inflammatory chemokines
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2022 ◽  
Vol 23 (1) ◽  
pp. 553
Author(s):  
Ga-Yul Min ◽  
Ji-Hye Kim ◽  
Tae-In Kim ◽  
Won-Kyung Cho ◽  
Ju-Hye Yang ◽  
...  

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with a type 2 T helper cell (Th2) immune response. The IndigoPulverata Levis extract (CHD) is used in traditional Southeast Asian medicine; however, its beneficial effects on AD remain uninvestigated. Therefore, we investigated the therapeutic effects of CHD in 2,4-dinitrochlorobenzene (DNCB)-induced BALB/c mice and tumor necrosis factor (TNF)-α- and interferon gamma (IFN)-γ-stimulated HaCaT cells. We evaluated immune cell infiltration, skin thickness, and the serum IgE and TNF-α levels in DNCB-induced AD mice. Moreover, we measured the expression levels of pro-inflammatory cytokines, mitogen-activated protein kinase (MAPK), and the nuclear factor-kappa B (NF-κB) in the mice dorsal skin. We also studied the effect of CHD on the translocation of NF-κB p65 and inflammatory chemokines in HaCaT cells. Our in vivo results revealed that CHD reduced the dermis and epidermis thicknesses and inhibited immune cell infiltration. Furthermore, it suppressed the proinflammatory cytokine expression and MAPK and NF-κB phosphorylations in the skin tissue and decreased serum IgE and TNF-α levels. In vitro results indicated that CHD downregulated inflammatory chemokines and blocked NF-κB p65 translocation. Thus, we deduced that CHD is a potential drug candidate for AD treatment.


2021 ◽  
Vol 23 (6) ◽  
pp. 1239-1270
Author(s):  
M. Z. Saidov

Cell infiltrate is a morphological substrate of immunoinflammatory rheumatic diseases. The systemic wide progressive disorganization of loose fibrous connective tissue is accompanied by the loss of tolerance with its own autoantigenes, activation of macrophagal-monocyte cells and autoreactive clones of T and B lymphocytes. Hyperproduction of pro-inflammatory chemokines and cytokines, local adhesive ligandreceptor interactions, endothelial reaction and angiogenesis contribute to the formation of cell infiltrate, ectopic lymphoid structures and GZT-granulomas in situ. The autoimmune response is the result of successive systemic and local molecular cellular events in which the mechanisms of congenital and adaptive immunity are involved. When interpreting immunopathogenesis of rheumatic diseases, all models and schemes adopted in the field of fundamental immunology are used. This is a model of MHC-restrictions, a model of molecular mimicry, or cross of the antigen presentation, a model of disrupting central or peripheral tolerance to auto-antigens, a model of candidate “triggers” of autoimmune and autoinflammatory processes, a model of associations of alleles MHC I and II classes with specific, nosologically unique, rheumatic diseases.


Author(s):  
Déborah Neyrinck-Leglantier ◽  
Julien Lesage ◽  
Silvia Blacher ◽  
Arnaud Bonnomet ◽  
Walter Hunziker ◽  
...  

Delocalization of zonula occludens-1 (ZO-1) from tight junctions plays a substantial role in epithelial cell plasticity observed during tumor progression. In vitro, we reported an impact of ZO-1 cyto-nuclear content in modulating the secretion of several pro-inflammatory chemokines. In vivo, we demonstrated that it promotes the recruitment of immune cells in mouse ear sponge assays. Examining lung cancers, we showed that a high density of CD8 cytotoxic T cells and Foxp3 immunosuppressive regulatory T cells in the tumor microenvironment correlated with a cyto-nuclear expression of ZO-1. Taken together, our results support that, by affecting tumor cell secretome, the cyto-nuclear ZO-1 pool may recruit immune cells, which could be permissive for tumor progression.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Deepak Kumar Kaushik ◽  
Anindita Bhattacharya ◽  
Brian Mark Lozinski ◽  
V. Wee Yong

