAβ1-42 without causing any cytotoxicity or notable side effects. This study suggests that 4-PSB-2 is a promising drug candidate for attenuation of AMD.

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AB0713 PERIODONTAL DISEASES AND ITS ASSOCIATION WITH ANKYLOSING SPONDYLITIS/SPA: A SYSTEMATIC REVIEW

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2020-eular.1564 ◽

2020 ◽

Vol 79 (Suppl 1) ◽

pp. 1652.1-1652

Author(s):

A. Pandey ◽

V. Ravindran ◽

M. Pandey ◽

R. Rajak ◽

V. Pandey

Keyword(s):

Systematic Review ◽

Ankylosing Spondylitis ◽

Connective Tissue ◽

Inflammatory Response ◽

Periodontal Disease ◽

Close Association ◽

Case Control ◽

Clinical Attachment Loss ◽

Tnf Α ◽

Host Inflammatory Response

Background:A close association between periodontal disease and Ankylosing spondylitis (AS) has long been specualted. Both diseases are characterized by dysregulation of the host inflammatory response, leading to further destruction of soft and hard connective tissue with there being evidence of increased levels of TNF-α and various interleukins in both patients of AS and periodontitis.Objectives:The aim of this systematic review was to appraise the available literature exploring the relationship between AS and periodontal disease.Methods:We searched Medline & Embase databases (from their inception till October 2019) using appropriate combinations of following search items with limits ‘(English, Human)’; Ankylosing spondylitis, spondyloarthritis, spondyloarthropathies, spondyloarthritides, spinal disease, musculoskeletal disease, Rheumatic disease AND periodontitis, periodontal disease, periodontoses, parodontoses, chronic periodontitis, gum disease, gingivitis, oral health, dental health, plaque index, bleeding on probing, probing pocket depth, clinical attachment loss. This search was supplemented by the manual search of bibliographies of articles selected and conferences proceedings of EULAR. Only be reviews, observational study of cross-sectional, cohort or case control type on adult patients with AS were selected. Data was extracted from a predesigned proforma. A close association between periodontal disease and Ankylosing spondylitis (AS) has long been specualted. Both diseases are characterized by dysregulation of the host inflammatory response, leading to further destruction of soft and hard connective tissue with there being evidence of increased levels of TNF-α and various interleukins in both patients of AS and periodontitis.Results:A total number of 984 articles were identified and 12 were selcted for detailed appraisal (Figure 1, PRISMA flow chart). They were all case control studies. The prevalence of periodontitis ranged from 38% to 88% in patients with AS whereas in the control group from 26% to 71 % in controls. Out of 12 studies, two showed significant changes in Plaque Index (PI), two studies showed altered Pocket Probing Depth (PPD), three showed significant increased in Clinical Attachment Loss (CAL) and increased Bleeding On Probing (BOP) was seen in 2 studies. In 7 studies, periodontitis was seen in a significant number of patients with AS (P<0.05). All studies reported that the prevalence of periodontal disease in AS patients was higher as compared to non-AS patients.Conclusion:Our systematic review found an association between AS and periodontal disease. Patients with AS show higher prevalence of periodontitis and a poor oral hygiene as compared to healthy controls. At practice level, this systematic review underscores the need for a collaboration between dentists and rheumatologist.Disclosure of Interests:None declared

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Comparing the protective effects of resveratrol, curcumin and sulforaphane against LPS/IFN-γ-mediated inflammation in doxorubicin-treated macrophages

Scientific Reports ◽

10.1038/s41598-020-80804-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Haidy A. Saleh ◽

Eman Ramdan ◽

Mohey M. Elmazar ◽

Hassan M. E. Azzazy ◽

Anwar Abdelnaser

Keyword(s):

