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A Patent Landscape of the Emerging Nanomolecules for the Treatment of Leishmaniasis
Published in Chetan Keswani, Intellectual Property Issues in Nanotechnology, 2020
Priyanka Gautam, Abhishek Pathak, Sandeep Kumar Singh
Evasion of the parasite inside the host by adopting different strategies such as: (1) inactivation of effector molecules, one key strategy of immune evasion. The inhibition of complement activation is vital for many parasitic diseases. Antibodies can be rendered ineffective by highly specific proteases secreted by parasites, and cytotoxic effector molecules of immune cells, such as reactive oxygen and nitrogen products, are counteracted by increased production of detoxifying parasite enzymes (glutathione-S-transferase, glutathione peroxidase, catalase, etc. (Hewitson et al., 2009; Evering and Weiss, 2006) and, (2) by secreting specifically-active products, parasites can also interfere with the cytokine network, enabling them to modulate local systemic host immune responses. Macrophages are proposed primary host cells for Leishmania but the role of these cells has not been well characterized either in disease prevention or in progression independent of T cells. The effector functions of macrophages for Leishmania have always been described in a T-dependent manner (Gupta et al., 2013; Soulat and Bogdan, 2017). The fate of infected macrophages in T cell activation is not well known. This is because of the T cells come later during infection.
Osteomyelitis: Therapeutic Management using Nanomedicines
Published in Bhupinder Singh, Rodney J. Y. Ho, Jagat R. Kanwar, NanoBioMaterials, 2018
Ashish Ranjan, Teenu Sharma, Atul Jain, Sumant Saini, Shantanu Bandyopadhyay, Shreeniwas Singh, Bhupinder Singh
Antibiotics face mechanical and osmotic challenges during penetration in a biofilm, and with the progression of the diseased state, the biofilm-based bacteria become even more resilient (Donlan and Costerton, 2002). Biofilm formation allows for immune evasion via the persistence of a small colony variant bacteria within host cells (Grant and Hung, 2013). The persistor bacterial subpopulation is shielded from host defenses and antibiotics, thereby causing recurrence in chronic OSM after the initial infection (Ciampolini and Harding, 2000). OSM is characterized by subtle morphological changes in the bone structure as shown in Figure 11.5. Typically, the interruption of the blood supply to the bone and the death of bone cells is observed (Fondi and Franchi, 2007). Clinical symptoms of OSM is generally nonspecific, and can include, chronic pain, a persistent sinus tract or wound drainage, poor wound healing, malaise, and sometimes fever (Ciampolini and Harding, 2000).
Nanotechnology at the Frontier of Biology and Medicine
Published in Tuan Vo-Dinh, Nanotechnology in Biology and Medicine, 2017
A new photoimmunotherapy is based on the Synergistic Immuno Photothermal Nanotherapy (SYMPHONY) concept, which combines anti-PD-L1 immunotherapy with GNS-mediated PTT for a two-pronged treatment modality aimed at achieving three main goals: (1) GNS-mediated photothermal heating and ablation of the primary tumor, (2) induction of a strong immunogenic cell lethality, and (3) reversal of factors contributing to immune suppression. One therapeutic arm uses laser light to irradiate the primary tumor area where GNS have accumulated, resulting in generation of heat, which kills the primary tumor cells (Figure 1.6) [21]. Not only is there an immediate killing effect at the site treated with light, but this treatment also results in a general activation of the immune system, as evidenced by the fact that distant tumors that are not treated with light also show cancer cell killing. The second therapeutic arm involves administration of PD-L1 immune checkpoint blockade to disable cancer resistance. Many cancers exploit immune checkpoints to evade the anticancer immune response. Immune checkpoint inhibition is a promising immunotherapy that aims to reverse signals from immunosuppressive tumor microenvironments. Programmed death-ligand 1 (PD-L1), a protein overexpressed by many cancers, contributes to the suppression of the immune system and cancer immune evasion. PD-L1 binds to its receptor, PD-1 found on activated T cells, and inhibits cytotoxic T-cell function, thus escaping the immune response. To reverse tumor-mediated immunosuppression, therapeutic anti-PD-1/PD-L1 antibodies have been designed to block the PD-L1/PD-1 interaction. By suppressing this tumor defense, the tumor cells are now vulnerable to the killing action of immune system cells that have been primed against the tumor by the NP phototherapy [21].
