Displaying publications 1 - 20 of 464 in total

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  1. Pang T
    Med J Malaysia, 1992 Mar;47(1):1-2.
    PMID: 1387441
    Matched MeSH terms: Cytokines/therapeutic use*
  2. Lawler NG, Gray N, Kimhofer T, Boughton B, Gay M, Yang R, et al.
    J Proteome Res, 2021 May 07;20(5):2796-2811.
    PMID: 33724837 DOI: 10.1021/acs.jproteome.1c00052
    We performed quantitative metabolic phenotyping of blood plasma in parallel with cytokine/chemokine analysis from participants who were either SARS-CoV-2 (+) (n = 10) or SARS-CoV-2 (-) (n = 49). SARS-CoV-2 positivity was associated with a unique metabolic phenotype and demonstrated a complex systemic response to infection, including severe perturbations in amino acid and kynurenine metabolic pathways. Nine metabolites were elevated in plasma and strongly associated with infection (quinolinic acid, glutamic acid, nicotinic acid, aspartic acid, neopterin, kynurenine, phenylalanine, 3-hydroxykynurenine, and taurine; p < 0.05), while four metabolites were lower in infection (tryptophan, histidine, indole-3-acetic acid, and citrulline; p < 0.05). This signature supports a systemic metabolic phenoconversion following infection, indicating possible neurotoxicity and neurological disruption (elevations of 3-hydroxykynurenine and quinolinic acid) and liver dysfunction (reduction in Fischer's ratio and elevation of taurine). Finally, we report correlations between the key metabolite changes observed in the disease with concentrations of proinflammatory cytokines and chemokines showing strong immunometabolic disorder in response to SARS-CoV-2 infection.
    Matched MeSH terms: Cytokines
  3. Atan R, Crosbie DC, Bellomo R
    Ren Fail, 2013 Sep;35(8):1061-70.
    PMID: 23866032 DOI: 10.3109/0886022X.2013.815089
    Hypercytokinemia is believed to be harmful and reducing cytokine levels is considered beneficial. Extracorporeal blood purification (EBP) techniques have been studied for the purpose of cytokine reduction. We aimed to study the efficacy of various EBP techniques for cytokine removal as defined by technical measures.
    Matched MeSH terms: Cytokines/blood*
  4. Vellasamy DM, Lee SJ, Goh KW, Goh BH, Tang YQ, Ming LC, et al.
    Int J Mol Sci, 2022 Oct 27;23(21).
    PMID: 36361845 DOI: 10.3390/ijms232113059
    Atherosclerosis is one of the main underlying causes of cardiovascular diseases (CVD). It is associated with chronic inflammation and intimal thickening as well as the involvement of multiple cell types including immune cells. The engagement of innate or adaptive immune response has either athero-protective or atherogenic properties in exacerbating or alleviating atherosclerosis. In atherosclerosis, the mechanism of action of immune cells, particularly monocytes, macrophages, dendritic cells, and B- and T-lymphocytes have been discussed. Immuno-senescence is associated with aging, viral infections, genetic predispositions, and hyperlipidemia, which contribute to atherosclerosis. Immune senescent cells secrete SASP that delays or accelerates atherosclerosis plaque growth and associated pathologies such as aneurysms and coronary artery disease. Senescent cells undergo cell cycle arrest, morphological changes, and phenotypic changes in terms of their abundances and secretome profile including cytokines, chemokines, matrix metalloproteases (MMPs) and Toll-like receptors (TLRs) expressions. The senescence markers are used in therapeutics and currently, senolytics represent one of the emerging treatments where specific targets and clearance of senescent cells are being considered as therapy targets for the prevention or treatment of atherosclerosis.
    Matched MeSH terms: Cytokines/metabolism
  5. Soh GT, Mohammad AH, Syed Isa SNL, Chin KY, Mohamed N
    PMID: 36380416 DOI: 10.2174/1871530323666221114111029
    BACKGROUND: Chronic low-grade inflammation is involved in the pathogenesis of postmenopausal osteoporosis, but the cytokines implicated remain elusive.

    OBJECTIVE: This study aimed to compare the difference in cytokine profile between postmenopausal women with and without osteoporosis in Klang Valley, Malaysia.

    METHODS: Postmenopausal women with (n = 20) and without osteoporosis (n = 20) were recruited for this study. Their bone health status was determined using dual-energy X-ray absorptiometry. Their fasting blood was collected for proteomic analysis. A protein array was performed for four subjects randomly selected from each group to screen the potential cytokines. Three cytokines at least 20% different between groups and consistently expressed by each subject were selected for validation using enzyme-linked immunosorbent assays (ELISA).