Nitric Oxide ◽

Inflammatory Response ◽

Raw 264.7 Cells ◽

Inos Mrna ◽

No Production ◽

Raw 264.7 ◽

Mrna Levels ◽

Protective Effects ◽

Tnf Α ◽

Ifn Γ

AbstractDoxorubicin (DOX) chemotherapy is associated with the release of inflammatory cytokines from macrophages. This has been suggested to be, in part, due to DOX-mediated leakage of endotoxins from gut microflora, which activate Toll-like receptor 4 (TLR4) signaling in macrophages, causing severe inflammation. However, the direct function of DOX on macrophages is still unknown. In the present study, we tested the hypothesis that DOX alone is incapable of stimulating inflammatory response in macrophages. Then, we compared the anti-inflammatory effects of curcumin (CUR), resveratrol (RES) and sulforaphane (SFN) against lipopolysaccharide/interferon-gamma (LPS/IFN-γ)-mediated inflammation in the absence or presence of DOX. For this purpose, RAW 264.7 cells were stimulated with LPS/IFN-γ (10 ng/mL/10 U/mL) in the absence or presence of DOX (0.1 µM). Our results showed that DOX alone is incapable of stimulating an inflammatory response in RAW 264.7 macrophages. Furthermore, after 24 h of incubation with LPS/IFN-γ, a significant increase in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) mRNA levels was observed. Similarly, nitric oxide (NO) production and TNF-α and IL-6 protein levels were significantly upregulated. Moreover, in LPS/IFN-γ-treated macrophages, the microRNAs (miRNAs) miR-146a, miR-155, and miR-21 were significantly overexpressed. Interestingly, upon testing CUR, RES, and SFN against LPS/IFN-γ-mediated inflammation, only SFN was able to significantly reverse the LPS/IFN-γ-mediated induction of iNOS, TNF-α and IL-6 and attenuate miR-146a and miR-155 levels. In conclusion, SFN, at the transcriptional and posttranscriptional levels, exhibits potent immunomodulatory action against LPS/IFN-γ-stimulated macrophages, which may indicate SFN as a potential treatment for DOX-associated inflammation.

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Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

Diagnostic Pathology ◽

10.1186/s13000-021-01089-0 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Jianwei Zhang ◽

Lei Han ◽

Feng Chen

Keyword(s):

Inflammatory Response ◽

Chronic Rhinosinusitis ◽

Nasal Polyps ◽

Mapk Pathway ◽

Inhibitory Effect ◽

Luciferase Reporter ◽

Western Blot Assay ◽

Protein Levels ◽

Tnf Α

Abstract Background Let-7a-5p is demonstrated to be a tumor inhibitor in nasopharyngeal carcinoma. However, the role of let-7a-5p in chronic rhinosinusitis with nasal polyps (CRSwNP) has not been reported. This study is designed to determine the pattern of expression and role of let-7a-5p in CRSwNP. Methods The expression level of let-7a-5p, TNF-α, IL-1β, and IL-6 in CRSwNP tissues and cells were detected by RT-qPCR. Western blot assay was carried out to measure the protein expression of the Ras-MAPK pathway. Dual luciferase reporter assay and RNA pull-down assay were used to explore the relationship between let-7a-5p and IL-6. Results Let-7a-5p was significantly downregulated in CRSwNP tissues and cells. Moreover, the mRNA expression of TNF-α, IL-1β and IL-6 was increased in CRSwNP tissues, while let-7a-5p mimic inhibited the expression of TNF-α, IL-1β and IL-6. Besides that, let-7a-5p was negatively correlated with TNF-α, IL-1β and IL-6 in CRSwNP tissues. In our study, IL-6 was found to be a target gene of let-7a-5p. Additionally, let-7-5p mimic obviously reduced the protein levels of Ras, p-Raf1, p-MEK1 and p-ERK1/2, while IL-6 overexpression destroyed the inhibitory effect of let-7a-5p on the Ras-MAPK pathway in CRSwNP. Conclusion We demonstrated that let-7a-5p/IL-6 interaction regulated the inflammatory response through the Ras-MAPK pathway in CRSwNP.

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ER Stress, UPR Activation and the Inflammatory Response to Viral Infection

Viruses ◽

10.3390/v13050798 ◽

2021 ◽

Vol 13 (5) ◽

pp. 798

Author(s):

Mara Cirone

Keyword(s):

Inflammatory Response ◽

Viral Infection ◽

Viral Infections ◽

Protective Role ◽

Microbial Infection ◽

Unfolded Protein ◽

Cytokines And Chemokines ◽

Complex Process ◽

Protein Response ◽

Recognition Receptor

The response to invading pathogens such as viruses is orchestrated by pattern recognition receptor (PRR) and unfolded protein response (UPR) signaling, which intersects and converges in the activation of proinflammatory pathways and the release of cytokines and chemokines that harness the immune system in the attempt to clear microbial infection. Despite this protective intent, the inflammatory response, particularly during viral infection, may be too intense or last for too long, whereby it becomes the cause of organ or systemic diseases itself. This suggests that a better understanding of the mechanisms that regulate this complex process is needed in order to achieve better control of the side effects that inflammation may cause while potentiating its protective role. The use of specific inhibitors of the UPR sensors or PRRs or the downstream pathways activated by their signaling could offer the opportunity to reach this goal and improve the outcome of inflammation-based diseases associated with viral infections.

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