Abstract Background Multiple sclerosis (MS) is a neurodegenerative condition of the central nervous system (CNS). It is associated with blood–brain barrier (BBB) breakdown and intravasation of leukocytes, particularly monocyte-derived macrophages, into the CNS. Pericytes are mural cells that are encased within the basement membrane of vasculature, and they contribute functionally to the neurovascular unit. These cells play an important role in maintaining BBB integrity and CNS homeostasis. However, the critical role of pericytes in mediating inflammation in MS or its models is unclear. Whether pericytes infiltrate into the CNS parenchyma in MS also needs clarification. Methods CNS samples from the experimental autoimmune encephalomyelitis (EAE) mouse model of MS were collected at different time points for immunohistochemical analysis of pericytes along the inflamed vasculature. These findings were validated using MS brain specimens, and further analysis of pericyte involvement in inflammation was carried out by culturing primary pericytes and macrophages. Multiplex ELISA, transmigration assay and real-time PCR were used to study the inflammatory potential of pericytes in cultures. Results We found that pericytes exhibit a heterogenous morphology, with notable elongation in the inflamed perivascular cuffs of EAE. This was manifested by a decrease in pericyte density but an increase in the coverage by pericytes along the vasculature. Chondroitin sulfate proteoglycans (CSPGs), a family of extracellular matrix proteins enriched within inflamed perivascular cuffs, elevated levels of pro-inflammatory chemokines/cytokines in pericytes in culture. Importantly, pericytes stimulated with CSPGs enhanced macrophage migration. We did not detect pericytes in the CNS parenchyma during EAE, and this was corroborated in MS brain samples. Conclusions Our data suggest that pericytes seek to restore the BBB through increased coverage, but that their exposure to CSPGs prompt their facilitation of macrophages to enter the CNS to elevate neuroinflammation in EAE and MS.


2021 ◽  
Vol 20 (10) ◽  
pp. 2099-2107
Author(s):  
Hao Li ◽  
Yan Gao

Purpose: To investigate the effectiveness of luteolin treatment in postmenopausal model of osteoarthritis (OA)Methods: Sprague-Dawley rats were divided into five groups. Luteolin was given orally to rats at doses of 50 and 100 mg/kg for 4 months, while aceclofenac was administered at a dose of 10 mg/kg. The antiinflammatory and anti-arthritic effects of luteolin and aceclofenac were determined using paw-withdrawal method. Knee joint thickness was measured using X-ray imaging. Pathological changes in bone slices were determined with immuno-histochemical evaluation. The levels of inflammatory cytokines were assessed by reverse transcription-polymerase chain reaction (RT-PCR) and western blot analysis.Results: Oral ingestion of luteolin significantly reduced manifestations of OA and suppressed levels of serum cytokines (p < 0.05). Moreover, luteolin increased expression of bone marker protein and reduced the gene expression levels of matrix metalloproteinases (MMPs, p < 0.05), suggesting its protective effects on chondrocytes. Luteolin significantly reduced the production of inflammatory chemokines and cytokines (IFN-γ, IL-1, and IL-6). Histopathological examination showed that luteolindecreased pathological lesions in monoiodoacetate-mediated OA in ovariectomized rats, indicatingprevention of cartilage loss.Conclusion: These results suggest that luteolin exerts protective effects against monoiodoacetateinduced (MIA) OA in ovariectomized rats by suppressing the expressions of inflammation-related mediators (IL-1β, Cox-2, and PGE-2). Thus, luteolin is a prospective option for the suppression of postmenopausal OA in humans.


2021 ◽  
Vol 6 (3) ◽  
pp. 96-107
Author(s):  
Abubakar Auwal Nasir ◽  
Erhabor Osaro ◽  
Ibrahim Mohammed ◽  
Ahmed Hamidu Marafa ◽  
Yakubu Abdulrahman

