ORCID Profile
0000-0003-4924-8982
Current Organisations
Macquarie University
,
UNSW Sydney
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Publisher: Elsevier BV
Date: 04-2022
Publisher: Frontiers Media SA
Date: 14-03-2018
Publisher: Royal Society of Chemistry (RSC)
Date: 2019
DOI: 10.1039/C9AN01300H
Abstract: A sandwich immunosensor was successfully developed for monitoring of interleukin-1β (IL-1β) in rat whole blood.
Publisher: Elsevier BV
Date: 03-2021
Publisher: Springer Science and Business Media LLC
Date: 15-12-2022
Publisher: IOSR Journals
Date: 2013
DOI: 10.9790/3008-0633038
Publisher: Elsevier BV
Date: 03-2017
DOI: 10.1016/J.JNEUROIM.2016.12.004
Abstract: Innate immunity relies on a set of germline-encoded receptors including Toll-like receptors (TLRs) that enable the host to discriminate between self and non-self. Multiple sclerosis (MS) is an autoimmune inflammatory demyelinating disease of the central nervous system (CNS). Infections are thought to play an important role in disease susceptibility. The role of innate immunity in MS has been recently appreciated. TLR2, a member of the TLR family, forms heterodimers with either TLR1 or TLR6 and detects a wide range of microbial as well as self-derived molecular structures. It may thus be important both in fighting infection and in activating autoimmunity. In this review, we discuss innate regulation of autoimmunity in MS with a focus on the role of TLR2 signaling.
Publisher: Elsevier BV
Date: 05-2022
Publisher: Springer Science and Business Media LLC
Date: 14-07-2023
DOI: 10.1186/S12967-023-04289-Y
Abstract: Immune checkpoint inhibitor therapy has revolutionized the clinical management of a erse range of cancer types, including advanced cutaneous melanoma. While immunotherapy targeting the PD-1/PD-L1 system has become standard of care, overall response rates remain unsatisfactory for most patients and there are no approved small molecule inhibitors of the PD-1/PD-L1 system. Flubendazole (FLU) is an anthelmintic that has been used to treat worm infections in humans and animals for decades. Here we tested the anti-cancer activity of systemically delivered FLU with suppression of PD-1 in immunocompetent mice. In C57BL/6J mice bearing subcutaneous B16F10 melanoma, FLU reduced both tumor growth and PD-1 protein levels without affecting levels of PD-L1. FLU’s suppression of PD-1 was accompanied by increased CD3 + T cell infiltration. Western blotting with extracts from human Jurkat T cells showed that FLU inhibited PD-1 protein expression, findings confirmed by flow cytometry. To gain mechanistic insights on FLU’s ability to suppress PD-1 protein levels, we performed bulk RNA sequencing on extracts of Jurkat T cells exposed to the benzimidazole for 4 h. From a pool of 14,475 genes there were 1218 differentially-expressed genes 687 with increased expression and 531 with decreased expression. Among the genes induced by FLU was the AP-1 family member, JUN and surprisingly, pdcd1 . KEGG pathway analysis showed FLU up-regulated genes over-represented in multiple pathways (p 0.01), the top hit being amoebiasis. FLU also affected the expression of genes in cancer-associated pathways, both through down-regulation and up-regulation. Gene set enrichment analysis revealed a large number of immunological signature gene sets correlated with FLU treatment, including gene sets associated with T cell differentiation, proliferation and function. The AP-1 inhibitor T5224 rescued PD-1 protein expression from inhibition by FLU. This study is the first to show that FLU can inhibit melanoma growth with PD-1 suppression in immunocompetent mice.
Publisher: Korean Diabetes Association
Date: 31-03-2022
Abstract: Diabetic peripheral neuropathy (DPN) affects over half of type 2 diabetes mellitus (T2DM) patients, with an urgent need for effective pharmacotherapies. While many rat and mouse models of T2DM exist, the phenotyping of DPN has been challenging with inconsistencies across laboratories. To better characterize DPN in rodents, a consensus guideline was published in 2014 to accelerate the translation of preclinical findings. Here we review DPN phenotyping in rat models of T2DM against the ‘Neurodiab’ criteria to identify uptake of the guidelines and discuss how DPN phenotypes differ between models and according to diabetes duration and sex. A search of PubMed, Scopus and Web of Science databases identified 125 studies, categorised as either diet and/or chemically induced models or transgenic/spontaneous models of T2DM. The use of diet and chemically induced T2DM models has exceeded that of transgenic models in recent years, and the introduction of the Neurodiab guidelines has not appreciably increased the number of studies assessing all key DPN endpoints. Combined high-fat diet and low dose streptozotocin rat models are the most frequently used and well characterised. Overall, we recommend adherence to Neurodiab guidelines for creating better animal models of DPN to accelerate translation and drug development.