    RESULTS: The protein array screening demonstrated that platelet-derived growth factor-BB, interleukin- 6 receptor (IL-6R), and tissue inhibitor of metallopeptidase-2 were higher in women with osteoporosis than women without osteoporosis (n = 4 per group), and consistently expressed by all women. Only body mass index (BMI)-adjusted logarithmically transformed IL-6R levels were lower among postmenopausal women with osteoporosis compared to women with normal bone health (p = 0.026) (n = 16 per group) in the ELISA test.

    CONCLUSION: IL-6R was lower among postmenopausal women with osteoporosis compared to women with normal bone health after adjusting for BMI. However, a large-scale epidemiological study with proteomic analysis needs to confirm the findings.

    Matched MeSH terms: Cytokines/metabolism
  6. Ng CT, Fong LY, Abdullah MNH
    Cytokine, 2023 Jun;166:156208.
    PMID: 37088004 DOI: 10.1016/j.cyto.2023.156208
    Interferon-gamma (IFN-γ) is a pleiotropic cytokine that plays a critical role in mediating an array of immune responses including promotes antiviral activity, facilitates macrophage activation, controls Th1/Th2 balance, and regulates cellular apoptosis and proliferation. A few articles have previously reviewed the effects of IFN-γ in the regulation of barrier permeability, but none of these articles focuses on barrier function of endothelial cells. This review aims to discuss the regulatory mechanisms of IFN-γ on endothelial barrier function and its underlying signaling pathways. Articles were retrieved from electronic databases such as PubMed and Google Scholar using keywords "Interferon-gamma", "endothelial cells", "barrier function", and "signaling pathway". The articles published between 2000 and 2022 that are related to the aforementioned topics were selected. A few journals published beyond this period were also included due to limited information available. The results showed that IFN-γ modulates endothelial barrier function, mainly involves small GTPases, STAT1-dependent pathway, p38 MAPK and nitric oxide. In conclusion, more in depth cellular and molecular studies are needed to elucidate the pathways of IFN-γ in the regulation of endothelial barrier function.
    Matched MeSH terms: Cytokines/metabolism
  7. Nirenjen S, Narayanan J, Tamilanban T, Subramaniyan V, Chitra V, Fuloria NK, et al.
    Front Immunol, 2023;14:1216321.
    PMID: 37575261 DOI: 10.3389/fimmu.2023.1216321
    BACKGROUND: Impaired wound healing is the most common and significant complication of Diabetes. While most other complications of Diabetes have better treatment options, diabetic wounds remain a burden as they can cause pain and suffering in patients. Wound closure and repair are orchestrated by a sequence of events aided by the release of pro-inflammatory cytokines, which are dysregulated in cases of Diabetes, making the wound environment unfavorable for healing and delaying the wound healing processes. This concise review provides an overview of the dysregulation of pro-inflammatory cytokines and offers insights into better therapeutic outcomes.

    PURPOSE OF REVIEW: Although many therapeutic approaches have been lined up nowadays to treat Diabetes, there are no proper treatment modalities proposed yet in treating diabetic wounds due to the lack of understanding about the role of inflammatory mediators, especially Pro-inflammatory mediators- Cytokines, in the process of Wound healing which we mainly focus on this review.

    RECENT FINDINGS: Although complications of Diabetes mellitus are most reported after years of diagnosis, the most severe critical complication is impaired Wound Healing among Diabetes patients. Even though Trauma, Peripheral Artery Disease, and Peripheral Neuropathy are the leading triggering factors for the development of ulcerations, the most significant issue contributing to the development of complicated cutaneous wounds is wound healing impairment. It may even end up with amputation. Newer therapeutic approaches such as incorporating the additives in the present dressing materials, which include antimicrobial molecules and immunomodulatory cytokines is of better therapeutic value.

    SUMMARY: The adoption of these technologies and the establishment of novel therapeutic interventions is difficult since there is a gap in terms of a complete understanding of the pathophysiological mechanisms at the cellular and molecular level and the lack of data in terms of the assessment of safety and bioavailability differences in the individuals' patients. The target-specific pro-inflammatory cytokines-based therapies, either by upregulation or downregulation of them, will be helpful in the wound healing process and thereby enhances the Quality of life in patients, which is the goal of drug therapy.

