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Interleukins and cytokines are involved in the pathogenesis of uveitis of heterogeneous origin. Understanding the basics of the ocular immune privilege is a fulcrum to discern their specific role in diverse uveitis to potentially translate as therapeutic targets. This review attempts to cover these elements in uveitis of infectious, noninfectious and masquerade origin. Insights of the molecular targets in novel therapy along with the vision of future research are intriguing.
Interleukins have been well described in mice and humans. In large domestic animals the situation is drastically different and there is still a need for further researches aiming at identifying all the homologous interleukins and comparing their functions among species. We performed here a bibliometric analysis of all interleukins described in the literature in various large animal species to identify what is known so far and to underline where there is a need for new studies. Using indicators such as H index but also M quotient, A index, G index, GH ratio, and HG index we ranked 39 interleukins identified so far in bovine, caprine, equine, ovine, and porcine, the main large domestic animals. Indexes and ratio under investigations were higher for IL1, IL2, IL4, IL5, IL6, IL8, IL10, IL12, and IL18 than for other interleukins, particularly in bovine and porcine species and to a certain extent in equine species. Recently discovered interleukins presented low values for the different indexes, quotient, and ratio. Even some "old" interleukins showed low values highlighting the need for further developments in comparative immunology. For instance an interleukin such as IL4 demonstrated variation in its functions between species. In conclusion, this study provides the first bibliometric analysis dedicated to large domestic animal interleukins and underlines the need for more studies to fully determine the structure and the functions of interleukins in other mammal species.
The mechanisms by which prenatal events affect development of adult disease are incompletely characterized. Based on findings in a murine model of maternal transmission of asthma risk, we sought to test the role of the pro-asthmatic cytokines interleukin IL-4 and -13. To assess transplacental passage of functional cytokines, we assayed phosphorylation of STAT-6, a marker of IL-4 and -13 signaling via heterodimeric receptor complexes which require an IL-4 receptor alpha subunit. IL-4 receptor alpha-/- females were mated to wild-type males, and pregnant females were injected with supraphysiologic doses of IL-4 or 13. One hour after injection, the receptor heterozygotic embryos were harvested and tissue nuclear proteins extracts assayed for phosphorylation of STAT-6 by Western blot. While direct injection of embryos produced a robust positive control, no phosphorylation was seen after maternal injection with either IL-4 or -13, indicating that neither crossed the placenta in detectable amounts. The data demonstrate a useful approach to assay for transplacental passage of functional maternal molecules, and indicate that molecules other than IL-4 and IL-13 may mediate transplacental effects in maternal transmission of asthma risk.
Calculous cholecystitis connects to inflammation and various complications. It is a common disease in the paediatric population, yet it is still uncertain how inflammation factors are involved in its morphopathogenesis. Twenty calculous cholecystitis surgery tissue samples were obtained from 20 children. As a control, seven unaffected gallbladders were used. Tissues were immunohistochemically stained for IL-1α, IL-4, IL-6, IL-7, IL-8, IL-10, and IL-17A, and the slides were inspected by light microscopy. To evaluate statistical differences and correlations between interleukins, Mann-Whitney U and Spearman's tests were used. Statistically significant difference between patient and control gallbladder epithelium was for IL-1α and IL-17A, but connective tissue-IL-1α, IL-4, IL-6, IL-7, IL-8, and IL-17A positive structures. A strong positive correlation in patients was detected between epithelial IL-1α and IL-1α in connective tissue, epithelial IL-6 and IL-7, IL-6 and IL-17A, IL-7 and IL-10, IL-7 and IL-17A, as well as between IL-6 and IL-7, IL-7 and IL-10 in connective tissue. The increase of IL-1α, IL-4, IL-6, IL-7, IL-8 and IL-17A positive structures suggests their role in the morphopathogenesis of calculous cholecystitis. The correlations between interleukins in epithelium and in connective tissues prove that the epithelial barrier function and inflammatory response in deeper layers are sustained through intercellular signalling pathways.