Publisher: Springer New York
Date: 2016
DOI: 10.1007/978-1-4939-3335-8_23
Abstract: Experimental autoimmune encephalomyelitis (EAE) is the most relevant and commonly used animal model to study autoimmune demyelinating diseases like Multiple Sclerosis (MS). In EAE, the activation of CD4+ T-cells is considered to be the main trigger leading to inflammation and central nervous system (CNS) demyelination. Toll-like receptors (TLRs) are the most important and first class of pattern recognition receptors (PRRs) in innate immune system and play critical roles in initiating inflammatory responses and promoting adaptive immune responses due to their ability to recognize a wide range of pathogen associated molecular patterns (PAMPs) and being expressed in a wide range of cell types both in the innate and adaptive immune systems. Upon TLR stimulation by appropriate ligand, innate immune cells produce pro-inflammatory cytokines and can serve as antigen-presenting cells (APCs) to prime naïve T cells to recognize antigens. Thus, TLRs play an important role in linking the innate to the adaptive immune response. To date, large numbers of studies have been done to investigate the role of adaptive immunity in both EAE and MS but delineating the role of innate immunity in EAE received very little focus and appreciation taking into account that it might contribute to both the initiation and progression of the disease. Moreover, EAE is not only a model to study inflammatory demyelination in the CNS it is in general a model to study cell-mediated organ-specific autoimmune conditions. Roles of different TLRs were studied in relation to EAE and MS. More recently, some studies demonstrated the immune adjuvant properties of certain TLR ligands including TLR2, TLR4, and TLR9 in EAE. This chapter outlines different methods employed in our labs to investigate the role of TLRs in EAE model.
Publisher: Impact Journals, LLC
Date: 08-10-2023
Publisher: Elsevier BV
Date: 11-2020
Publisher: Frontiers Media SA
Date: 24-03-2021
Publisher: MDPI AG
Date: 28-08-2020
DOI: 10.3390/BIOMEDICINES8090313
Abstract: Peripheral neuropathy (PN) is a debilitating complication of diabetes that affects % of patients. Recent evidence suggests that obesity and metabolic disease, which often precede diabetes diagnosis, may influence PN onset and severity. We examined this in a translationally relevant model of prediabetes induced by a cafeteria (CAF) diet in Sprague–Dawley rats (n = 15 CAF versus n = 15 control). Neuropathy phenotyping included nerve conduction, tactile sensitivity, intraepidermal nerve fiber density (IENFD) and nerve excitability testing, an in vivo measure of ion channel function and membrane potential. Metabolic phenotyping included body composition, blood glucose and lipids, plasma hormones and inflammatory cytokines. After 13 weeks diet, CAF-fed rats demonstrated prediabetes with significantly elevated fasting blood glucose, insulin and impaired glucose tolerance as well as obesity and dyslipidemia. Nerve conduction, tactile sensitivity and IENFD did not differ however, superexcitability was significantly increased in CAF-fed rats. Mathematical modeling demonstrated this was consistent with a reduction in sodium–potassium pump current. Moreover, superexcitability correlated positively with insulin resistance and adiposity, and negatively with fasting high-density lipoprotein cholesterol. In conclusion, prediabetic rats over-consuming processed, palatable foods demonstrated altered nerve function that preceded overt PN. This work provides a relevant model for pathophysiological investigation of diabetic complications.
Publisher: American Diabetes Association
Date: 06-2020
DOI: 10.2337/DB20-530-P
Abstract: Diabetic peripheral neuropathy is a major complication of diabetes with complex and incompletely understood pathophysiology. We utilised a cafeteria-style diet (Caf) and low dose streptozotocin (STZ) to model varying degrees of hyperglycemia. Adult male Sprague-Dawley rats were ided into four groups: control (chow diet), prediabetic (Caf diet for 21 weeks), diet reversal (13 weeks Caf diet then 8 weeks chow all n=12) and type 2 diabetic (T2D - Caf+STZ 25mg/kg i.p, n=24). STZ was administered after 5 weeks of diet one week later, non-fasted blood glucose was 16.09 ± 1.19 [SEM] and 78% of T2D rats had glucose levels ≥10mmol/L. Metabolic phenotyping revealed significantly increased body weight, fat mass, fasting blood HDL cholesterol, plasma insulin and impaired glucose tolerance in both prediabetic and T2D rats compared to controls fasting glucose and HbA1c were significantly elevated only in T2D. Neuropathy phenotyping included sensory behavioural testing (thermal and mechanical nociceptive sensibility) and electrophysiology (nerve conduction studies and nerve excitability) which were assessed at two timepoints, early (8-11 weeks of diet) and late (17-19 weeks of diet). Nerve excitability abnormalities were present in prediabetes and T2D groups at the early stage (superexcitability p& .05) while changes in nerve conduction velocity and litude emerged later. Mechanical and thermal hypoalgesia was observed in prediabetic and T2D rats only at the late stage. Diet reversal improved body weight, fat mass, HDL, HbA1c, glucose clearance and mechanical nociception response, with no changes in nerve conduction and excitability. Together these data suggest that Caf diet combined with low dose STZ could be utilized to investigate the onset of neuropathological changes in T2D and assessment of subsequent peripheral neuropathy. M. Hossain: None. M.D. Kendig: None. B.M. Wild: None. M.J. Morris: None. R. Arnold: None. National Health and Medical Research Council of Australia (1126929, 1091006) Rebecca L. Cooper Foundation (RG160627)
Location: United Kingdom of Great Britain and Northern Ireland
Location: Australia
No related grants have been discovered for Md Jakir Hossain.