    Matched MeSH terms: Cytokines*
  8. Hasan N, Hasani NAH, Omar E, Sham FR, Fuad SBSA, Karim MKA, et al.
    Cancer Biomark, 2023;38(1):61-75.
    PMID: 37522193 DOI: 10.3233/CBM-220268
    BACKGROUND: A complicated interplay between radiation doses, tumour microenvironment (TME), and host immune system is linked to the active participation of immune response.

    OBJECTIVE: The effects of single targeted 2 Gy and 8 Gy gamma-ray irradiations on the immune cell population (lymphocytes, B-cells, T-cells, neutrophils, eosinophils, and macrophages) in EMT6 mouse-bearing tumour models was investigated.

    METHODS: The effects of both irradiation doses in early (96 hours) and acute phase (5 to 11 days) post-irradiation on immune parameters were monitored in blood circulation and TME using flow cytometry. Simultaneously, selected cytokines related to immune cells within the TME were measured using multiplex ELISA.

    RESULTS: A temporary reduction in systemic total white blood count (TWBC) resulted from an early phase (96 hours) of gamma-ray irradiation at 2 Gy and 8 Gy compared to sham control group. No difference was obtained in the acute phase. Neutrophils dominated among other immune cells in TME in sham control group. Eosinophils in TME was significantly increased after 8 Gy treatment in acute phase compared to sham control (p< 0.005). Furthermore, the increment of tumour necrosis (TNF)-α, eotaxin and interleukin (IL)-7 (p< 0.05) in both treatment groups and phases were associated with anti-tumour activities within TME by gamma-ray irradiation.

    CONCLUSION: The temporary changes in immune cell populations within systemic circulation and TME induced by different doses of gamma-ray irradiation correlated with suppression of several pro-tumorigenic cytokines in mouse-bearing EMT6 tumour models.