It is well known that exposure to cis-diaminedichloroplatinum (CDDP) results in impairment of spermatogenesis; however, little is known about the signal mechanisms involved in CDDP regulation of Sertoli cell (SC) function. This study was designed to evaluate how CDDP regulates SC signal molecules and mechanisms. Purified rat SC was cultured under serum-free conditions and treated with CDDP (10 ng/ml) at various time points. Western blot analysis was used to determine the activation of extracellular signal-related kinases 1 and 2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), cJun-N-terminal kinase (JNK), cyclooxygenase (COX)-1 and COX-2, inducible and endothelial nitric oxide synthase (iNOS and eNOS). The levels of transferrin (TF) and prostaglandin (PG)E2, PGF2alpha, PGD2, carbaprostacyclin (cPGI2 analog) in culture medium were quantified by ELISA. Nitrite (NO2(-)) and nitrate (NO3(-)) in culture medium were also quantified by Griess assay. Interleukin (IL)-1beta and IL-6 mRNAs were measured by quantitative real-time PCR (QRT-PCR) analysis. CDDP activated the phosphorylation of ERK1/2 (p-ERK1/2) in the early phase (within 5 min) and the level of transferrin (TF) fell significantly. In addition, CDDP significantly increased the level of COX-2, PGs, and ILs in the late phase (within 24h). When ERK activity inhibitor (PD98059, 10 microM) or COX-2 activity inhibitor (NS-398, 10 microM) was used, CDDP reduction of TF and induction of PG and IL expression were prevented, suggesting that the detrimental effects on spermatogenesis through the impairment of SC induced by CDDP are mediated by the activation of ERK1/2 and COX-2 pathways in SC.
Anastomotic dehiscence is the most severe complication of colorectal surgery and its incidence increases in the presence of infection. It has been reported that immune factors or the activity of matrix metalloproteinases (MMP) may mediate the loss of anastomotic strength in the first postoperative days. In this study, we investigated the effects of abdominal sepsis on the MMP and interleukin (IL) gene expression in left colonic anastomoses in rats.
Our data show that botulinum toxin A (BoNT/A) didn't influence motor functions in naïve and CCI-exposed rats, but diminished the neuropathic pain-related behavior. The results indicate that BoNT/A administration diminished the spinal Iba-1 positive cells activation and, in parallel, downregulated IL-1beta. Moreover, we observed that in DRG the protein level of pronociceptive factors (IL-1beta and IL-18) decreased and antinociceptive (IL-10 and IL-1RA) factors increased. Additionally, our behavioral analysis shows that chronic minocycline treatment together with a single BoNT/A injection in CCI-exposed rats has beneficial analgesic effects (M. Zychowska, E. Rojewska, W. Makuch, S. Luvisetto, F. Pavone, S. Marinelli, B. Przewlocka, J. Mika, 2016) [1].
There is a wealth of biological pathway information available in the scientific literature, but it is spread across many thousands of publications. Alongside publications that contain definitive experimental discoveries are many others that have been dismissed as spurious, found to be irreproducible, or are contradicted by later results and consequently now considered controversial. Many descriptions and images of pathways are incomplete stylized representations that assume the reader is an expert and familiar with the established details of the process, which are consequently not fully explained. Pathway representations in publications frequently do not represent a complete, detailed, and unambiguous description of the molecules involved; their precise posttranslational state; or a full account of the molecular events they undergo while participating in a process. Although this might be sufficient to be interpreted by an expert reader, the lack of detail makes such pathways less useful and difficult to understand for anyone unfamiliar with the area and of limited use as the basis for computational models.
This study monitored the changes in the expression of inflammatory IL-6 and IL-1β during the treatment period of Fluoropyrimidine (FP) based therapy. RNA was extracted from the peripheral blood of 102 CRC patients before treatment with FP therapy, and from 48 and 32 patients after 3 and 6 months of treatment, respectively. The genetic transcription of IL-6 and IL-1β was determined by real time PCR. Patients were stratified according to their levels of IL-6 and IL-1β genes expression for subgroup and survival analyses. Baseline CRC patients showed overexpression of IL-6 and IL-1β compared to healthy control. FP therapy significantly induced IL-6 and IL-1β expression. Subgroup analysis showed that patients with right colon tumors had significant elevation in both IL-6 and IL-1β with FP therapy. FP therapy significantly induced IL-1β expression in patients ⩽45 years, smokers, with high baseline level of CA19.9, right colon tumors, low grade pathology, T3 tumors and positive lymph nodes. Survival analysis showed that baseline levels of interleukins expression had insignificant effect on overall survival and event free survival. FP therapy has an impact on the level of interleukins expression declared in certain clinicopathological subgroups of CRC patients, but without a prognostic significance on patients' survival.
More and more studies have suggested that single-nucleotide polymorphisms (SNPs) in interleukin (IL) genes are correlated with an increased risk of developing oral lichen planus (OLP). However, these results were inconsistent. Therefore, the aim of this meta-analysis is to retrieve and comprehensively analyze all related clinical studies to investigate the association of ILs gene polymorphisms with the OLP risk.
In-depth knowledge of cancer molecular and cellular mechanisms have revealed a strong regulation of cancer development and progression by the inflammation which orchestrates the tumor microenvironment. Immune cells, residents or recruited, in the inflammation milieu can have rather contrasting effects during cancer development. Accumulated clinical and experimental data support the notion that acute inflammation could exert an immunoprotective effect leading to tumor eradication. However, chronic immune response promotes tumor growth and invasion. These reactions are mediated by soluble mediators or cytokines produced by either host immune cells or tumor cells themselves. Herein, we provide an overview of the current understanding of the role of the best-validated cytokines involved in tumor progression, IL-1, IL-4 and IL-6; in addition to IL-2 cytokines family, which is known to promote tumor eradication by immune cells. Furthermore, we summarize the clinical attempts to block or bolster the effect of these tumor-related interleukins in anti-cancer therapy development.
