Review paperCytokines and the Koch phenomenon
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Cited by (76)
Preferred product characteristics for therapeutic vaccines to improve tuberculosis treatment outcomes: Key considerations from World Health Organization consultations
2020, VaccineCitation Excerpt :For initial proof-of-concept generation, the administration of vaccines at the end of treatment in individuals enrolled only after end of treatment delivered in a routine setting, may be an appropriate way of mitigating the generalizability question. The potential for the injection of antigenic components of Mtb precipitating a delayed-type (Type IV) hypersensitivity reaction, resulting in necrosis at the site of injection, in persons with Mtb infection or active TB [37] represents a possibility that must be considered when testing therapeutic TB vaccines on persons with active TB disease. The possibility of pulmonary and systemic inflammatory reactions [38] , and the breakdown of granuloma structure potentially resulting in Mtb dissemination should be considered and monitored.
Safety and immunogenicity of the M72/AS01<inf>E</inf> candidate tuberculosis vaccine in adults with tuberculosis: A phase II randomised study
2016, TuberculosisCitation Excerpt :The increased reactogenicity could also be caused by an extreme form of delayed hypersensitivity, similar to previously reported exaggerated reactions to the Mantoux test [36,37]. In contrast, the increased reactogenicity was unlikely to be due to Koch reactions, which correspond to disease exacerbations in M. tuberculosis-infected individuals upon newly exposure to mycobacterial compounds [33,38]. Although the immunological mechanism behind the Koch phenomenon is not known, the absence of AEs suggestive of pulmonary pathology indicated that the vaccine did not induce lung inflammation and that Koch reactions did not lie behind the large, self-resolving (without sequel) skin reactions in TB-infected patients [39].
Mycobacterium tuberculosis PE25/PPE41 protein complex induces necrosis in macrophages: Role in virulence and disease reactivation?
2014, FEBS Open BioCitation Excerpt :M. tuberculosis induces apoptosis in APCs through TNF-α, toll like receptors (TLRs), Fas or by altering the expression of Bax/Bcl-xL via an oxygen dependent pathway [1–4]. Virulent strains of M. tuberculosis have been known to develop mechanisms that resist host apoptotic cell death [5–8], however they are capable of inducing necrotic cell death, which helps in bacterial multiplication and dissemination [9–12]. On the other hand non-virulent strains like Mycobacterium bovis BCG and Mycobacterium smegmatis fail to induce necrosis of the host cells [10,11], suggesting that the factors released by the virulent strains interfere with the host cell death machinery for their release and subsequent infection of the neighboring (fresh) cells [8].
Nonlytic Fc-fused IL-7 synergizes with Mtb32 DNA vaccine to enhance antigen-specific T cell responses in a therapeutic model of tuberculosis
2013, VaccineCitation Excerpt :The discrepancy may reflect differences in pathogen (LCMV vs. MTB), concentration of IL-7 (5 μg of protein which daily injected for 25 days vs. 50 μg of DNA plasmid five times with two week intervals), and timing of treatment (contraction phase vs. under chemotherapy) [18,30–32]. Safety issues of TB therapeutic vaccines were raised after a subcutaneous injection of culture filtrate into tuberculosis patients evoked necrosis in established tuberculosis lesions at distant sites, which is now known as the “Koch reaction” and implicates the development of immunopathology due to severe inflammation reaction caused by exaggerated immune response to MTB [33]. It is therefore noteworthy to mention a recent study that evaluated the effects of recombinant human IL-7 (rhIL-7) in a sepsis model showed improved survival, indicating that diminished exacerbation was the result of highly activated immune cells [16].
N-3 Fatty acids uniquely affect anti-microbial resistance and immune cell plasma membrane organization
2011, Chemistry and Physics of LipidsCitation Excerpt :For example, IL-12 is critical for activation and migration of murine dendritic cells (Cooper et al., 1995) and TNFα is required for granuloma formation in mice (Flynn et al., 1995). On the other hand, TNFα is also associated with the histopathological damage during TB, mediating necrosis and tissue dysfunction (Rook and al Attiyah, 1991). Lipids serve as structural membrane components, a source of energy and regulators of the host immune response.
Early clinical trials with a new tuberculosis vaccine, MVA85A, in tuberculosis-endemic countries: issues in study design
2006, Lancet Infectious Diseases