    Matched MeSH terms: Cytokines*
  9. Yap SH, Lee CS, Zulkifli ND, Suresh D, Hamase K, Das KT, et al.
    Amino Acids, 2024 Feb 03;56(1):6.
    PMID: 38310167 DOI: 10.1007/s00726-023-03360-8
    Studies in vivo have demonstrated that the accumulation of D-amino acids (D-AAs) is associated with age-related diseases and increased immune activation. However, the underlying mechanism(s) of these observations are not well defined. The metabolism of D-AAs by D-amino oxidase (DAO) produces hydrogen peroxide (H2O2), a reactive oxygen species involved in several physiological processes including immune response, cell differentiation, and proliferation. Excessive levels of H2O2 contribute to oxidative stress and eventual cell death, a characteristic of age-related pathology. Here, we explored the molecular mechanisms of D-serine (D-Ser) and D-alanine (D-Ala) in human liver cancer cells, HepG2, with a focus on the production of H2O2 the downstream secretion of pro-inflammatory cytokine and chemokine, and subsequent cell death. In HepG2 cells, we demonstrated that D-Ser decreased H2O2 production and induced concentration-dependent depolarization of mitochondrial membrane potential (MMP). This was associated with the upregulation of activated NF-кB, pro-inflammatory cytokine, TNF-α, and chemokine, IL-8 secretion, and subsequent apoptosis. Conversely, D-Ala-treated cells induced H2O2 production, and were also accompanied by the upregulation of activated NF-кB, TNF-α, and IL-8, but did not cause significant apoptosis. The present study confirms the role of both D-Ser and D-Ala in inducing inflammatory responses, but each via unique activation pathways. This response was associated with apoptotic cell death only with D-Ser. Further research is required to gain a better understanding of the mechanisms underlying D-AA-induced inflammation and its downstream consequences, especially in the context of aging given the wide detection of these entities in systemic circulation.
    Matched MeSH terms: Cytokines/metabolism
  10. Foo YY, Tiah A, Aung SW
    Clin Exp Immunol, 2023 Jun 05;212(3):212-223.
    PMID: 36866467 DOI: 10.1093/cei/uxad030
    Natural killer (NK) cells possess the innate ability to eliminate cancerous cells effectively. Their crucial role in immunosurveillance has been widely recognized and exploited for therapeutic intervention. Despite the fast-acting nature of NK cells, NK adoptive cell transfer lacks favorable response in some patients. Patient NK cells often display diminished phenotype in preventing cancer progression resulting in poor prognosis. Tumor microenvironment plays a significant role in causing the downfall of NK cells in patients. The release of inhibitory factors by tumor microenvironment hinders normal function of NK cells against tumor. To overcome this challenge, therapeutic strategies such as cytokine stimulation and genetic manipulation are being investigated to improve NK tumor-killing capacity. One of the promising approaches includes generation of more competent NK cells via ex vivo cytokines activation and proliferation. Cytokine-induced ML-NK demonstrated phenotypic alterations such as enhanced expression of activating receptors which help elevate their antitumor response. Previous preclinical studies showed enhanced cytotoxicity and IFNγ production in ML-NK cells compared to normal NK cells against malignant cells. Similar effects are shown in clinical studies in which MK-NK demonstrated encouraging results in treating hematological cancer. However, there is still a lack of in-depth studies using ML-NK in treating different types of tumors and cancers. With convincing preliminary response, this cell-based approach could be used to complement other therapeutic modalities to achieve better clinical outcomes.
    Matched MeSH terms: Cytokines/metabolism
  11. Pang T
    Med J Malaysia, 1993 Mar;48(1):9-11.
    PMID: 8341179
    Cytokines are central to the development of effective immunity against microbial pathogens and their beneficial effects in the control of a variety of infections of man and animals are well-documented. However, it appears that cytokines may also have detrimental effects in infections by actually enhancing microbial growth. These observations emphasise the fact that many successful pathogens possess mechanisms enabling them to evade the immune response and that caution needs to be exercised in using cytokines as therapeutic agents to control infections in various human diseases.
    Matched MeSH terms: Cytokines/immunology; Cytokines/metabolism; Cytokines/therapeutic use*
  12. Yunus MHM, Nordin A, Kamal H
    Medicina (Kaunas), 2020 Nov 16;56(11).
    PMID: 33207632 DOI: 10.3390/medicina56110614
    Osteoarthritis (OA) is the most well-known degenerative disease among the geriatric and is a main cause of significant disability in daily living. It has a multifactorial etiology and is characterized by pathological changes in the knee joint structure including cartilage erosion, synovial inflammation, and subchondral sclerosis with osteophyte formation. To date, no efficient treatment is capable of altering the pathological progression of OA, and current therapy is broadly divided into pharmacological and nonpharmacological measures prior to surgical intervention. In this review, the significant risk factors and mediators, such as cytokines, proteolytic enzymes, and nitric oxide, that trigger the loss of the normal homeostasis and structural changes in the articular cartilage during the progression of OA are described. As the understanding of the mechanisms underlying OA improves, treatments are being developed that target specific mediators thought to promote the cartilage destruction that results from imbalanced catabolic and anabolic activity in the joint.
    Matched MeSH terms: Cytokines
  13. Mehta M, Paudel KR, Shukla SD, Allam VSRR, Kannaujiya VK, Panth N, et al.
    J Control Release, 2021 09 10;337:629-644.
    PMID: 34375688 DOI: 10.1016/j.jconrel.2021.08.010
