Displaying all 6 publications

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  1. Goh YC, Chan SW, Siar CH
    Malays J Pathol, 2019 Dec;41(3):303-311.
    PMID: 31901915
    INTRODUCTION: Ameloblastoma is a benign but locally invasive odontogenic epithelial neoplasm with a high recurrence rate after treatment. The two main subsets encountered clinically are unicystic (UA) and solid/multicystic ameloblastoma (SMA). Currently neoplastic progression of many tumour types are believed to be related to parenchyma-stromal cell-cell interactions mediated by cytokines notably interleukins (IL). However their roles in ameloblastoma remain ill-understood.

    MATERIALS AND METHODS: Thirty-nine formalin-fixed paraffin-embedded ameloblastoma cases comprising unicystic ameloblastoma (n=19) and solid/multicystic ameloblastoma (n=20) were subjected to IHC staining for IL-1α, IL-1β, IL-6 and IL-8. A semi-quantitative method was used to evaluate the expression levels of these cytokines according to cell types in the tumoural parenchyma and stroma.

    RESULTS: Major findings were upregulations of IL-1α and IL-6 in SMA compared to UA. Both cytokines were heterogeneously detected in the tumoural parenchyma and stroma. Within the neoplastic epithelial compartment, IL-1α expression was more frequently detected in PA-like cells in UA whereas it was more frequently encountered in SR-like cells in SMA. IL-6 demonstrated higher expression levels in the stromal compartment of SMA. IL-1β and IL-8 were markedly underexpressed in both tumour subsets.

    CONCLUSIONS: Overexpression of IL-1α in SMA suggests that this growth factor might play a role in promoting bone resorption and local invasiveness in this subtype. The expression levels of IL-1α and IL-6 in three cellular localizations indicate that parenchymal-stromal components of ameloblastoma interact reciprocally via IL-1α and IL-6 to create a microenvironment conducive for tumour progression.

    Matched MeSH terms: Interleukin-1alpha/metabolism*
  2. Mohamad S, Hamid SSA, Azlina A, Md Shukri N
    Asia Pac Allergy, 2019 Jul;9(3):e22.
    PMID: 31384577 DOI: 10.5415/apallergy.2019.9.e22
    Background: Chronic rhinosinusitis (CRS) is one of the most common and complex chronic inflammatory disease of sinonasal mucosa. Even though the pathogenesis of CRS is multifactorial and still unclear, the role of cytokines especially interleukin-1 (IL-1) is being investigated worldwide in different population because of varying results obtained.

    Objective: To study the association of IL-1 (A and B) gene polymorphisms with chronic rhinosinusitis with nasal polyp (CRSwNP) and without nasal polyp (CRSsNP), and other factors related.

    Methods: This is a case-controlled study which include a total of 138 subjects recruited from Otorhinolaryngology-Head and Neck Surgery clinic in Hospital Universiti Sains Malaysia. Genotyping of the IL-1A (+4845G, +4845T) and IL-1B (-511C, -511T) were performed with restriction fragment length polymorphism analysis.

    Results: There was a statistical significant association between IL-1B (-511C, -511T) polymorphism with CRSwNP and CRSsNP (p < 0.001). The CT genotype of IL-1B was markedly increased in CRSwNP subjects (52.2%). However, there was no significant association found between IL-1A (+4845G, +4845T) with CRSwNP and CRSsNP (p = 0.093). No association was found in factors related to CRS, which included asthma, atopy, allergy, aspirin sensitivity, and family history of nasal polyp (p value of 0.382, 0.382, 0.144, >0.95, and 0.254, respectively).

    Conclusion: This study indicates an association of IL-1B (-511C, -511T) polymorphism with CRSwNP and CRSsNP in our population, hence there is a possibility of IL-1B involvement in modulating pathogenesis of CRS. There was no significant association of IL-1A (+4845G, +4845T) polymorphism with CRSwNP and CRSsNP, and other factors related.

    Matched MeSH terms: Interleukin-1alpha
  3. Chin, V.K., Chong, W.C., Hassan, H., Zakaria, Z.A., Nordin, N., Basir, R., et al.
    JUMMEC, 2019;22(2):4-12.
    MyJurnal
    Background: The cytokine cascade in the immunopathogenesis of malaria infection had been widely studied.
    However, their specific association with survival and severe infection remained obscure.

    Methods: The study investigated the cytokine profiles and histopathological features of malaria in the severe
    infection and survival models by using male ICR mice and male Sprague Dawley rats respectively.

    Results: The severe model, the infected ICR mice, exhibited a high parasitemia with 100% mortality after
    peak parasitemia at day 5 post-infection. The survival model, the infected Sprague Dawley rats, showed
    mild parasitemia with full recovery by day 14 of infection. Both severe and survival models showed similar
    histopathological severity during peak parasitemia. The severe model produced highly elevated levels of proinflammatory
    cytokines, TNF-α and IL-1α, and low levels of the anti-inflammatory cytokine, IL-4; while the
    survival model showed low levels of TNF-α and IL-1α with high levels of IL-4.