Atherosclerosis is a chronic inflammatory process that results in coronary artery disease, peripheral artery disease and in many cases of stroke. It is a disease that involves multiple inflammatory cytokine which is regarded as the primary underlying cause of cardiovascular diseases (CVD). CVD is the leading cause of death in the developed and developing countries like Nigeria. From pathological perspective, the chronic inflammatory condition of atherosclerosis occurs due to interplay between platelets, monocytes, macrophages. Physiologically platelets play a significant role in coagulation and repair of endothelial injury. Pathologically, studies have shown that activated platelets release multiple inflammatory cytokines and chemokines that serve as positive mediators of atherosclerosis. This chemokine is (RANTES, P-selectin and PF-4). Activated platelet release p-selectin that mediate platelet adhesion and rolling to injured endothelial cell, RANTES trigger the recruitment of monocytes into the sub- endothelium and PF4 promote the differentiation of monocytes into macrophages in the intimal layer of the endothelium which engulf ox-LDL to form FOAM cells. Thus, the aim of this review is to understand and describe the role of activated platelets in atherosclerosis as well as therapeutic target of these platelet inflammatory chemokines which is the major mediator of atherosclerosis in human.


2021 ◽  
Vol 2 ◽  
Author(s):  
Dione Kawamoto ◽  
Rodrigo Borges ◽  
Rodolfo Alvarenga Ribeiro ◽  
Robson Franciso de Souza ◽  
Pâmela Pontes Penas Amado ◽  
...  

Inflammation is a driven force in modulating microbial communities, but little is known about the interplay between colonizing microorganisms and the immune response in periodontitis. Since local and systemic inflammation may play a whole role in disease, we aimed to evaluate the oral and fecal microbiome of patients with periodontitis and to correlate the oral microbiome data with levels of inflammatory mediator in saliva.Methods: Nine patients with periodontitis (P) in Stage 3/Grade B and nine age-matched non-affected controls (H) were evaluated. Microbial communities of oral biofilms (the supra and subgingival from affected and non-affected sites) and feces were determined by sequencing analysis of the 16SrRNA V3–V4 region. Salivary levels of 40 chemokines and cytokines were correlated with oral microbiome data.Results: Supragingival microbial communities of P differed from H (Pielou's evenness index, and Beta diversity, and weighted UniFrac), since relative abundance (RA) of Defluviitaleaceae, Desulfobulbaceae, Mycoplasmataceae, Peptostreococcales-Tissierellales, and Campylobacteraceae was higher in P, whereas Muribaculaceae and Streptococcaceae were more abundant in H. Subgingival non-affected sites of P did not differ from H, except for a lower abundance of Gemellaceae. The microbiome of affected periodontitis sites (PD ≥ 4 mm) clustered apart from the subgingival sites of H. Oral pathobionts was more abundant in sub and supragingival biofilms of P than H. Fecal samples of P were enriched with Acidaminococcus, Clostridium, Lactobacillus, Bifidobacterium, Megasphaera, and Romboutsia when compared to H. The salivary levels of interleukin 6 (IL-6) and inflammatory chemokines were positively correlated with the RA of several recognized and putative pathobionts, whereas the RA of beneficial species, such as Rothia aeria and Haemophilus parainfluenzae was negatively correlated with the levels of Chemokine C-C motif Ligand 2 (CCL2), which is considered protective. Dysbiosis in patients with periodontitis was not restricted to periodontal pockets but was also seen in the supragingival and subgingival non-affected sites and feces. Subgingival dysbiosis revealed microbial signatures characteristic of different immune profiles, suggesting a role for candidate pathogens and beneficial organisms in the inflammatory process of periodontitis.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mengyao Li ◽  
Ying Chen ◽  
Huihan Li ◽  
Dehua Yang ◽  
Yunlian Zhou ◽  
...  

Abstract Background How to early distinguish the severity of Mycoplasma pneumoniae pneumonia (MPP) is a worldwide concern in clinical practice. We therefore conducted this study to assess the relationship between levels of serum inflammatory chemokines and the severity of MPP. Methods In this prospective study, we enrolled 39 children with MPP, whose clinical information was collected, blood samples were assayed for cytokines and chemokines by ELISA. Results The levels of serum CXCL10 in children with severe MPP were significantly higher than those in children with mild MPP (2500.0 [1580.9–2500.0] vs. 675.7 [394.7–1134.9], P < 0.001). Measurement of CXCL10 levels in serum enabled the differentiation of children with severe MPP with an area under the curve (AUC) of 0.885 (95 % CI 0.779–0.991, P < 0.001), with a sensitivity of 81.0 % and a specificity of 83.3 %. Conclusions Serum CXCL10 level may be a potential biomarker for severe MPP in children.