    Nuclear factor κB (NFκB) is a unique protein complex that plays a major role in lung inflammation and respiratory dysfunction. The NFκB signaling pathway, therefore becomes an avenue for the development of potential pharmacological interventions, especially in situations where chronic inflammation is often constitutively active and plays a key role in the pathogenesis and progression of the disease. NFκB decoy oligodeoxynucleotides (ODNs) are double-stranded and carry NFκB binding sequences. They prevent the formation of NFκB-mediated inflammatory cytokines and thus have been employed in the treatment of a variety of chronic inflammatory diseases. However, the systemic administration of naked decoy ODNs restricts their therapeutic effectiveness because of their poor pharmacokinetic profile, instability, degradation by cellular enzymes and their low cellular uptake. Both structural modification and nanotechnology have shown promising results in enhancing the pharmacokinetic profiles of potent therapeutic substances and have also shown great potential in the treatment of respiratory diseases such as asthma, chronic obstructive pulmonary disease and cystic fibrosis. In this review, we examine the contribution of NFκB activation in respiratory diseases and recent advancements in the therapeutic use of decoy ODNs. In addition, we also highlight the limitations and challenges in use of decoy ODNs as therapeutic molecules, cellular uptake of decoy ODNs, and the current need for novel delivery systems to provide efficient delivery of decoy ODNs. Furthermore, this review provides a common platform for discussion on the existence of decoy ODNs, as well as outlining perspectives on the latest generation of delivery systems that encapsulate decoy ODNs and target NFκB in respiratory diseases.
    Matched MeSH terms: Cytokines
  14. Nine MJ, Choudhury D, Hee AC, Mootanah R, Osman NAA
    Materials (Basel), 2014 Feb 10;7(2):980-1016.
    PMID: 28788496 DOI: 10.3390/ma7020980
    Wear debris, of deferent sizes, shapes and quantities, generated in artificial hip and knees is largely confined to the bone and joint interface. This debris interacts with periprosthetic tissue and may cause aseptic loosening. The purpose of this review is to summarize and collate findings of the recent demonstrations on debris characterization and their biological response that influences the occurrence in implant migration. A systematic review of peer-reviewed literature is performed, based on inclusion and exclusion criteria addressing mainly debris isolation, characterization, and biologic responses. Results show that debris characterization largely depends on their appropriate and accurate isolation protocol. The particles are found to be non-uniform in size and non-homogeneously distributed into the periprosthetic tissues. In addition, the sizes, shapes, and volumes of the particles are influenced by the types of joints, bearing geometry, material combination, and lubricant. Phagocytosis of wear debris is size dependent; high doses of submicron-sized particles induce significant level of secretion of bone resorbing factors. However, articles on wear debris from engineered surfaces (patterned and coated) are lacking. The findings suggest considering debris morphology as an important parameter to evaluate joint simulator and newly developed implant materials.
    Matched MeSH terms: Cytokines
  15. Mohd Zawawi Z, Kalyanasundram J, Mohd Zain R, Thayan R, Basri DF, Yap WB
    Int J Mol Sci, 2023 Mar 24;24(7).
    PMID: 37047115 DOI: 10.3390/ijms24076142
    The coronavirus disease 2019 (COVID-19) became a worldwide concern at the beginning of 2020 and has affected millions. Several previous studies revealed the impact of the imbalanced innate immune response on the progression of COVID-19 and its disease outcomes. High levels of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukins are produced readily by innate immune cells to fight Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) infections. Nonetheless, cytokine-mediated inflammatory events are also linked to detrimental lung injury and respiratory failure, which can result in deaths among COVID-19 patients. TNF-α is amongst the early cytokines produced to mediate proinflammatory responses and enhance immune cell infiltration in response to SARS-CoV-2 infections. In COVID-19, TNF-α-mediated inflammation can cause detrimental tissue damage and gradually promotes lung fibrosis, which later results in pneumonia, pulmonary edema, and acute respiratory distress syndrome. This review, therefore, aims to deliberate the immunomodulatory roles of TNF-α in promoting inflammation and its relation with COVID-19 morbidity and mortality. In addition, this review also proposes the potential of TNF-α as a biomarker for the prognosis of severe COVID-19 and its related complications and as a molecular target for anti-TNF-α therapy.
    Matched MeSH terms: Cytokines
  16. Gour A, Manhas D, Bag S, Gorain B, Nandi U
    Phytother Res, 2021 Aug;35(8):4258-4283.
    PMID: 33786876 DOI: 10.1002/ptr.7092
    Emergence of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, COVID-19, has become the global panic since December 2019, which urges the global healthcare professionals to identify novel therapeutics to counteract this pandemic. So far, there is no approved treatment available to control this public health issue; however, a few antiviral agents and repurposed drugs support the patients under medical supervision by compromising their adverse effects, especially in emergency conditions. Only a few vaccines have been approved to date. In this context, several plant natural products-based research studies are evidenced to play a crucial role in immunomodulation that can prevent the chances of infection as well as combat the cytokine release storm (CRS) generated during COVID-19 infection. In this present review, we have focused on flavonoids, especially epicatechin, epigallocatechin gallate, hesperidin, naringenin, quercetin, rutin, luteolin, baicalin, diosmin, ge nistein, biochanin A, and silymarin, which can counteract the virus-mediated elevated levels of inflammatory cytokines leading to multiple organ failure. In addition, a comprehensive discussion on available in silico, in vitro, and in vivo findings with critical analysis has also been evaluated, which might pave the way for further development of phytotherapeutics to identify the potential lead candidatetoward effective and safe management of the SARS-CoV-2 disease.