    Conclusion: There were differences in the pathogenesis of the severe and survival models of malaria infection.
    These could be a basis for immunotherapy of malaria in the future.
    Matched MeSH terms: Interleukin-1alpha
  4. Mohd Zohdi R, Abu Bakar Zakaria Z, Yusof N, Mohamed Mustapha N, Abdullah MN
    PMID: 21941590 DOI: 10.1155/2012/843025
    A novel cross-linked honey hydrogel dressing was developed by incorporating Malaysian honey into hydrogel dressing formulation, cross-linked and sterilized using electron beam irradiation (25 kGy). In this study, the physical properties of the prepared honey hydrogel and its wound healing efficacy on deep partial thickness burn wounds in rats were assessed. Skin samples were taken at 7, 14, 21, and 28 days after burn for histopathological and molecular evaluations. Application of honey hydrogel dressings significantly enhanced (P < 0.05) wound closure and accelerated the rate of re-epithelialization as compared to control hydrogel and OpSite film dressing. A significant decrease in inflammatory response was observed in honey hydrogel treated wounds as early as 7 days after burn (P < 0.05). Semiquantitative analysis using RT-PCR revealed that treatment with honey hydrogel significantly (P < 0.05) suppressed the expression of proinflammatory cytokines (IL-1α, IL-1β, and IL-6). The present study substantiates the potential efficacy of honey hydrogel dressings in accelerating burn wound healing.
    Matched MeSH terms: Interleukin-1alpha
  5. Ali Salim KM, Abd Jalil A, Radzi Z, Ismail SM, Czernuszka JT, Rahman MT
    Materials (Basel), 2020 Oct 06;13(19).
    PMID: 33036128 DOI: 10.3390/ma13194436
    OBJECTIVE: Reconstruction of oral and facial defects often necessitate replacement of missing soft tissue. The purpose of tissue expanders is to grow healthy supplementary tissue under a controlled force. This study investigates the inflammatory responses associated with the force generated from the use of anisotropic hydrogel tissue expanders.

    METHODS: Sprague Dawley rats (n = 7, body weight = 300 g ± 50 g) were grouped randomly into two groups-control (n = 3) and expanded (n = 4). Anisotropic hydrogel tissue expanders were inserted into the frontal maxillofacial region of the rats in the expanded group. The rats were sacrificed, and skin samples were harvested, fixed in formalin, and embedded in paraffin wax for histological investigation. Hematoxylin and eosin staining was performed to detect histological changes between the two groups and to investigate the inflammatory response in the expanded samples. Three inflammatory markers, namely interleukin (IL)-1α, IL-6, and tumor necrosis factor-α (TNF-α), were analyzed by immunohistochemistry.

    RESULT: IL-1-α expression was only observed in the expanded tissue samples compared to the controls. In contrast, there was no significant difference in IL-6, and TNF-α production. Histological analysis showed the absence of inflammatory response in expanded tissues, and a negative non-significant correlation (Spearman's correlation coefficient) between IL-1-α immune-positive cells and the inflammatory cells (r = -0.500). In conclusion, tissues that are expanded and stabilized using an anisotropic self-inflating hydrogel tissue expander might be useful for tissue replacement and engraftment as the expanded tissue does not show any sign of inflammatory responses. Detection of IL-1-α in the expanded tissues warrants further investigation for its involvement without any visible inflammatory response.

    Matched MeSH terms: Interleukin-1alpha
  6. Sarkar S, Leo BF, Carranza C, Chen S, Rivas-Santiago C, Porter AE, et al.
    PLoS One, 2015;10(11):e0143077.
    PMID: 26580078 DOI: 10.1371/journal.pone.0143077
    Exposure to silver nanoparticles (AgNP) used in consumer products carries potential health risks including increased susceptibility to infectious pathogens. Systematic assessments of antimicrobial macrophage immune responses in the context of AgNP exposure are important because uptake of AgNP by macrophages may lead to alterations of innate immune cell functions. In this study we examined the effects of exposure to AgNP with different particle sizes (20 and 110 nm diameters) and surface chemistry (citrate or polyvinlypyrrolidone capping) on cellular toxicity and innate immune responses against Mycobacterium tuberculosis (M.tb) by human monocyte-derived macrophages (MDM). Exposures of MDM to AgNP significantly reduced cellular viability, increased IL8 and decreased IL10 mRNA expression. Exposure of M.tb-infected MDM to AgNP suppressed M.tb-induced expression of IL1B, IL10, and TNFA mRNA. Furthermore, M.tb-induced IL-1β, a cytokine critical for host resistance to M.tb, was inhibited by AgNP but not by carbon black particles indicating that the observed immunosuppressive effects of AgNP are particle specific. Suppressive effects of AgNP on the M.tb-induced host immune responses were in part due to AgNP-mediated interferences with the TLR signaling pathways that culminate in the activation of the transcription factor NF-κB. AgNP exposure suppressed M.tb-induced expression of a subset of NF-κB mediated genes (CSF2, CSF3, IFNG, IL1A, IL1B, IL6, IL10, TNFA, NFKB1A). In addition, AgNP exposure increased the expression of HSPA1A mRNA and the corresponding stress-induced Hsp72 protein. Up-regulation of Hsp72 by AgNP can suppress M.tb-induced NF-κB activation and host immune responses. The observed ability of AgNP to modulate infectious pathogen-induced immune responses has important public health implications.
    Matched MeSH terms: Interleukin-1alpha/genetics; Interleukin-1alpha/immunology
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