2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Carlos Cabalag ◽  
Owen Prall ◽  
John Ciciulla ◽  
Laurence Galea ◽  
Niko Thio ◽  
...  

Abstract   Significant advances have been made in our understanding of the tumor immune microenvironment (TIM) and tumor infiltrating lymphocytes (TILs). Nevertheless, there is little understanding of the changes in the TIM in response to neoadjuvant chemoradiotherapy (CRT). Thus, our aim was to investigate the changes in the TIM with neoadjuvant CRT in EC by assessing the immune cell infiltrate, the expression of immune related genes, and their association with treatment response and prognosis. Methods To decipher the effects of neoadjuvant CRT on the TIM, we obtained 58 paired pre-treatment and post neoadjuvant CRT treated EC specimens. TILs and tumor infiltrating neutrophils (TIN) were quantified in pre-treatment biopsies and surgical resection specimens following neoadjuvant CRT. To evaluate the immune transcriptomics, RNA was extracted from these specimens and gene expression was assessed using the Nanostring Platform based on the PanCancer Immune Profiling Panel. Immunohistochemistry (IHC) was performed to validate findings from the immune transcriptomics. Results TIL counts were not prognostic for disease specific survival (DSS). We observed higher expression of immune-suppressive inflammatory chemokines (TGFß-1 and IL-16) in post-neoadjuvant treated samples compared to pre-treatment biopsies. In samples collected after neoadjuvant CRT, low expression of genes related to anti-tumor T cell cytotoxic activity1 was significantly associated with disease recurrence. In patients with residual disease, multivariate analysis revealed a high neutrophil count, but not TIL count, was significantly associated with inferior DSS (HR 3.8 [1.3– 10.8]; p = 0.01). Conclusion In EC, the tumor microenvironment after neoadjuvant CRT remains largely immune-suppressive. We discovered that the presence of TINs in patients with residual disease post neoadjuvant CRT is an independent adverse prognostic factor. Collectively, our results suggest that an inflammatory pro-tumoral microenvironment associated with TINs may contribute to treatment resistance and progressive disease in EC.


2021 ◽  
Author(s):  
Xiaodong Shan ◽  
Feifei Chen ◽  
Huikang Lin ◽  
Hangjun Zhang ◽  
Yuchi Zhong ◽  
...  

Abstract Zinc oxide nanoparticles (ZnO-NPs) can affect human health primarily via inhalation. This study evaluated the protective effects of theaflavins (TFs) and epigallocatechin gallate (EGCG) against ZnO-NP-induced cytotoxicity in rat tracheal epithelial (RTE) cells. After exposure to ZnO-NPs (100 µg/L), treatment with TFs and EGCG (10, 100 and 1000 µg/L) significantly inhibited the levels of reactive oxygen species (ROS), and the content of malondialdehyde (MDA). Treatment also alleviated apoptosis induced by oxidative stress, which was achieved by inhibiting cytochrome C (CytoC) and Caspase 3/8/9 mRNA expression. Upon treatment with the highest concentrations of TFs and EGCG (1000 µg/L), CytoC gene expression was downregulated by 59.10% and 77.27%, Caspase 3 gene expression by 50.03% and 60.01%, Caspase 8 gene expression by 45.11% and 55.57%, and Caspase 9 gene expression by 51.33% and 66.67%. In addition, about the interleukin family as interleukin 1β (IL-1β) and interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and the other inflammatory chemokines like C-C motif chemokine 2 (CCL2), C-X-C motif chemokine 8 (CXCL8) were upregulated in RTE cells in the presence of ZnO-NPs. All factors were gradually rescued after the addition of TFs and EGCG. These results showed that TFs and EGCG could effectively protect RTE cells from oxidative damage induced by ZnO-NPs through antiapoptotic and antioxidant effects.


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