Overview of methodologies for the culturing, recovery and detection of Campylobacter
Published in International Journal of Environmental Health Research, 2023
Marcela Soto-Beltrán, Bertram G. Lee, Bianca A. Amézquita-López, Beatriz Quiñones
Carbohydrate structures on the surface of the Campylobacter cell can serve to facilitate host cell adhesion, invasion, immune evasion, and pathogenicity (Table 2). In particular, galactosyltransferases genes cgtB and wlaN are associated with modification to the lipooligosaccharides on the surface of Campylobacter that trigger immune responses underpinning Guillain-Barré and Miller Fisher syndromes (Bolton 2015). Still, our knowledge of the interactions between the invading Campylobacter and the host cells has some gaps. In transcriptome experiments with almost 200 C. jejuni clinical isolates and a mammalian cell line (INT-407 cells), over 900 genes were upregulated compared to controls grown without a host (Kovács et al. 2020). In addition to the known virulence factors genes, other functional groups including transmembrane proteins, bacterial shape determinants, regulatory systems, energy systems, respiration, iron uptake, protein synthesis/modifications/secretion were also upregulated to support Campylobacter intracellular survival (Kovács et al. 2020). Future experiments involving gene inactivation, phenotypic assays, and transcriptomics with a diverse Campylobacter strain collection are thus needed to improve our understanding of Campylobacter pathogenesis.
A cellular automata model of chemotherapy effects on tumour growth: targeting cancer and immune cells
Published in Mathematical and Computer Modelling of Dynamical Systems, 2019
Fateme Pourhasanzade, S. H. Sabzpoushan
It can be also seen that except for p0= 0.5, the applied drug led to complete removal of immune cells from the tissue. If the base probability of division of proliferating tumour cells increases, the tumour growth will be faster. Therefore, the probability of killing tumour cells by immune system and the recruitment of immune cells will decrease due to the rules of the model. These results show the drug-induced immune evasion that enhanced tumour growth and failure of the host immune system in clinical trials. When the base probability of division of proliferating tumour cells is small, the tumour growth will be slower. We think antigenic changes created by individual mutations do not induce a strong immune response. Then, we applied chemotherapy which kills all types of cells, including immune cells. Since there is no recruitment, the number of immune cells will dramatically decrease in advance. If p0= 0.5; we can see that the recruitment of immune cells has occurred. Therefore, although the appropriate therapy is the one that shrinks the tumour volume, we prefer to have less damage in the normal and immune cells in the studied tissue. Similarly, the number of cancer non-stem cells decreases by applying a high half-life drug and decreasing p0.
Analysis of coronavirus envelope protein with cellular automata model
Published in International Journal of Parallel, Emergent and Distributed Systems, 2022
Raju Hazari, Parimal Pal Chaudhuri
High transmissibility of CoV-2, as per our analysis, is a combined effect of mutations on structural proteins (Envelope E, Spike S, and Nucleocapsid N) and the role played by non-structural proteins (nsps) and accessory proteins (ORFs). Viral life cycle in host cell is controlled by these proteins for replication and host immune evasion. The current paper is the first one in the series of three papers (we shall report) investigating the reason of highest transmissibility of SARS CoV-2 (2019) compared to SARS CoV(2003) and MERS (2012). The Cellular Automata enhanced Machine Learning (CAML) model is presented in the current paper to investigate the contribution of envelop protein for high transmissibility of SARS CoV-2. The ML framework is designed to learn the threshold limit of CA model parameter so that the list of mutants identified by the ML framework cover the mutants reported in published literature for in vitro/in vivo mutational studies on two case studies. The ML framework identifies the mutants for each of the two case studies reported in Section 6. Large difference in CA model parameter DCLVS between CoV-2 and CoV and (also CoV-2 and MERS) confirms difference in transmissibility of CoV-2 (2019) from that of CoV(2003) and MERS (2012). Further, CAML model also confirms same level of transmissibility for CoV-2 (2003) and MERS (2012). CAML platform can be employed to predict possible mutations in viral proteins. Six mutants predicted for CoV-2 are reported. We expect the results presented in our current and future papers will provide a platform to design therapeutic agents and robust vaccine with broader coverage to combat the CoV-2 epidemic. This epidemic is likely to persist for some more time due to new type of viral strains which may appear once the virus encounters vaccine administered on infected patients. Further, the CAML platform will provide an efficient workbench to develop therapeutic drug/vaccine for other types of viruses which may appear in future generating next pandemic situation.