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Immuno-Pathologic Basis of COVID-19 and the Management of Mild and Moderate Cases
Published in Srijan Goswami, Chiranjeeb Dey, COVID-19 and SARS-CoV-2, 2022
Debdeep Dasgupta, Srijan Goswami, Chiranjeeb Dey
The levels of IL-2, IL-7, IL-10, GSCF, IP-10, MCP1, MIP1a, and TNF-α in the blood of severely ill COVID-19 patients were also elevated. In short, the aberrant release of multiple cytokines appears to trigger a cytokine storm that produces immunopathogenic damage to tissues and organs, even while the immune response seeks to suppress and eradicate the virus (Wiersinga et al., 2020). Thus, it can be mentioned that the cytokine storm involves an immune response that causes collateral damage that may be greater than the immediate benefit of the immune response. Figure 7.5 and Table 7.1 represent specific organs involved and respective signs and symptoms of a systemic cytokine storm. Further studies should be done to find out the detailed pathogenesis of COVID-19 and cytokine storms (Wiersinga et al., 2020; Price et al., 2020; Dutta et al., 2020; Fajgenbaum and June, 2020; WHO, 2020a; Yuki et al., 2020; Kumar and Al Khodor, 2020; Parasher, 2021; Cevik et al., 2020; Abbas et al., 2016; Oliveira et al, 2020).
Anaphylaxis
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
IgG-mediated anaphylaxis has been demonstrated in mouse models and is postulated to be involved in anaphylaxis in humans to omalizumab or other monoclonal antibodies (Cox et al. 2007, Cheifetz et al. 2003). Immune complex/complement-mediated mechanisms may be involved in reactions to protamine and some other drugs. In reactions to Radio Contrast Media (RCM), RCM molecules may interact with the Fc portion of IgE or IgG already bound to mast cells or basophils, directly causing cross-linking and cell activation (Brockow and Ring 2011). Cytokine storm-like reactions, characterized by chills and fever, followed by hypotension, desaturation and cardiovascular collapse can occur with chimeric, humanized and human monoclonal antibodies and chemotherapy. Cytokine storm reactions are systemic inflammatory responses instigated by leukocyte release of pro-inflammatory cytokines (TNF-α, IL-1B, and IL-6) (Castells 2017).
Diagnosis and Treatment of COVID-19
Published in Wenguang Xia, Xiaolin Huang, Rehabilitation from COVID-19, 2021
The blood purification system includes plasma exchange, adsorption, perfusion, blood/plasma filtration, etc., which can remove inflammatory factors and block the “cytokine storm”, thereby reducing the damage to the body caused by the inflammatory response. It can be used for treatment of early and midstage cytokine storms in severe and critically severe patients.
Nanocurcumin formulation: a possible therapeutic agent for post COVID inflammatory syndrome
Published in Immunopharmacology and Immunotoxicology, 2022
Asha D. Kushwaha, K. P. Mishra, Mrinalini Singh, Lilly Ganju, Deepika Saraswat
Along with repurposing approved drugs [20], researchers are also actively seeking safe, natural products with antiviral pharmacological activity as potential prophylactic/therapeutics for COVID-19. There are no effective therapeutic candidates are available to curb cytokine release syndrome and its associated multi-organ damage and post-COVID inflammatory syndrome. Recently various review has published that curcumin/nano-curcumin has potential antiviral and immunomodulatory activity [21]. Curcumin (diferuloylmethane) is a phytonutrient found in turmeric (Curcuma longa) which is used as traditional medicine and dietary supplement, exhibit wide range of health benefits including anti-inflammation [22], cardiorespiratory regulation [23], respiratory [24] and immunomodulation [25,26].
Cytokine release syndrome in COVID-19: a major mechanism of morbidity and mortality
Published in International Reviews of Immunology, 2022
Yifan Que, Chao Hu, Kun Wan, Peng Hu, Runsheng Wang, Jiang Luo, Tianzhi Li, Rongyu Ping, Qinyong Hu, Yu Sun, Xudong Wu, Lei Tu, Yingzhen Du, Christopher Chang, Guogang Xu
The term "cytokine release syndrome” generally refers to a severely over-reactive immune system that progresses in an unregulated manner. We now know that unfettered cytokine release can occur in many conditions, including infections, but the first introduction of the term was in a paper by Ferrera et al describing the effects of cytokine dysregulation in graft-versus-host disease (GVHD) in 1993 [1]. Since the early 2000s, this term has also been used to describe abnormal release of large quantities of inflammatory mediators in infectious diseases caused by cytomegalovirus, Epstein-Barr virus, SARS-CoV and H5N1 influenza virus [2]. CRS may be a feature of infection related secondary hemophagocytic lymphohistiocytosis (HLH) and is thought to be associated with acute lung injury (ALI) and ARDS occurring in SARS and the Middle East Respiratory Syndrome (MERS). Although this term has gained recognition and acceptance in the medical community, the triggers and mechanisms that lead to CRS remain elusive.
Factors Involved in the onset of infection following bacterially contaminated platelet transfusions
Published in Platelets, 2021
Joels Wilson-Nieuwenhuis, Mohamed El-Mohtadi, Kurtis Edwards, Kathryn Whitehead, Nina Dempsey-Hibbert
Perhaps of more importance to our understanding of T-ABI and T-AS is the mechanism of immunological priming of platelets by bacteria prior to transfusion, and the platelet immunological responses elicited. Platelets express Pattern Recognition Receptors (PRRs), allowing direct recognition of Pathogen-Associated Molecular Patterns (PAMPs) on the invading microorganisms[111]. Ligation of these PRRs results in the release of a plethora of cytokines and chemokines from the platelets (including IL-1β, MIP-1α, RANTES, PF4, and TGF-β1, amongst others) that orchestrate immune responses (Figure 2). It is often this ‘cytokine storm’ that can exacerbate the symptoms of an immune reaction in the host (recipient)[112]. Interestingly, it has been shown that platelets are capable of differentiating different isoforms of bacterial LPS via TLRs, releasing different cytokine profiles and effector peptides depending on the stimulus [109,113]. Further, activated platelets can directly phagocytose bacteria [114–116], release AMPs, hydrogen peroxide, and other reactive oxygen species to ultimately kill pathogens[117].