Interleukins (ILs) are the most typical inflammatory and immunoregulatory cytokines. Evidences have shown that polymorphisms in ILs are associated with cerebral infarction risk. However, the results remain inconclusive. The present study was to evaluate the role of ILs polymorphisms in cerebral infarction susceptibility. Relevant case-control studies published between January 2000 and December 2015 were searched and retrieved from the electronic databases of Web of Science, PubMed, Embase and the Chinese Biomedical Database. The odds ratio (OR) with its 95% confidence interval (CI) were employed to calculate the strength of association. A total of 55 articles including 12619 cerebral infarction patients and 14436 controls were screened out. Four ILs (IL-1, IL-6, IL-10 and IL-18) contained nine single nucleotide polymorphisms (SNPs; IL-1α -899C/T, IL-1β -511C/T and IL-1β +3953C/T; IL-6 -174G/C and -572C/G; IL-10 -819C/T and -1082A/G; IL-18 -607C/A and -137G/C). Our result showed that IL-1α -899C/T and IL-18 -607C/A (under all the genetic models), and IL-6 -572C/G (under the allelic model, heterogeneity model and dominant model) were associated with increased the risk of cerebral infarction (P<0.05). Subgroup analysis by ethnicity showed that IL-6 -174G/C polymorphism (under all the five models) and IL-10 -1082A/G polymorphism (under the allelic model and heterologous model) were significantly associated with increased the cerebral infarction risk in Asians. Other genetic polymorphisms were not related with cerebral infarction susceptibility under any genetic models. In conclusion, IL-1α -899C/T, IL-6 -572C/G and IL-18 -607C/A might be risk factors for cerebral infarction development. Further studies with well-designed and large sample size are still required.
T lymphocytes require signals from self-peptides and cytokines, most notably interleukins 7 and 15 (IL-7, IL-15), for survival. While mouse T cells die rapidly if IL-7 or IL-15 is withdrawn, human T cells can survive prolonged withdrawal of IL-7 and IL-15. Here we show that IL-7 and IL-15 are required to maintain human T cell proliferative capacity through the STAT5 signaling pathway. T cells from humanized mice proliferate better if stimulated in the presence of human IL-7 or IL-15 or if T cells are exposed to human IL-7 or IL-15 in mice. Freshly isolated T cells from human peripheral blood lose proliferative capacity if cultured for 24 hours in the absence of IL-7 or IL-15. We further show that phosphorylation of STAT5 correlates with proliferation and inhibition of STAT5 reduces proliferation. These results reveal a novel role of IL-7 and IL-15 in maintaining human T cell function, provide an explanation for T cell dysfunction in humanized mice, and have significant implications for in vitro studies with human T cells.
There is a perplexity in the association between interleukin (IL) polymorphisms and periodontitis among patients with and without diabetes mellitus (DM). The aim of the present study was to evaluate indexed data regarding the association between periodontitis and genetic polymorphisms in interleukins among patients with and without DM. The addressed question was "Is there an association between periodontitis and polymorphisms in interleukins among patients with and without DM?" Original studies were included. Indexed databases were searched, and the pattern of the present literature review was customized to summaries' the pertinent information. Eight studies were included and processed for data extraction. Two studies showed that polymorphisms in IL-1B genes aggravate periodontitis in patients with type-2 DM, and two studies showed that IL-1B genes either do not or are less likely to contribute towards the progression of periodontitis in patients with type-2 DM. Two studies reported that IL genes do not show cross-susceptibility with periodontitis and type-2 DM. One study reported that the primary factor that governs the occurrence and progression of periodontitis in patients with and without type-2 DM is poor routine oral hygiene maintenance. Seven studies had a high risk of bias. The role of IL gene polymorphisms in the development and progression of periodontitis in patients with and without DM remains controversial.
Aromatic-aromatic hydrogen bonds are important in many areas of chemistry, biology and materials science. In this study we have analyzed the roles played by the π-π interactions in interleukins (ILs) and tumor necrosis factor (TNF) proteins. Majority of π-π interacting residues are conserved in ILs and TNF proteins. The accessible surface area calculations in these proteins reveal that these interactions might be important in stabilizing the inner core regions of these proteins. In addition to π-π interactions, the aromatic residues also form π-networks in ILs and TNF proteins. The results obtained in the present study indicate that π-π interactions and π-π networks play important roles in the structural stability of ILs and TNF proteins.
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