    Matched MeSH terms: Cytokines
  17. Hossain MM, Norazmi MN
    Biomed Res Int, 2013;2013:179174.
    PMID: 24350246 DOI: 10.1155/2013/179174
    Tuberculosis, an infectious disease caused by Mycobacterium tuberculosis (Mtb), remains a major cause of human death worldwide. Innate immunity provides host defense against Mtb. Phagocytosis, characterized by recognition of Mtb by macrophages and dendritic cells (DCs), is the first step of the innate immune defense mechanism. The recognition of Mtb is mediated by pattern recognition receptors (PRRs), expressed on innate immune cells, including toll-like receptors (TLRs), complement receptors, nucleotide oligomerization domain like receptors, dendritic cell-specific intercellular adhesion molecule grabbing nonintegrin (DC-SIGN), mannose receptors, CD14 receptors, scavenger receptors, and FCγ receptors. Interaction of mycobacterial ligands with PRRs leads macrophages and DCs to secrete selected cytokines, which in turn induce interferon-γ- (IFNγ-) dominated immunity. IFNγ and other cytokines like tumor necrosis factor-α (TNFα) regulate mycobacterial growth, granuloma formation, and initiation of the adaptive immune response to Mtb and finally provide protection to the host. However, Mtb can evade destruction by antimicrobial defense mechanisms of the innate immune system as some components of the system may promote survival of the bacteria in these cells and facilitate pathogenesis. Thus, although innate immunity components generally play a protective role against Mtb, they may also facilitate Mtb survival. The involvement of selected PRRs and cytokines on these seemingly contradictory roles is discussed.
    Matched MeSH terms: Cytokines/immunology*
  18. Appanna R, Wang SM, Ponnampalavanar SA, Lum LC, Sekaran SD
    Am J Trop Med Hyg, 2012 Nov;87(5):936-42.
    PMID: 22987650 DOI: 10.4269/ajtmh.2012.11-0606
    Plasma leakage in severe dengue has been postulated to be associated with skewed cytokine immune responses. In this study, the association of cytokines with vascular permeability in dengue patients was investigated. Human serum samples collected from 48 persons (13 with dengue fever, 29 with dengue hemorrhagic fever, and 6 healthy) were subjected to cytokines analysis by using Luminex Multiplex Technology. Selected serum samples from patients with dengue hemorrhagic fever sera and recombinant human cytokines were then tested for roles on inducing vascular permeability by treatment of human umbilical vein endothelial cells. Confocal immunofluorescence staining indicated morphologic alteration of human umbilical vein endothelial cells treated with serum samples from patients with dengue hemorrhagic fever compared with serum samples from healthy persons. The findings suggest that cytokines produced during dengue hemorrhagic infections could induce alterations in the vascular endothelium, which may play a fundamental role in the pathophysiology of dengue.
    Matched MeSH terms: Cytokines/blood*
  19. Balaram P, Kien PK, Ismail A
    Int J Med Microbiol, 2009 Mar;299(3):177-85.
    PMID: 18845475 DOI: 10.1016/j.ijmm.2008.08.004
    Bacterial persistence is of major concern worldwide in the control of a number of bacterial infections. The carriers who are asymptomatic act as reservoirs of the bacteria. Knowledge of the host response, of the persistence process, and of the potential of biological mediators as diagnostic markers is essential towards development of prophylactic and treatment modalities for these diseases. Immune mechanisms related to recognition and elimination of the bacteria play pivotal roles in the control of bacterial infections. The majority of the studies on bacterial infections detail the immune mechanisms in the active phase of infection, and reports on the immune status in carriers are scanty. The present review describes the role of recognition molecules (TLRs) and the immune mediators (cytokines) in bacterial persistence. It appears that the TLR-mediated induction of cytokine profiles differs in active infection and bacterial persistence, with an active Th1 response being beneficial for the clearance of a high load of bacteria and at the same time conducive for the persistence of low bacterial load. Immunomodulation aiming at stimulation of the immune responses should be carried out with care as it could give rise to a carrier state in individuals with low load of the bacteria.
    Matched MeSH terms: Cytokines/immunology*
  20. Lim KJ
    Malays J Pathol, 2003 Jun;25(1):1-13.
    PMID: 16196373
    Successful human reproduction remains an enigma, but this is slowly changing in the current era of expanding scientific knowledge. The discovery of various molecular factors such as adhesion molecules, proteases and cytokines have in recent years been at the forefront of medical research. The growing importance of immunology in particular has led to novel new immuno-modulatory therapies and increasing research into this new aspect of reproductive immunology may well prove to be the most important breakthrough in understanding the fundamentals of human reproduction. Implantation represents the first step in the complex interactions and processes involved in foetal-maternal interaction, which continues throughout pregnancy gestation and culminates in the birth of an infant. It is therefore vital that we understand the myriad processes controlling implantation in order to build a firm foundation for exploring reproductive immunology research in the new millennium. This review brings together and presents an overview of the potential roles of currently known molecular factors such as adhesion molecules, proteases, cytokines and its interaction with the maternal immune response, incorporating the findings of previous published research performed by the author on cytokines and reproductive immunology.
    Matched MeSH terms: Cytokines/metabolism*
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